Chronic stable angina overview: Difference between revisions

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Overview
Historical Perspective
Classification
Classic Chronic Stable Angina
Atypical Walk through Angina Mixed Angina Nocturnal Angina Postprandial Angina Cardiac Syndrome X Vasospastic Angina
Differentiating Chronic Stable Angina from Acute Coronary Syndromes
Pathophysiology
Epidemiology and Demographics
Risk Stratification
Pretest Probability of CAD in a Patient with Angina
Prognosis
Diagnosis
History and Symptoms
Physical Examination
Test Selection Guideline for the Individual Basis
Laboratory Findings
Electrocardiogram
Exercise ECG
Chest X Ray
Myocardial Perfusion Scintigraphy with Pharmacologic Stress
Myocardial Perfusion Scintigraphy with Thallium
Echocardiography
Exercise Echocardiography
Computed coronary tomography angiography(CCTA)
Positron Emission Tomography
Ambulatory ST Segment Monitoring
Electron Beam Tomography
Cardiac Magnetic Resonance Imaging
Coronary Angiography
Treatment
Medical Therapy
Revascularization
PCI
CABG
Hybrid Coronary Revascularization
Alternative Therapies for Refractory Angina
Transmyocardial Revascularization (TMR)
Spinal Cord Stimulation (SCS)
Enhanced External Counter Pulsation (EECP)
ACC/AHA Guidelines for Alternative Therapies in patients with Refractory Angina
Discharge Care
Patient Follow-Up
Rehabilitation
Secondary Prevention
Guidelines for Asymptomatic Patients
Noninvasive Testing in Asymptomatic Patients
Pharmacotherapy to Prevent MI and Death in Asymptomatic Patients
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Latest revision as of 00:00, 10 July 2017

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]; Associate Editor(s)-In-Chief: Maheep Singh Sangha, M.B.B.S.; Cafer Zorkun, M.D., Ph.D. [4]

Overview

Angina pectoris, commonly known as angina, is chest pain^[1] due to ischemia (a lack of blood and subsequent lack of oxygen supply) of the heart muscle. It is most often due to obstruction or spasm of the coronary arteries (the heart's blood vessels). Coronary artery disease, also referred to as atherosclerosis of the coronary arteries, is the most common cause of angina. The term derives from the Greek ankhon ("strangling") and the Latin pectus ("chest") meaning "a strangling feeling in the chest". In angina pectoris, symptomatic onset may include chest discomfort indicated by a feeling of tightness, heaviness, or pain in the chest cavity.

Historical Perspective

Chronic stable angina is a form of chest pain characterized by an insufficient blood flow to the myocardium of the heart to match myocardial energy demands (ischemia). The term angina was originally derived from the Greek word ankhon and the Latin word pectus, which when combined, loosely translates as "a strangling feeling in the chest". Attempts to classify this disease state began as early as the 4th century B.C., when Lucius Annaeus Seneca first described the symptoms he was experiencing as "to have any other malady is to be sick; to have this is to be dying". Throughout history many renowned researchers and health care professionals have contributed to the understanding, definition, and recognition of angina.

Classification

Chronic Stable Angina

Angina pectoris is a sensation of chest discomfort that is often described as: a feeling of tightness, heaviness, or pain. Angina pectoris is a characteristic of coronary heart disease. When it occurs chronically, this is referred to as stable angina.

Walk Through Angina

Walk through angina is the appearance of anginal chest discomfort early in the course of exertion which subsequently subsides despite continued exertion.

Mixed Angina

Mixed or variable threshold angina pectoris is a syndrome in which there is substantial variation in the magnitude of physical activity that induces anginal chest pain.

Nocturnal Angina

Nocturnal angina is the occurrence of anginal discomfort either during the first hours of sleep or during the early morning hours. It is speculated that discomfort caused during the first hours of sleep is due to increased venous return, whereas the discomfort caused during the early morning hours is due to increased vascular tone.

Postprandial Angina

Postprandial angina pectoris is anginal chest discomfort that occurs following meals. It is thought to be due to an increase in vascular tone or a reduction in coronary blood flow.

Cardiac Syndrome X

Cardiac syndrome X is angina associated with objective evidence of myocardial ischemia in the absence of epicardial coronary artery disease. Syndrome X has been hypothesized to be a disorder of the coronary microvasculature rather than the large caliber epicardial coronary arteries.

Vasospastic Angina

Coronary vasospasm is a multi-factorial, transient, and abrupt reduction of luminal diameter of an epicardial coronary artery due to inappropriate constriction of coronary smooth muscle that can generate distal ischemia. This may occur spontaneously or in the context of angioplasty, particularly if denudation of the endothelium or dissection occurs. In addition, the vasospasm can either be focal or multifocal (which compromises more than one vessel).

Differentiating Chronic Stable Angina from Urgent Conditions

Stable angina must be differentiated from unstable angina and acute coronary syndromes. If the pattern of angina is stable, this is termed chronic stable angina. If the magnitude, threshold or frequency of chest pain accelerates, this is termed an acute coronary syndrome.

Pathophysiology

The primary causes of myocardial ischemia in chronic stable angina are: fixed epicardial stenosis, spasm of the epicardial artery and/or microvascualar disease. The causation of angina is not mutually exclusive. Two or more causes may coexist in the same patient.

Epidemiology and Demographics

Coronary artery disease (CAD) remains the single leading cause of death in the United States. Stable angina is the initial manifestation of ischemic heart disease in approximately 50% of these patients.

Risk Stratification

The average mortality in patients with stable angina ranges from 1-3%. However, the prognosis varies widely depending on various factors such as: the duration and severity of symptoms, resting ECG abnormalities, abnormal left ventricular function and associated comorbidities.^[2]

Pretest Probability

Pretest probability is defined as the probability of the target disorder before the result of a diagnostic test is known. A number of studies have emphasized the importance of pretest probability of coronary artery disease (CAD).^[3] Once a thorough patient history and physical examination is complete, it is important to assess the probability of underlying CAD, as this helps both the physician and the patient to determine the next step in the diagnosis and treatment. In patients with chronic stable angina, the strongest predictors contributing to underlying significant CAD include: the age, gender and type of pain (typical, atypical) experienced.^[3]

Prognosis

Ischemic heart disease remains as the number one cause of mortality in developed countries. The prognosis of stable angina varies widely depending on severity of symptoms, extent of atherosclerosis and presence of other risk factors and co-morbidities. The presence of impaired left ventricular function is associated with a poor prognosis. Reduced LV function, number and location of stenoses, workload in METs calculated using Duke score are the strongest predictors of survival in patients with chronic stable angina.

Diagnosis

History and Symptoms

The name 'angina pain' can be thought of as a misnomer as patients often describe the sensation as discomfort rather than physical pain. The best method to characterize this discomfort/pain is through the 'PQRST system'.

Physical Examination

Among patients with chronic stable angina, the physical examination may be asymptomatic or characteristically normal. Patients that present with left ventricular dysfunction are associated with a poorer prognosis than patients who do not present with dysfunction. All patients should be examined carefully for the presence of rales and other signs of heart failure. The majority of patients present with history of either, chest pain or discomfort categorized as: typical or atypical. Typical presentation would include pain or discomfort in the front or anterior precordium. Atypical presentation can be more convoluted in presentation and involve a wide range of symptoms. For example, an atypical patient may present with dyspnea instead of chest pain and this is termed an angina equivalent. In addition to the historical presentation of chest pain or discomfort, the patient history should be extensively evaluated to include an assessment of cardiovascular risk factors. Physical examination may be normal or asymptomatic. In some cases, a physical examination may reveal heart failure. Additional findings can be important in understanding the onset of the condition. For instance, the presence of peripheral vascular disease may be associated with an increased risk of coronary artery disease (CAD).

Test Selection Guideline for the Individual Basis

Criteria for test selection hinges largely on the current disease state of the individual patient and subsequent level of fitness for testing. Potential diagnostic testing modalities include: exercise ECG, ECG at rest, exercise echocardiography, echocardiography at rest, and stress scintigraphy.

Laboratory Findings

In patients with chronic stable angina, initial laboratory investigations are used to: identify potential causes of ischemia, establish risk factors, and determine the overall prognosis for the patient. An initial laboratory test can provide a wide variety of clinical information. For instance, low hemoglobin levels can cause ischemia. Therefore, assessing hemoglobin as a part of complete blood count provides prognostic information.^[4] Biomarkers, such as troponin and CK-MB, are used to exclude myocardial injury. In assessment for risk factor stratification, all patients with ischemic heart disease are recommended to have a a standard round of blood work conducted including fasting plasma glucose levels and a complete lipid profile. Serum creatinine^[5] is used to assess renal dysfunction^[6] due to associated hypertension or diabetes and remains a negative prognostic factor. In patients with chronic stable angina, an elevation in fasting glucose^[7] independently predicts the adverse outcome. Recent research on NT-pro-BNP has demonstrated the ability to predict long-term mortality in patients with chronic stable angina independent of age, ventricular ejection fraction and other risk factors.^[8]

Electrocardiography

A resting 12-lead ECG is performed and recorded in all patients with suspected angina pectoris. However, a normal resting ECG does not exclude the diagnosis of ischemia. Abnormalites commonly observed on resting ECG include: ST-segment changes, left ventricular hypertrophy (LVH), left branch bundle blockage (LBBB), signs of coronary artery disease (CAD) such as previous myocardial infarction (MI) or abnormal repolarization patterns.^[9] An ECG recorded during pain helps to identify an underlying vasospasm.

Exercise EKG

In patients with chronic stable angina, exercise ECG is more sensitive and specific to identify inducible ischemia and to diagnose coronary artery disease.^[10] ECG abnormalities associated with MI include: down sloping of ST-segment depression or elevation, accompanying angina that occurs at a low workload during early stages of exercise and persistent for more than 3-minutes after exercise. The reliability of diagnosis is shown to improve with the evaluation of ST changes in relation to heart rate.^[11] Bruce protocol or treadmill (expressed in terms of METs) or bicycle ergometer (expressed in terms of watts) are used to detect MI. Exercise ECG test must be terminated on the achievement of maximal predicted heart rate and/or if the patient becomes symptomatic or develops pain with significant ST-segment changes. Exercise ECG test also provides prognostic stratification to evaluate the response to medical therapy or revascularization.^[12]

Chest X-Ray

Routine chest x-ray examination is important in the evaluation of patients with signs or symptoms of congestive heart failure,^[13] valvular heart disease, pericardial disease, or aortic dissection/aneurysm. The presentation of cardiomegaly, characterized by pulmonary congestion on a chest x-ray, is indicative of a poor prognosis for the patient.^[14]

Myocardial Perfusion Scintigraphy with Pharmacologic Stress

Pharmacologic stress testing using myocardial perfusion scintigraphy or echocardiography can be employed in patients with known or suspected angina pectoris who are unable to perform adequate exercise tests. These patients often owe their ineligibility status to associated conditions such as: peripheral vascular disease, musculoskeletal disorders, diseases of the lower extremities, severe obesity, or deconditioning. Pharmacologic stress testing is achieved with the infusion of either dobutamine in incremental dose, which acts by increasing myocardial oxygen consumption and thereby mimic effect of exercise, or with the use of coronary vasodilators such as adenosine or dipyridamole, which acts by differentiating regions based on perfusion. Stress imaging is of great value in the evaluation of patients with low pretest probability of CAD.^[15] However, in patients with LBBB, perfusion scintigraphy is shown to have poor diagnostic accuracy.^[16]

Myocardial Perfusion Scintigraphy with Thallium

In patients with baseline ECG abnormalities,a myocardial perfusion test can be used to localize the region of ischemia. Thallium-201 and technetium-99m are the two radio-labeled agents that are frequently used for the assessment of myocardial perfusion. Myocardial uptake of thallium-201 chloride is directly proportional to the regional myocardial blood flow and is dependent on the presence of viable myocardium. In patients with known CAD, a normal thallium stress test without a perfusion defect is indicative of a benign process and associated with excellent prognosis. Patients with a normal thallium scan are at low risk for CAD and subsequent coronary angiography is indicated only if the patient has a high probabilty Duke treadmill score. Contraindications for thallium stress test include the presence of arrhythmia, acute myocarditis, severe aortic stenosis and acute MI within the past 2 days.

Echocardiography

Echocardiography is useful to evaluate ventricular function^[17] and detect ischemia induced regional wall motion abnormality that occurs at rest, during exercise or with pharmacologic stress test. As a testing modality, two-dimensional echocardiography is often coupled with other testing modalities to detect regional wall motion abnormalities that most frequently occur during induced myocardial ischemia associated with coronary artery disease (CAD). Potential paired testing modalities include: upright treadmill exercise, supine bicycle ergometry, pacing, and pharmacologic stress, particularly with dobutamine. Patients with CAD may respond more adversely to testing modalities than their counterparts. Often, an adverse outcome such as the inability to perform a bicycle ergometry test or exercise treadmill protocol can be characterized as a poor prognostic factor.

Exercise Echocardiography

Stress echocardiography is echocardiography that is paired with different forms of stressors, such as exercise or pharmacological. Exercise stress echocardiography is the preferred stress echocardiography modality. However, it is not suitable for all patients and may not be feasible in populations that do not meet a minimum level of fitness. In patients who are ineligible for exercise stress echocardiography, pharmacological stress echocardiography can be a useful alternative. Common pharmacological stressors include: adenosine, dipyridamole, and dobutamine. As a testing modality, exercise echocardiography is noted as more sensitive, more specific and has a higher predictive value than exercise ECG. Exercise echocardiography can be helpful in the evaluation of regional wall motion response, location and extent of ischemia during stress in patients with MI. During exercise, the normal myocardium is hyperdynamic while in patients with MI, the ischemic myocardium is either akinetic or hypokinetic.

Positron Emission Tomography

Positron emission tomography is of particular value in the assessment of regional coronary blood flow reserve, myocardial perfusion, and the presence and extent of hibernating myocardium.

Ambulatory ST Segment Monitoring

Ambulatory ECG monitoring (Holter monitor) is used to detect major arrhythmias and myocardial ischemia occurring during normal activities. Ambulatory ECG monitoring adds very little prognostic value in patients with chronic stable angina, however, does play a role in the detection of major arrhythmias in patients with chronic stable angina and suspected vasospastic angina.

Electron Beam Tomography

The extent of coronary artery calcification directly correlates to the area of atheromatous plaque.^[18] Hence in patients with chest pain, coronary artery calcium (CAC) scoring is one of the factor to be considered in the risk assessment for coronary artery disease. The methods used for detection and quantification of CAC include electron beam computed tomography (EBCT) and multi-detector computed tomography (MDCT).^[19] Agatston score is a computed software that is commonly used to measure CAC based on the density and area of calcified plaques.^[20]

Cardiac Magnetic Resonance Imaging

Cardiac magnetic resonance imaging (CMRI) is a non-invasive test that is useful in the evaluation of overall coronary anatomy and function. CMRI also helps in the identification of inflammation,^[21] neovascularization^[22] and fibrous cap.^[23] It, therefore, holds the potential for plaque characterization.

Coronary Angiography

Coronary angiography is a gold standard test in the evaluation of severity of coronary artery disease and the possibility for revascularization. Coronary angiography is indicated in patients with a high pretest probability of CAD and in symptomatic patients with inconclusive initial noninvasive tests. Provocative testing with ergonovine during angiography may be useful in patients with vasospastic angina. Major complications such as death, MI and stroke associated with routine angiography is as low as 0.1% - 0.2%.^[24]

Treatment

Treatment of chronic stable angina aims at minimizing symptoms, reducing recurrent ischemia, improving the quality of life and improving prognosis by preventing MI and death. Treatment options include lifestyle modification, pharmacotherapy and revascularization that help in slowing the disease progression, preserving the endothelial function and preventing thrombosis.

Patients with single-vessel CAD may be started on initial pharmacologic therapy and if non-responsive or symptomatic despite on therapy, PCI may be a preferred alternative.

Patients with double-vessel CAD and with normal LV function may be started on initial medical management and in non-responders, PCI may be considered. However, the decision of PCI versus CABG depends on the coronary anatomy, LV function and the need for complete revascularization.

Patients with triple-vessel CAD or left main disease or reduced left ventricular function, CABG is the mainstay of management. However, in cases of mild symptoms or preserved LVEF in patients with triple-vessel disease, initial pharmacologic therapy or PCI may be tried.

Pharmacotherapy

The goal of the management of chronic stable angina is to improve the quality of life by decreasing the severity and frequency of symptoms and to decrease premature cardiovascular death caused by myocardial infarction or development of heart failure. The mainstays of the treatment of chronic stable angina are patient education, lifestyle changes and medical therapy.^[25] In patients with chronic stable angina, immediate symptomatic relief is achieved with short-acting sublingual nitrates and long term symptom relief is achieved with beta blockers as first line therapy, or calcium channel blockers and long-acting nitrates when beta blockers are contraindicated. Drugs that improve the quality of life and are associated with a better prognosis include: low dose aspirin, beta-blockers and ACEIs.

Anti-platelet Agents

Aspirin

In patients with ischemic heart disease, prophylactic low dose aspirin prevents arterial thrombosis by irreversible inactivation of platelet aggregation.^[26]^[27]^[28]^[29]

Dipyridamole

Dipyridamole is a pyrimidopyrimidine derivative with poor anti-thrombotic efficacy and therefore not recommended for anti-platelet therapy in patients with chronic stable angina.^[29] Dipyridamole may also exacerbate anginal symptoms due to coronary steal phenomenon.^[30]

Clopidogrel

Thienopyridines, such as clopidogrel and ticlopidine, selectively inhibit ADP-induced platelet aggregation and are used as an alternative to aspirin in patients with significant risk of arterial thrombosis.

Anti-anginal Agents

Nitrates

In patients with chronic stable angina, nitrates remain the mainstay of therapy. Organic nitrates are therapeutic precursors of endothelium-derived relaxing factor that produce their beneficial effects both, by decreasing myocardial oxygen requirements and by improving myocardial perfusion. The most commonly used nitrates are nitroglycerin, isosorbide dinitrate and isosorbide mononitrate. Short acting nitrates, such as sublingual nitroglycerin, are best suited to treat acute episodes of angina and are effective when used for situational prophylaxis. Long-acting nitrates help to reduce the frequency and severity of angina and may increase exercise tolerance in patients with stable angina.^[31]^[32]^[33] Nitrates at therapeutic doses do not affect coronary vascular resistance, thereby reducing the risk of myocardial ischemia due to coronary steal phenomena that is consistent with the use of dipyridamole and other short acting dihydropyridines.

Beta Blockers

In patients with stable angina, beta blockers are used as a first line of therapy for both, symptomatic relief^[34]^[35]^[36] and the prevention of ischemic events.^[37] The physiologic mechanism of benefit of this therapy is a marked reduction in myocardial oxygen consumption by reducing the heart rate and myocardial contractility. Selective beta-1 blockers are preferred to non-selective beta-blockers due to fewer associated side effects.^[33] The most commonly used selective beta-1 blockers are metoprolol, atenolol, and bisoprolol.

Calcium Channel Blockers

Calcium channel blockers (CCBs) consist of three sub-classes namely, dihydropyridines (e.g., nifedipine), phenylalkylamines (e.g., verapamil) and modified benzothiazepines (e.g., diltiazem). The beneficial anti-anginal effects of CCB include: reduction in the afterload consequent to systemic vasodilation as well as epicardial vessel vasodilation, enhancement of the coronary collateral flow with subsequent sub-endocardial perfusion due to the inhibition of calcium influx via L-type channels.^[38] Long-acting calcium channel blockers are an effective antianginal agent and are considered to be the first choice in post-MI patients with a contraindication to beta-blocker.^[39] Long-acting CCBs are also specifically used to control symptoms in patients with vasospastic angina.^[40] However short-acting CCBs, such as nifedipine, are avoided due to an increased risk of myocardial infarction and mortality.^[41]^[35]^[36]

Potassium Channel Openers

Nicorandil has both, anti-anginal effects due to nitrate-like and ATP-sensitive potassium channel activating properties and provides cardio-protective effects as well. Therefore, nicorandil usage in addition to standard anti-anginal therapy may be indicated in patients who are intolerant to beta-blocker therapy or in whom CCB monotherapy or combination therapy CCB is unsuccessful.^[42]^[43]^[44]

Newer Anti-anginal Agents

Ranolazine is a one of the newer FDA approved anti-anginal medication for management of chronic stable angina. Perhexiline is another anti-anginal, primarily used in Australia and New Zealand, being studied for use in the United States and UK. In patients with chronic stable angina, other effective agents with anti-anginal and anti-ischemic properties are ivabradine, trimetazidine and molsidomine.

ACEI/RAAS Blockers

Patients diagnosed with syndrome X and hypertension may have microvascular angina characterized by a reduced coronary vasodilator reserve and increased sympathetic drive. ACE inhibition in such patients may attenuate sympathetic coronary vasoconstriction, normalize thallium perfusion defects and reduce exercise-induced ischemia with subsequent increased myocardial oxygen supply.^[45]^[46] Based on the recent AHA and ESC guidelines, the recommended goal blood pressure in patients with atherosclerotic coronary vascular disease is less than 130/80 mm Hg.^[47]^[44]^[48]

Anti-lipid Agents

Statins by inhibiting HMG-CoA reductase subsequently reduce serum cholesterol levels and have been shown to be effective in the primary prevention of various hyperlipidemias and secondary prevention of ischemic heart disease.^[49]^[50] The most commonly used statins are simvastatin, atorvastatin, pravastatin and rosuvastatin. The incidence of major cardiovascular mortality was reduced by 30% with the use of simvastatin^[49] and pravastatin^[51]^[52] in patients with coronary artery disease and therefore may be used for both primary and secondary prevention.^[53]^[54]^[55]^[56] However, there are no trials specifically performed on patients with stable angina but they form a significant portion in other major trials studying the efficacy of lipid-lowering drugs on the overall mortality from cardiovascular events.^[57] In patients with low HDL and high triglycerides as an adjunctive to statin therapy, fibrates or niacin may be used.^[58]

Revasularization

The goal of the treatment of chronic stable angina is to reduce the symptoms, delay the progression of atherosclerosis, and prevent cardiovascular events. In order to achieve these goals, lifestyle modifications and medical therapy are the first line treatment. Revascularization is done to increase survival in specific conditions where the stenosis of the coronary arteries is anatomically and functionally significant and the symptoms are refractory to medical therapy. There are currently two well-established revascularization approaches for the treatment of chronic stable angina caused by coronary atherosclerosis: CABG and PCI. Since the introduction of coronary artery bypass surgery in 1967 and percutaneous transluminal coronary angioplasty (PTCA) in 1977, research has supported the effective usage of both strategies for treatment of patients with chronic stable angina. However, as with any treatment method, both methodologies have weaknesses. The choice between PCI and CABG is based upon anatomy and other factors such as left ventricular function and the presence or absence of diabetes. In general, PTCA is reserved for single or some cases of two vessel disease, while CABG is reserved for patients with two or three vessel disease or left main disease. With the availability of drug-eluting stents, PCI is increasingly being performed for many lesions including more complex ones.

PCI

Percutaneous coronary intervention for coronary artery disease first began in 1977, as a valuable mode of revascularization, wherein at the point of coronary stenosis a catheter-borne balloon is inflated to relieve the stenosis.

CABG

Coronary artery bypass surgery, also coronary artery bypass graft (CABG, pronounced "cabbage") surgery, and colloquially heart bypass or bypass surgery is a surgical procedure performed to relieve angina and reduce the risk of death from coronary artery disease. Arteries or veins from elsewhere in the patient's body are grafted to the coronary arteries to bypass atherosclerotic narrowings and improve the blood supply to the coronary circulation supplying the myocardium (heart muscle). This surgery is usually performed with the heart stopped, necessitating the usage of cardiopulmonary bypass; techniques are available to perform CABG on a beating heart, so-called "off-pump" surgery.

PCI vs Medical Therapy

An increased risk of mortality and morbidity is associated with untreated coronary artery disease.^[59] The main aim of therapy in patients with chronic stable angina is to alleviate symptoms, delay the progression of atherosclerosis, reduce the incidence of adverse coronary events and improve prognosis. This may be achieved with either initial medical therapy or with initial revascularization that includes percutaneous coronary intervention or coronary artery bypass grafting. Medical therapy alleviates symptom and improves prognosis; however, on the contrary, revascularization procedures provide symptomatic relief but generally does not improve mortality.

CABG vs Medical Therapy

It is well established that revascularization with CABG has shown to provide better symptomatic relief and improved survival rates in comparison to medical therapy in some patients with stable angina.^[60] However, the long term benefit of CABG is limited by the progression of atherosclerosis in other unbypassed vessels and stenosis of the graft itself.

PCI and CABG vs Medical Therapy

The Mass and Mass-II trials directly compared the effect of medical therapy, CABG and PCI for the management of chronic stable angina.^[61]^[62] However, there are a few reservations to the application of results from these studies as they did not include the current optimal strategies of therapy.

PCI vs CABG

PCI and CABG have become the standard of care in the management of patients with symptomatic coronary artery disease. Patients with multi-vessel disease, the overall mortality and freedom from myocardial infarction appear to be similar in both the treatment strategies; however, the need for repeat revascularization is significantly higher in patients who initially underwent PCI secondary to a higher incidence of restenosis.

Alternative Therapies for Refractory Angina

Transmyocardial Revascularization (TMR)

As the survival of patients with primary coronary events continue to increase, the number of patients presenting with refractory ischemia despite maximal medical therapy and unsuitable for further traditional revascularization techniques also continues to rise.^[63] Transmyocardial revascularization (TMR) is one of the emerging techniques that has been studied in many randomized trials and has shown to reduce the incidence of recurrent angina, increase exercise tolerance time and improve quality of life.^[63]^[64] TMR can be performed using either a laser beam or a percutaneous approach. However, only laser TMR is currently FDA approved.

Spinal Cord Stimulation (SCS)

In patients with refractory angina, spinal cord stimulation (SCS) is used to provide analgesia in the region of radiation of anginal-pain with the help an implanted device consisting of a stimulating electrode tip that extends into the dorsal epidural space, usually at the C7-T1 level.

Enhanced External Counter Pulsation (EECP)

Enhanced external counter pulsation (EECP) is another alternative therapy in the management of refractory angina. Most data from observational studies have demonstrated significant improvement in the exercise tolerance and reduction in the frequency of anginal symptoms as well as the use of nitroglycerin among patients treated with EECP.^[65]

Discharge Care

Patient Follow-Up

Ongoing follow-up of the patient with chronic stable angina is necessary to monitor symptoms and to optimize antianginal therapy. It is generally recommended that these patients be evaluated every 4-6 months during first year of diagnosis/initiation of therapy and annually thereafter. Based upon clinical judgement, if the patient is poorly responsive to therapy, if the episodes are severe or frequent, or if the patient is fragile with multiple co-morbidities, they may need to be seen more frequently.

During a follow-up visit, the patient should be asked about the frequency and severity of their anginal symptoms, their level of exercise capacity, whether they have been able to modify his/her risk factors, how well they are tolerating and complying with the therapy and whether he/she has developed new illnesses or co-morbidities.

Rehabilitation

Cardiac rehabilitation, also called cardiac rehab (CR), is a medically supervised program to help cardiac patients recover quickly and improve their overall well being. The main goal of rehabilitation is to help patients understand their disease and inculcate a regimen to stabilize and reduce, or even reverse the progression of cardiovascular disease. Cardiac rehab is often divided into phases that involve monitored exercise, counseling, emotional support, and education about lifestyle changes to reduce the risks of heart problems. It also helps reverse limitations experienced by patients who have suffered the adverse patho-physiologic and psychological consequences of cardiac events, thus, also helping patients to return to work early. Traditionally, cardiac rehabilitation has been provided to lower-risk patients who could exercise without physical limitations. However, rapid evolution in the management of CAD has now changed the demographics of the patients, so that, even patients with recent revascularization can be candidates for rehabilitation training.

Secondary Prevention

Smoking Cessation

The 1989 Surgeon General’s report, which assessed numerous case-control and cohort studies, reported that smoking increased cardiovascular disease mortality by 50%.^[66] Cigarette smoking, likely due to the hemodynamic consequences of sympathetic neural stimulation and systemic catecholamine release, plays an important role in the pathogenesis of coronary artery disease. Cigarette smoking also forms a major risk factor for acute cardiovascular events as it relates to an associated increase in blood coagulability.^[67] Hence, cigarette smoking is an important reversible risk factor in the pathogenesis of CAD and cessation of which improves prognosis and is associated with a substantial decrease in the risk of mortality.^[68]^[69]^[70] In patients with stable angina pectoris, nicotine replacement therapy has shown to be potentially beneficial despite the associated cardiovascular risks of nicotine, such as increase in heart rate with a small rise in blood pressure. Nicotine replacement therapy may be initiated as early as 2–3 days after acute myocardial infarction or cardiac arrhythmias.^[67] Additionally, nicotine patches have been used successfully in high-risk patients without any adverse effects such as aggravation of MI or arrhythmia.^[71]^[72]

Weight Management

Obesity is directly associated with the development of coronary artery disease (CAD) risk factors such as: hypertension, diabetes, reduced levels of HDL-C and elevated levels of triglyceride. Research has demonstrated that CAD risk factors contribute to a strong, graded, J-shaped univariable relationship between BMI and cardiovascular disease mortality. This increased mortality, when adjusted for age, self-reported smoking status, total cholesterol, and systolic blood pressure, maintained significant hazard ratios.^[73] Hence, in obese patients with CAD, weight reduction and/or dietary interventions may be warranted to reduce the incidence of above-mentioned risk factors and prevent future coronary events. Weight reduction is strongly recommended in patients with a BMI greater than 30 kg/m² and in patients with increased waist circumference (greater than 102 cms for men and 89 cms for women), characteristic of truncal obesity.^[47] Based on the plasma lipid abnormalities, adequate dietary modification may also be indicated.^[74]

Physical Activity

Based on an individual's ability to exercise and severity of the symptoms, physical activity may be indicated as a treatment. As a treatment, increased physical activity has demonstrated improvements in an individual's sustained exercise duration, reduced the frequency of symptoms and also provided beneficial effects on blood pressure, diabetes and the overall lipid profile. Before the initiation of an exercise regimen, an exercise test is indicated as a useful guide to assess the level of tolerance.^[75]

Lipid Management

In patients with established coronary artery disease, the recommended goal for total cholesterol is 130 mg/dl and LDL-C is 100 mg/dl, while the HDL-C and triglyceride concentrations serve as preferred markers for risk assessment.^[47] In patients with CAD, a fasting lipid-profile may be repeated at 5 year intervals to assess the overall risk of cardiovascular mortality and morbidity.^[76] Based on the individual’s lipid abnormalities, necessary dietary interventions and/or lipid-lowering agents are suggested to prevent the risk of future coronary events.^[74] A Mediterranean diet consisting of fruits, vegetables, lean meat and fish has also been shown to be beneficial. Omega-3 fatty acid supplementation may be indicated in patients with stable angina for secondary prevention, as it has been shown to reduce elevated triglycerides and also reduce the risk of sudden cardiac death.^[77]^[78]^[79]^[80] Fish consumption once a week has also been associated with reduced risk of mortality from coronary artery disease and, for this reason, is strongly recommended.^[81]^[82]

BP Control

The risk of progression of atherosclerosis is proportional to the increase in elevated blood pressure, hyperglycemia and dyslipidemia. Therefore, the control of hypertension, hyperglycemia and other features of metabolic syndrome deserves special attention in the prevention of mortality and morbidity due to coronary artery disease. In patients with established CAD, concomitant diabetes and/or renal dysfunction, the blood pressure goal is 130/80-85 and the decision to lower blood pressure depends on the total cardiovascular risk and the extent of target organ damage.^[76]^[83] Close monitoring and lifestyle changes may be indicated in low-risk patients without documented target organ damage. However, in high-risk patients with a sustained SBP of ≥140 mm Hg and/or DBP ≥90 mm Hg, the goal is to lower blood pressure less than 140/90 with the help of combined drug therapy and life style modification. Anti-hypertensive therapies that have shown to significantly reduce cardiovascular mortality and morbidity in patients with coronary artery disease include diuretics, beta-blockers, ACEIs, ARBs and calcium channel blockers.

Diabetes Control

Diabetes is one of the major modifiable risk factors for coronary artery disease. Maintaining a good glycemic control has been demonstrated to delay the disease progression in patients with impaired glycemic control and further prevent microvascular complications.^[83]^[84]^[85] In type 1 diabetics, appropriate insulin therapy and concomitant dietary modification may be required. However, in patients with type 2 diabetes, a multi-factorial intervention involving increased physical activity, weight reduction, dietary modification and/or drug therapy has shown to reduce the risk of overall cardiovascular and microvascular events by approximately 50%.^[76]^[86]

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Template:WikiDoc Sources

[urlMerckMedicus_:_Dorlands_Medical_Dictionary-1] "MerckMedicus : Dorland's Medical Dictionary". Retrieved 2009-01-09.

[pmid16415069-2] Daly CA, De Stavola B, Sendon JL, Tavazzi L, Boersma E, Clemens F et al. (2006) Predicting prognosis in stable angina--results from the Euro heart survey of stable angina: prospective observational study. BMJ 332 (7536):262-7. DOI:10.1136/bmj.38695.605440.AE PMID: 16415069

[pmid7258092-3] 3.0 ^3.1 Diamond GA, Forrester JS (1981) Improved interpretation of a continuous variable in diagnostic testing: probabilistic analysis of scintigraphic rest and exercise left ventricular ejection fractions for coronary disease detection. Am Heart J 102 (2):189-95. PMID: 7258092

[pmid15893180-4] Horne BD, Anderson JL, John JM, Weaver A, Bair TL, Jensen KR et al. (2005) Which white blood cell subtypes predict increased cardiovascular risk? J Am Coll Cardiol 45 (10):1638-43. DOI:10.1016/j.jacc.2005.02.054 PMID: 15893180

[pmid14712425-5] Shlipak MG, Stehman-Breen C, Vittinghoff E, Lin F, Varosy PD, Wenger NK et al. (2004) Creatinine levels and cardiovascular events in women with heart disease: do small changes matter? Am J Kidney Dis 43 (1):37-44. PMID: 14712425

[pmid12706933-6] Fried LF, Shlipak MG, Crump C, Bleyer AJ, Gottdiener JS, Kronmal RA et al. (2003) Renal insufficiency as a predictor of cardiovascular outcomes and mortality in elderly individuals. J Am Coll Cardiol 41 (8):1364-72. PMID: 12706933

[pmid14760320-7] Arcavi L, Behar S, Caspi A, Reshef N, Boyko V, Knobler H (2004) High fasting glucose levels as a predictor of worse clinical outcome in patients with coronary artery disease: results from the Bezafibrate Infarction Prevention (BIP) study. Am Heart J 147 (2):239-45. DOI:10.1016/j.ahj.2003.09.013 PMID: 14760320

[pmid15716560-8] Kragelund C, Grønning B, Køber L, Hildebrandt P, Steffensen R (2005) N-terminal pro-B-type natriuretic peptide and long-term mortality in stable coronary heart disease. N Engl J Med 352 (7):666-75. DOI:10.1056/NEJMoa042330 PMID: 15716560

[pmid10728321-9] Kléber AG (2000) ST-segment elevation in the electrocardiogram: a sign of myocardial ischemia. Cardiovasc Res 45 (1):111-8. PMID: 10728321

[pmid11075788-10] Ashley EA, Myers J, Froelicher V (2000) Exercise testing in clinical medicine. Lancet 356 (9241):1592-7. DOI:10.1016/S0140-6736(00)03138-X PMID: 11075788

[pmid6127094-11] Elamin MS, Boyle R, Kardash MM, Smith DR, Stoker JB, Whitaker W et al. (1982) Accurate detection of coronary heart disease by new exercise test. Br Heart J 48 (4):311-20. PMID: 6127094

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@@ Line 1: / Line 1: @@
-{{SI}}
+<div style="-webkit-user-select: none;">
-{{WikiDoc Cardiology Network Infobox}}
+{|class="infobox" style="position: fixed; top: 65%; right: 10px; margin: 0 0 0 0; border: 0; float: right;
-{{CMG}}
+|-
+| {{#ev:youtube|https://https://www.youtube.com/watch?v=zD9aXZY0pdY|350}}
+|-
+|}
+__NOTOC__
+{{Chronic stable angina}}
+{{CMG}}; {{AOEIC}} [[User:Maheep Sangha|Maheep Singh Sangha, M.B.B.S.]]; {{CZ}}
-'''Associate Editor-In-Chief:''' {{CZ}}
+==Overview==
+'''Angina pectoris''', commonly known as angina,  is [[chest pain]]<ref name="urlMerckMedicus : Dorlands Medical Dictionary">{{cite web |url=http://merckmedicus.com/pp/us/hcp/thcp_dorlands_content_split.jsp?pg=/ppdocs/us/common/dorlands/drlnd/one_04/000004934.htm#000004934 |title=MerckMedicus : Dorland's Medical Dictionary |format= |work= |accessdate=2009-01-09}}</ref> due to [[ischemia]] (a lack of blood and subsequent lack of [[oxygen]] supply) of the [[myocardium|heart muscle]]. It is most often due to obstruction or spasm of the [[coronary circulation|coronary arteries]] (the heart's blood vessels). [[Coronary heart disease|Coronary artery disease]], also referred to as atherosclerosis of the coronary arteries, is the most common cause of angina. The term derives from the [[Greek language|Greek]] ''ankhon'' ("strangling") and the [[Latin]] ''pectus'' ("chest") meaning "a strangling feeling in the chest". In [[angina pectoris]], symptomatic onset may include [[chest discomfort]] indicated by a feeling of tightness, heaviness, or pain in the chest cavity.
+==Historical Perspective==
+Chronic stable angina is a form of chest pain characterized by an insufficient blood flow to the [[myocardium]] of the heart to match myocardial energy demands ([[ischemia]]). The term angina was originally derived from the Greek word ''ankhon'' and the Latin word ''pectus'', which when combined, loosely translates as "a strangling feeling in the chest". Attempts to classify this disease state began as early as the 4th century B.C., when [[Lucius Annaeus Seneca]] first described the symptoms he was experiencing as "to have any other malady is to be sick; to have this is to be dying".  Throughout history many renowned researchers and health care professionals have contributed to the understanding, definition, and recognition of angina.
+==Classification==
+====Chronic Stable Angina====
+[[Angina pectoris]] is a sensation of chest discomfort that is often described as: a feeling of tightness, heaviness, or pain.  [[Angina pectoris]] is a characteristic of [[coronary heart disease]]. When it occurs chronically, this is referred to as [[stable angina]].
+====Walk Through Angina====
+Walk through angina is the appearance of anginal chest discomfort early in the course of exertion which subsequently subsides despite continued exertion.
+====Mixed Angina====
+Mixed or variable threshold angina pectoris is a syndrome in which there is substantial variation in the magnitude of physical activity that induces anginal chest pain.
+====Nocturnal Angina====
+Nocturnal angina is the occurrence of anginal discomfort either during the first hours of sleep or during the early morning hours. It is speculated that discomfort caused during the first hours of sleep is due to increased venous return, whereas the discomfort caused during the early morning hours is due to increased vascular tone.
+====Postprandial Angina====
+Postprandial angina pectoris is anginal chest discomfort that occurs following meals. It is thought to be due to an increase in vascular tone or a reduction in [[coronary blood flow]].
+====Cardiac Syndrome X====
+Cardiac syndrome X is [[Angina pectoris|angina]] associated with objective evidence of myocardial ischemia in the absence of epicardial  [[coronary artery disease]].  Syndrome X has been hypothesized to be a disorder of the coronary microvasculature rather than the large caliber epicardial coronary arteries.
+====Vasospastic Angina====
+Coronary vasospasm is a multi-factorial, transient, and abrupt reduction of [[Lumen (anatomy)|luminal]] diameter of an [[epicardial]] coronary artery due to inappropriate constriction of coronary [[smooth muscle]] that can generate distal [[ischemia]].  This may occur spontaneously or in the context of [[angioplasty]], particularly if denudation of the [[endothelium]] or [[dissection]] occurs.  In addition, the vasospasm can either be focal or multifocal (which compromises more than one vessel).
+==Differentiating Chronic Stable Angina from Urgent Conditions==
+Stable angina must be differentiated from unstable angina and [[acute coronary syndromes]].  If the pattern of angina is stable, this is termed chronic stable angina. If the magnitude, threshold or frequency of [[chest pain]] accelerates, this is termed an [[acute coronary syndrome]].
+==Pathophysiology==
+The primary causes of [[myocardial ischemia]] in chronic stable angina are: fixed epicardial stenosis, spasm of the epicardial artery and/or microvascualar disease. The causation of angina is not mutually exclusive. Two or more causes may coexist in the same patient.
+==Epidemiology and Demographics==
+[[Coronary artery disease|Coronary artery disease (CAD)]] remains the single leading cause of death in the United States. Stable angina is the initial manifestation of [[ischemic heart disease]] in approximately 50% of these patients.
+==Risk Stratification==
+The average [[mortality]] in patients with stable angina ranges from 1-3%. However, the [[prognosis]] varies widely depending on various factors such as: the duration and severity of [[symptom]]s, [[Chronic stable angina risk stratification electrocardiogram/chest x-ray|resting ECG abnormalities]], [[Chronic stable angina risk stratification based upon rest left ventricular function|abnormal left ventricular function]] and associated [[comorbidity|comorbidities]].<ref name="pmid16415069">Daly CA, De Stavola B, Sendon JL, Tavazzi L, Boersma E, Clemens F et al. (2006) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=16415069 Predicting prognosis in stable angina--results from the Euro heart survey of stable angina: prospective observational study.] ''BMJ'' 332 (7536):262-7. [http://dx.doi.org/10.1136/bmj.38695.605440.AE DOI:10.1136/bmj.38695.605440.AE] PMID: [http://pubmed.gov/16415069 16415069]</ref>
-{{Editor Help}}
+==Pretest Probability==
+Pretest probability is defined as the probability of the target disorder before the result of a diagnostic test is known.  A number of studies have emphasized the importance of pretest probability of [[coronary artery disease|coronary artery disease (CAD)]].<ref name="pmid7258092">Diamond GA, Forrester JS (1981) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=7258092 Improved interpretation of a continuous variable in diagnostic testing: probabilistic analysis of scintigraphic rest and exercise left ventricular ejection fractions for coronary disease detection.] ''Am Heart J'' 102 (2):189-95. PMID: [http://pubmed.gov/7258092 7258092]</ref> Once a thorough patient [[Chronic stable angina symptoms|history]] and [[Physical examination|physical examination]] is complete, it is important to assess the probability of underlying CAD, as this helps both the physician and the patient to determine the next step in the [[Chronic stable angina test selection guideline for the individual basis|diagnosis]] and [[Chronic stable angina treatment|treatment]]. In patients with [[Chronic stable angina definition|chronic stable angina]], the strongest predictors contributing to underlying significant [[CAD]] include: the age, gender and type of pain (typical, atypical) experienced.<ref name="pmid7258092">Diamond GA, Forrester JS (1981) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=7258092 Improved interpretation of a continuous variable in diagnostic testing: probabilistic analysis of scintigraphic rest and exercise left ventricular ejection fractions for coronary disease detection.] ''Am Heart J'' 102 (2):189-95. PMID: [http://pubmed.gov/7258092 7258092]</ref>
+==Prognosis==
-'''Click [[Chronic stable angina|''here'']] for the Chronic stable angina main page'''
+Ischemic heart disease remains as the number one cause of mortality in developed countries. The prognosis of stable angina varies widely depending on severity of symptoms, extent of atherosclerosis and presence of other risk factors and co-morbidities.  The presence of impaired left ventricular function is associated with a poor prognosis. Reduced LV function, number and location of stenoses, workload in METs calculated using Duke score are the strongest predictors of survival in patients with chronic stable angina.
+==Diagnosis==
+===History and Symptoms===
+The name 'angina pain' can be thought of as a misnomer as patients often describe the sensation as discomfort rather than physical pain. The best method to characterize this discomfort/pain is through the 'PQRST system'.
+===Physical Examination===
+Among patients with chronic stable angina, the physical examination may be asymptomatic or characteristically normal. Patients that present with left ventricular dysfunction are associated with a poorer prognosis than patients who do not present with dysfunction. All patients should be examined carefully for the presence of [[rales]] and other signs of [[heart failure]]. The majority of patients present with history of either, chest pain or discomfort categorized as: typical or atypical. Typical presentation would include pain or discomfort in the front or anterior precordium. Atypical presentation can be more convoluted in presentation and involve a wide range of symptoms. For example, an atypical patient may present with [[dyspnea]] instead of chest pain and this is termed an angina equivalent. In addition to the historical presentation of chest pain or discomfort, the patient history should be extensively evaluated to include an assessment of cardiovascular risk factors. Physical examination may be normal or asymptomatic. In some cases, a physical examination may reveal [[heart failure]]. Additional findings can be important in understanding the onset of the condition. For instance, the presence of [[peripheral vascular disease]] may be associated with an increased risk of [[coronary artery disease| coronary artery disease (CAD)]].
-==Overview==
+===Test Selection Guideline for the Individual Basis===
-'''Angina pectoris''', commonly known as '''angina''', is [[chest pain]]<ref name="urlMerckMedicus : Dorlands Medical Dictionary">{{cite web |url=http://merckmedicus.com/pp/us/hcp/thcp_dorlands_content_split.jsp?pg=/ppdocs/us/common/dorlands/drlnd/one_04/000004934.htm#000004934 |title=MerckMedicus : Dorland's Medical Dictionary |format= |work= |accessdate=2009-01-09}}</ref> due to [[ischemia]] (a lack of blood and hence [[oxygen]] supply) of the [[myocardium|heart muscle]], generally due to obstruction or spasm of the [[coronary circulation|coronary arteries]] (the heart's blood vessels). [[Coronary heart disease|Coronary artery disease]], the main cause of angina, is due to [[atherosclerosis]] of the cardiac arteries. The term derives from the [[Greek language|Greek]] ''ankhon'' ("strangling") and the [[Latin]] ''pectus'' ("chest"), and can therefore be translated as "a strangling feeling in the chest".  In [[angina pectoris]] the sensation of [[chest discomfort]] can be a feeling of tightness, heaviness, or pain.
+Criteria for test selection hinges largely on the current disease state of the individual patient and subsequent level of fitness for testing. Potential diagnostic testing modalities include: [[chronic stable angina exercise electrocardiography|exercise ECG]], [[chronic stable angina electrocardiography|ECG at rest]], [[Chronic stable angina exercise electrocardiography|exercise echocardiography]], [[Chronic stable angina exercise electrocardiography|echocardiography at rest]], and [[Chronic stable angina perfusion scintigraphy with pharmacologic stress|stress scintigraphy]].
+===Laboratory Findings===
+In patients with chronic stable angina, initial laboratory investigations are used to: identify potential causes of [[ischemia]], establish risk factors, and determine the overall prognosis for the patient. An initial laboratory test can provide a wide variety of clinical information. For instance, low hemoglobin levels can cause ischemia. Therefore, assessing hemoglobin as a part of complete blood count provides prognostic information.<ref name="pmid15893180">Horne BD, Anderson JL, John JM, Weaver A, Bair TL, Jensen KR et al. (2005) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=15893180 Which white blood cell subtypes predict increased cardiovascular risk?] ''J Am Coll Cardiol'' 45 (10):1638-43. [http://dx.doi.org/10.1016/j.jacc.2005.02.054 DOI:10.1016/j.jacc.2005.02.054] PMID: [http://pubmed.gov/15893180 15893180]</ref> Biomarkers, such as [[troponin]] and [[CK-MB]], are used to exclude myocardial injury. In assessment for [[Chronic stable angina risk stratification|risk factor stratification]], all patients with ischemic heart disease are recommended to have a a standard round of blood work conducted including fasting plasma glucose levels and a complete lipid profile. Serum creatinine<ref name="pmid14712425">Shlipak MG, Stehman-Breen C, Vittinghoff E, Lin F, Varosy PD, Wenger NK et al. (2004) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=14712425 Creatinine levels and cardiovascular events in women with heart disease: do small changes matter?] ''Am J Kidney Dis'' 43 (1):37-44. PMID: [http://pubmed.gov/14712425 14712425]</ref> is used to assess renal dysfunction<ref name="pmid12706933">Fried LF, Shlipak MG, Crump C, Bleyer AJ, Gottdiener JS, Kronmal RA et al. (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=12706933 Renal insufficiency as a predictor of cardiovascular outcomes and mortality in elderly individuals.] ''J Am Coll Cardiol'' 41 (8):1364-72. PMID: [http://pubmed.gov/12706933 12706933]</ref> due to associated [[hypertension]] or [[diabetes]] and remains a negative prognostic factor. In patients with chronic stable angina, an elevation in fasting glucose<ref name="pmid14760320">Arcavi L, Behar S, Caspi A, Reshef N, Boyko V, Knobler H (2004) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=14760320 High fasting glucose levels as a predictor of worse clinical outcome in patients with coronary artery disease: results from the Bezafibrate Infarction Prevention (BIP) study.] ''Am Heart J'' 147 (2):239-45. [http://dx.doi.org/10.1016/j.ahj.2003.09.013 DOI:10.1016/j.ahj.2003.09.013] PMID: [http://pubmed.gov/14760320 14760320]</ref> independently predicts the adverse outcome. Recent research on NT-pro-BNP has demonstrated the ability to predict long-term mortality in patients with chronic stable angina independent of age, ventricular ejection fraction and other risk factors.<ref name="pmid15716560">Kragelund C, Grønning B, Køber L, Hildebrandt P, Steffensen R (2005) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=15716560 N-terminal pro-B-type natriuretic peptide and long-term mortality in stable coronary heart disease.] ''N Engl J Med'' 352 (7):666-75. [http://dx.doi.org/10.1056/NEJMoa042330 DOI:10.1056/NEJMoa042330] PMID: [http://pubmed.gov/15716560 15716560]</ref>
+===Electrocardiography===
+A resting 12-lead ECG is performed and recorded in all patients with suspected angina pectoris. However, a normal resting ECG does not exclude the diagnosis of [[ischemia]]. Abnormalites commonly observed on resting ECG include: ST-segment changes, [[left ventricular hypertrophy|left ventricular hypertrophy (LVH)]], left branch bundle blockage ([[LBBB]]), signs of [[coronary artery disease|coronary artery disease (CAD)]] such as previous [[myocardial infarction|myocardial infarction (MI)]] or abnormal repolarization patterns.<ref name="pmid10728321">Kléber AG (2000) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=10728321 ST-segment elevation in the electrocardiogram: a sign of myocardial ischemia.] ''Cardiovasc Res'' 45 (1):111-8. PMID: [http://pubmed.gov/10728321 10728321]</ref> An ECG recorded during pain helps to identify an underlying [[Coronary vasospasm|vasospasm]].
+===Exercise EKG===
+In patients with chronic stable angina, exercise ECG is more sensitive and specific to identify inducible ischemia and to diagnose [[coronary artery disease]].<ref name="pmid11075788">Ashley EA, Myers J, Froelicher V (2000) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11075788 Exercise testing in clinical medicine.] ''Lancet'' 356 (9241):1592-7. [http://dx.doi.org/10.1016/S0140-6736(00)03138-X DOI:10.1016/S0140-6736(00)03138-X] PMID: [http://pubmed.gov/11075788 11075788]</ref> ECG abnormalities associated with [[MI]] include: down sloping of ST-segment depression or elevation, accompanying angina that occurs at a low workload during early stages of exercise and persistent for more than 3-minutes after exercise. The reliability of diagnosis is shown to improve with the evaluation of ST changes in relation to heart rate.<ref name="pmid6127094">Elamin MS, Boyle R, Kardash MM, Smith DR, Stoker JB, Whitaker W et al. (1982) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=6127094 Accurate detection of coronary heart disease by new exercise test.] ''Br Heart J'' 48 (4):311-20. PMID: [http://pubmed.gov/6127094 6127094]</ref> Bruce protocol or treadmill (expressed in terms of METs) or bicycle ergometer (expressed in terms of watts) are used to detect [[MI]]. Exercise ECG test must be terminated on the achievement of maximal predicted heart rate and/or if the patient becomes symptomatic or develops pain with significant ST-segment changes. Exercise ECG test also provides prognostic stratification to evaluate the response to medical therapy or revascularization.<ref name="pmid1875969">Mark DB, Shaw L, Harrell FE, Hlatky MA, Lee KL, Bengtson JR et al. (1991) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=1875969 Prognostic value of a treadmill exercise score in outpatients with suspected coronary artery disease.] ''N Engl J Med'' 325 (12):849-53. [http://dx.doi.org/10.1056/NEJM199109193251204 DOI:10.1056/NEJM199109193251204] PMID: [http://pubmed.gov/1875969 1875969]</ref>
+===Chest X-Ray===
+Routine chest x-ray examination is important in the evaluation of patients with signs or symptoms of [[congestive heart failure]],<ref name="pmid1825901">Chakko S, Woska D, Martinez H, de Marchena E, Futterman L, Kessler KM et al. (1991) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=1825901 Clinical, radiographic, and hemodynamic correlations in chronic congestive heart failure: conflicting results may lead to inappropriate care.] ''Am J Med'' 90 (3):353-9. PMID: [http://pubmed.gov/1825901 1825901]</ref> valvular heart disease, pericardial disease, or [[aortic dissection]]/[[aortic aneurysm|aneurysm]]. The presentation of cardiomegaly, characterized by  pulmonary congestion on a chest x-ray, is indicative of a poor prognosis for the patient.<ref name="pmid9651709">Hemingway H, Shipley M, Christie D, Marmot M (1998) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=9651709 Cardiothoracic ratio and relative heart volume as predictors of coronary heart disease mortality. The Whitehall study 25 year follow-up.] ''Eur Heart J'' 19 (6):859-69. PMID: [http://pubmed.gov/9651709 9651709]</ref>
+===Myocardial Perfusion Scintigraphy with Pharmacologic Stress===
+Pharmacologic stress testing using myocardial perfusion scintigraphy or echocardiography can be employed in patients with known or suspected [[Chronic stable angina definition|angina pectoris]] who are unable to perform adequate exercise tests. These patients often owe their ineligibility status to associated conditions such as: [[peripheral vascular disease]], musculoskeletal disorders, diseases of the lower extremities, severe [[obesity]], or deconditioning. Pharmacologic stress testing is achieved with the infusion of either [[dobutamine]] in incremental dose, which acts by increasing myocardial oxygen consumption and thereby mimic effect of exercise, or with the use of coronary vasodilators such as [[adenosine]] or [[dipyridamole]], which acts by differentiating regions based on perfusion. Stress imaging is of great value in the evaluation of patients with low pretest probability of [[CAD]].<ref name="pmid11174875">Shaw LJ, Hachamovitch R, Redberg RF (2000) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11174875 Current evidence on diagnostic testing in women with suspected coronary artery disease: choosing the appropriate test.] ''Cardiol Rev'' 8 (1):65-74. PMID: [http://pubmed.gov/11174875 11174875]</ref> However, in patients with [[LBBB]], perfusion scintigraphy is shown to have poor diagnostic accuracy.<ref name="pmid16002158">Vigna C, Stanislao M, De Rito V, Russo A, Santoro T, Fusilli S et al. (2006) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=16002158 Inaccuracy of dipyridamole echocardiography or scintigraphy for the diagnosis of coronary artery disease in patients with both left bundle branch block and left ventricular dysfunction.] ''Int J Cardiol'' 110 (1):116-8. [http://dx.doi.org/10.1016/j.ijcard.2005.05.068 DOI:10.1016/j.ijcard.2005.05.068] PMID: [http://pubmed.gov/16002158 16002158]</ref>
+===Myocardial Perfusion Scintigraphy with Thallium===
+In patients with baseline [[Chronic stable angina electrocardiography|ECG abnormalities]],a myocardial perfusion test can be used to localize the region of [[ischemia]]. Thallium-201 and technetium-99m are the two radio-labeled agents that are frequently used for the assessment of  myocardial perfusion. Myocardial uptake of thallium-201 chloride is directly proportional to the regional myocardial blood flow and is dependent on the presence of viable myocardium. In patients with known [[CAD]], a normal thallium stress test without a perfusion defect is indicative of a benign process and associated with excellent prognosis. Patients with a normal thallium scan are at low risk for [[CAD]] and subsequent coronary angiography is indicated only if the patient has a [[Chronic stable angina prognosis#Duke Score (Exercise Treadmill Test)|high probabilty Duke treadmill score]]. Contraindications for thallium stress test include the presence of [[arrhythmia]], acute [[myocarditis]], [[aortic stenosis|severe aortic stenosis]] and acute [[MI]] within the past 2 days.
+===Echocardiography===
+Echocardiography is useful to evaluate ventricular function<ref name="pmid9091535">Cheitlin MD, Alpert JS, Armstrong WF, Aurigemma GP, Beller GA, Bierman FZ et al. (1997) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=9091535 ACC/AHA guidelines for the clinical application of echocardiography: executive summary. A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (Committee on Clinical Application of Echocardiography). Developed in collaboration with the American Society of Echocardiography.] ''J Am Coll Cardiol'' 29 (4):862-79. PMID: [http://pubmed.gov/9091535 9091535]</ref> and detect ischemia induced regional wall motion abnormality that occurs at rest, during exercise or with pharmacologic stress test. As a testing modality, [[two-dimensional echocardiography]] is often coupled with other testing modalities to detect regional wall motion abnormalities that most frequently occur during induced [[myocardial ischemia]] associated with [[coronary artery disease|coronary artery disease (CAD)]]. Potential paired testing modalities include: upright treadmill exercise, supine bicycle ergometry, pacing, and pharmacologic stress, particularly with [[dobutamine]]. Patients with CAD may respond more adversely to testing modalities than their counterparts. Often, an adverse outcome such as the inability to perform a bicycle ergometry test or exercise treadmill protocol can be characterized as a poor prognostic factor.
+===Exercise Echocardiography===
+[[Stress echocardiography]] is echocardiography that is paired with different forms of stressors, such as exercise or pharmacological. Exercise stress echocardiography is the preferred stress echocardiography modality. However, it is not suitable for all patients and may not be feasible in populations that do not meet a minimum level of fitness. In patients who are ineligible for exercise stress echocardiography, pharmacological stress echocardiography can be a useful alternative. Common pharmacological stressors include: [[adenosine]], [[dipyridamole]], and [[dobutamine]]. As a testing modality, exercise echocardiography is noted as more sensitive, more specific and has a higher predictive value than [[Chronic stable angina exercise electrocardiography|exercise ECG]]. Exercise echocardiography can be helpful in the evaluation of regional wall motion response, location and extent of [[ischemia]]  during stress in patients with [[MI]]. During exercise, the normal myocardium is hyperdynamic while in patients with [[MI]], the ischemic myocardium is either akinetic or hypokinetic.
+===Positron Emission Tomography===
+[[Positron emission tomography]] is of particular value in the assessment of regional coronary blood flow reserve, myocardial perfusion, and the presence and extent of [[hibernating myocardium]].
+===Ambulatory ST Segment Monitoring===
+Ambulatory ECG monitoring (Holter monitor) is used to detect major [[arrhythmias]] and [[myocardial ischemia]] occurring during normal activities. Ambulatory ECG monitoring adds very little prognostic value in patients with chronic stable angina, however, does play a role in the detection of major arrhythmias in patients with chronic stable angina  and  suspected [[Coronary Vasospasm|vasospastic angina]].
+===Electron Beam Tomography===
+The extent of coronary artery calcification directly correlates to the area of atheromatous plaque.<ref name="pmid7554196">Rumberger JA, Simons DB, Fitzpatrick LA, Sheedy PF, Schwartz RS (1995) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=7554196 Coronary artery calcium area by electron-beam computed tomography and coronary atherosclerotic plaque area. A histopathologic correlative study.] ''Circulation'' 92 (8):2157-62. PMID: [http://pubmed.gov/7554196 7554196]</ref> Hence in patients with [[chest pain]], coronary artery calcium (CAC) scoring is one of the factor to be considered in the risk assessment for [[coronary artery disease]]. The methods used for detection and quantification of CAC include electron beam computed tomography (EBCT) and multi-detector computed tomography (MDCT).<ref name="pmid17239724">Greenland P, Bonow RO, Brundage BH, Budoff MJ, Eisenberg MJ, Grundy SM et al. (2007) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=17239724 ACCF/AHA 2007 clinical expert consensus document on coronary artery calcium scoring by computed tomography in global cardiovascular risk assessment and in evaluation of patients with chest pain: a report of the American College of Cardiology Foundation Clinical Expert Consensus Task Force (ACCF/AHA Writing Committee to Update the 2000 Expert Consensus Document on Electron Beam Computed Tomography) developed in collaboration with the Society of Atherosclerosis Imaging and Prevention and the Society of Cardiovascular Computed Tomography.] ''J Am Coll Cardiol'' 49 (3):378-402. [http://dx.doi.org/10.1016/j.jacc.2006.10.001 DOI:10.1016/j.jacc.2006.10.001] PMID: [http://pubmed.gov/17239724 17239724]</ref> Agatston score is a computed software that is commonly used to measure CAC based on the density and area of calcified plaques.<ref name="pmid2407762">Agatston AS, Janowitz WR, Hildner FJ, Zusmer NR, Viamonte M, Detrano R (1990) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=2407762 Quantification of coronary artery calcium using ultrafast computed tomography.] ''J Am Coll Cardiol'' 15 (4):827-32. PMID: [http://pubmed.gov/2407762 2407762]</ref>
+===Cardiac Magnetic Resonance Imaging===
+Cardiac magnetic resonance imaging (CMRI) is a non-invasive test that is useful in the evaluation of overall coronary anatomy and function. CMRI also helps in the identification of inflammation,<ref name="pmid11157694">Ruehm SG, Corot C, Vogt P, Kolb S, Debatin JF (2001) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11157694 Magnetic resonance imaging of atherosclerotic plaque with ultrasmall superparamagnetic particles of iron oxide in hyperlipidemic rabbits.] ''Circulation'' 103 (3):415-22. PMID: [http://pubmed.gov/11157694 11157694]</ref> neovascularization<ref name="pmid12591755">Kerwin W, Hooker A, Spilker M, Vicini P, Ferguson M, Hatsukami T et al. (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=12591755 Quantitative magnetic resonance imaging analysis of neovasculature volume in carotid atherosclerotic plaque.] ''Circulation'' 107 (6):851-6. PMID: [http://pubmed.gov/12591755 12591755]</ref> and fibrous cap.<ref name="pmid11997569">Wasserman BA, Smith WI, Trout HH, Cannon RO, Balaban RS, Arai AE (2002) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11997569 Carotid artery atherosclerosis: in vivo morphologic characterization with gadolinium-enhanced double-oblique MR imaging initial results.] ''Radiology'' 223 (2):566-73. PMID: [http://pubmed.gov/11997569 11997569]</ref> It, therefore, holds the potential for plaque characterization.
+===Coronary Angiography===
+Coronary angiography is a gold standard test in the evaluation of severity of [[coronary artery disease]] and the possibility for revascularization. Coronary angiography is indicated in patients with a high pretest probability of [[CAD]] and in symptomatic patients with inconclusive initial noninvasive tests. Provocative testing with ergonovine during angiography may be useful in patients with [[Chronic stable angina clinical subset- vasospastic angina|vasospastic angina]]. Major complications such as death, [[MI]] and [[stroke]] associated with routine angiography is as low as 0.1% - 0.2%.<ref name="pmid1742788">Noto TJ, Johnson LW, Krone R, Weaver WF, Clark DA, Kramer JR et al. (1991) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=1742788 Cardiac catheterization 1990: a report of the Registry of the Society for Cardiac Angiography and Interventions (SCA&I).] ''Cathet Cardiovasc Diagn'' 24 (2):75-83. PMID: [http://pubmed.gov/1742788 1742788]</ref>
+==Treatment==
+Treatment of chronic stable angina aims at minimizing symptoms, reducing recurrent [[ischemia]], improving the quality of life and improving [[Chronic stable angina prognosis|prognosis]] by preventing [[MI]] and death. Treatment options include [[Chronic stable angina secondary prevention|lifestyle modification]], [[Chronic stable angina medical therapy|pharmacotherapy]] and [[Chronic stable angina revascularization|revascularization]] that help in slowing the disease progression, preserving the endothelial function and preventing [[thrombosis]].
+Patients with [[CAD|single-vessel CAD]] may be started on initial [[Chronic stable angina medical therapy|pharmacologic therapy]] and if non-responsive or symptomatic despite on therapy, [[Chronic stable angina revascularization percutaneous coronary intervention|PCI]] may be a preferred alternative.
+Patients with [[CAD|double-vessel CAD]] and with [[EF|normal LV function]] may be started on initial [[Chronic stable angina medical therapy|medical management]] and in non-responders, [[Chronic stable angina revascularization percutaneous coronary intervention|PCI]] may be considered. However, the decision of [[Chronic stable angina revascularization percutaneous coronary intervention|PCI]] versus [[Chronic stable angina revascularization coronary artery bypass grafting|CABG]] depends on the coronary anatomy, [[EF|LV function]] and the need for complete revascularization.
+Patients with [[CAD|triple-vessel CAD]] or [[left main]] [[CAD|disease]] or reduced [[EF|left ventricular function]], [[Chronic stable angina revascularization coronary artery bypass grafting|CABG]] is the mainstay of management. However, in cases of mild symptoms or preserved [[EF|LVEF]] in patients with triple-vessel disease, initial [[Chronic stable angina medical therapy|pharmacologic therapy]] or [[Chronic stable angina revascularization percutaneous coronary intervention|PCI]] may be tried.
+===Pharmacotherapy===
+The goal of the management of [[Chronic stable angina definition|chronic stable angina]] is to improve the quality of life by decreasing the severity and frequency of symptoms and to decrease premature cardiovascular death caused by [[myocardial infarction]] or development of [[heart failure]]. The mainstays of the treatment of [[chronic stable angina]] are patient education, lifestyle changes and medical therapy.<ref name="Qaseem">Qaseem A, Fihn SD, Dallas P, et al. Management of patients with stable ischemic heart disease: Executive summary of a clinical practice guideline from the American College of Physicians, American College of Cardiology Foundation/American Heart Association/American Association for Thoracic Surgery/Preventive Cardiovascular Nurses Association/Society of Thoracic Surgeons. Ann Intern Med 2012. </ref> In patients with chronic stable angina, immediate symptomatic relief is achieved with [[Chronic stable angina nitrate therapy|short-acting sublingual nitrates]] and long term symptom relief is achieved with [[Chronic stable angina beta blocker therapy|beta blockers]] as first line therapy, or [[Chronic stable angina treatment calcium channel blockers|calcium channel blockers]] and [[Chronic stable angina nitrate therapy|long-acting nitrates]] when beta blockers are contraindicated. Drugs that improve the quality of life and are associated with a better prognosis include: [[Chronic stable angina treatment aspirin|low dose aspirin]], [[Chronic stable angina beta blocker therapy|beta-blockers]] and [[Chronic stable angina treatment angiotensin converting enzyme inhibitors (ACEI) and renin angiotensin aldosterone system blockers (RAAS blockers)|ACEIs]].
+====Anti-platelet Agents====
+=====Aspirin=====
+In patients with [[ischemic heart disease]], prophylactic low dose aspirin prevents arterial thrombosis by irreversible inactivation of platelet aggregation.<ref name="pmid8298418"> (1994) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=8298418 Collaborative overview of randomised trials of antiplatelet therapy--I: Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. Antiplatelet Trialists' Collaboration.] ''BMJ'' 308 (6921):81-106. PMID: [http://pubmed.gov/8298418 8298418]</ref><ref name="pmid14720534">Patrono C, Bachmann F, Baigent C, Bode C, De Caterina R, Charbonnier B et al. (2004) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=14720534 Expert consensus document on the use of antiplatelet agents. The task force on the use of antiplatelet agents in patients with atherosclerotic cardiovascular disease of the European society of cardiology.] ''Eur Heart J'' 25 (2):166-81. PMID: [http://pubmed.gov/14720534 14720534]</ref><ref name="pmid15383474">Patrono C, Coller B, FitzGerald GA, Hirsh J, Roth G (2004) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=15383474 Platelet-active drugs: the relationships among dose, effectiveness, and side effects: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy.] ''Chest'' 126 (3 Suppl):234S-264S. [http://dx.doi.org/10.1378/chest.126.3_suppl.234S DOI:10.1378/chest.126.3_suppl.234S] PMID: [http://pubmed.gov/15383474 15383474]</ref><ref name="pmid11786451">Antithrombotic Trialists' Collaboration (2002) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11786451 Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients.] ''BMJ'' 324 (7329):71-86. PMID: [http://pubmed.gov/11786451 11786451]</ref>
+=====Dipyridamole=====
+Dipyridamole is a pyrimidopyrimidine derivative with  poor anti-thrombotic efficacy and therefore not recommended for anti-platelet therapy in patients with chronic stable angina.<ref name="pmid11786451">Antithrombotic Trialists' Collaboration (2002) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11786451 Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients.] ''BMJ'' 324 (7329):71-86. PMID: [http://pubmed.gov/11786451 11786451]</ref> Dipyridamole may also exacerbate anginal symptoms due to coronary steal phenomenon.<ref name="pmid10860181">Kaufmann PA, Mandinov L, Seiler C, Hess OM (2000) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=10860181 Impact of exercise-induced coronary vasomotion on anti-ischemic therapy.] ''Coron Artery Dis'' 11 (4):363-9. PMID: [http://pubmed.gov/10860181 10860181]</ref>
+=====Clopidogrel=====
+Thienopyridines, such as [[clopidogrel]] and [[ticlopidine]], selectively inhibit ADP-induced platelet aggregation and are used as an alternative to [[aspirin]] in patients with significant risk of arterial thrombosis.
+====Anti-anginal Agents====
+=====Nitrates=====
+In patients with chronic stable angina, nitrates remain the mainstay of therapy. Organic nitrates are therapeutic precursors of endothelium-derived relaxing factor that produce their beneficial effects both, by decreasing myocardial oxygen requirements and by improving myocardial perfusion. The most commonly used nitrates are [[nitroglycerin]], [[isosorbide dinitrate]] and [[isosorbide mononitrate]]. Short acting nitrates, such as sublingual nitroglycerin, are best suited to treat acute episodes of angina and are effective when used for situational prophylaxis. Long-acting nitrates help to reduce the frequency and severity of angina and may increase exercise tolerance in patients with stable angina.<ref name="pmid7848896">Thadani U, Lipicky RJ (1994) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=7848896 Short and long-acting oral nitrates for stable angina pectoris.] ''Cardiovasc Drugs Ther'' 8 (4):611-23. PMID: [http://pubmed.gov/7848896 7848896]</ref><ref name="pmid9468470">Parker JD, Parker JO (1998) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=9468470 Nitrate therapy for stable angina pectoris.] ''N Engl J Med'' 338 (8):520-31. [http://dx.doi.org/10.1056/NEJM199802193380807 DOI:10.1056/NEJM199802193380807] PMID: [http://pubmed.gov/9468470 9468470]</ref><ref name="pmid10351980">Gibbons RJ, Chatterjee K, Daley J, Douglas JS, Fihn SD, Gardin JM et al. (1999)[http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=10351980ACC/AHA/ACP-ASIM guidelines for the management of patients with chronic stable angina: executive summary and recommendations. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients with Chronic Stable Angina).]''Circulation'' 99 (21):2829-48. PMID: [http://pubmed.gov/10351980 10351980]</ref> Nitrates at therapeutic doses do not affect coronary vascular resistance, thereby reducing the risk of [[myocardial ischemia]] due to [[Subclavian steal syndrome|coronary steal phenomena]] that is consistent with the use of [[Chronic stable angina treatment dipyridamole|dipyridamole]] and other short acting dihydropyridines.
+=====Beta Blockers=====
+In patients with stable angina, [[beta blockers]] are used as a first line of therapy for both, symptomatic relief<ref name="pmid8044945">Pepine CJ, Cohn PF, Deedwania PC, Gibson RS, Handberg E, Hill JA et al. (1994) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=8044945 Effects of treatment on outcome in mildly symptomatic patients with ischemia during daily life. The Atenolol Silent Ischemia Study (ASIST)] ''Circulation'' 90 (2):762-8. PMID: [http://pubmed.gov/8044945 8044945]</ref><ref name="pmid9652879">Savonitto S, Ardissino D (1998) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=9652879 Selection of drug therapy in stable angina pectoris.] ''Cardiovasc Drugs Ther'' 12 (2):197-210. PMID: [http://pubmed.gov/9652879 9652879]</ref><ref name="pmid10448616">Thadani U (1999) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=10448616 Treatment of stable angina.] ''Curr Opin Cardiol'' 14 (4):349-58. PMID: [http://pubmed.gov/10448616 10448616]</ref> and the prevention of ischemic events.<ref name="pmid7010157"> (1981) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=7010157 Timolol-induced reduction in mortality and reinfarction in patients surviving acute myocardial infarction.] ''N Engl J Med'' 304 (14):801-7. [http://dx.doi.org/10.1056/NEJM198104023041401 DOI:10.1056/NEJM198104023041401] PMID: [http://pubmed.gov/7010157 7010157]</ref> The physiologic mechanism of benefit of this therapy is a marked reduction in myocardial oxygen consumption by reducing the heart rate and myocardial contractility. Selective beta-1 blockers are preferred to non-selective beta-blockers due to fewer associated side effects.<ref name="pmid10351980">Gibbons RJ, Chatterjee K, Daley J, Douglas JS, Fihn SD, Gardin JM et al. (1999) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=10351980 ACC/AHA/ACP-ASIM guidelines for the management of patients with chronic stable angina: executive summary and recommendations. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients with Chronic Stable Angina).] ''Circulation'' 99 (21):2829-48. [http://circ.ahajournals.org/content/99/21/2829.full.pdf] PMID: [http://pubmed.gov/10351980 10351980]</ref> The most commonly used selective beta-1 blockers are [[metoprolol]], [[atenolol]], and [[bisoprolol]].
+=====Calcium Channel Blockers=====
+Calcium channel blockers (CCBs) consist of three sub-classes namely, dihydropyridines (e.g., [[nifedipine]]), phenylalkylamines (e.g., [[verapamil]]) and modified benzothiazepines (e.g., [[diltiazem]]). The beneficial anti-anginal effects of CCB include: reduction in the afterload consequent to systemic vasodilation as well as epicardial vessel vasodilation, enhancement of the coronary collateral flow with subsequent sub-endocardial perfusion due to the inhibition of calcium influx via L-type channels.<ref name="pmid12515758">Gibbons RJ, Abrams J, Chatterjee K, Daley J, Deedwania PC, Douglas JS et al. (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=12515758 ACC/AHA 2002 guideline update for the management of patients with chronic stable angina--summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Chronic Stable Angina).] ''Circulation'' 107 (1):149-58.[http://content.onlinejacc.org/cgi/reprint/41/1/159.pdf] PMID: [http://pubmed.gov/12515758 12515758]</ref> [[verapamil|Long-acting calcium channel blockers]] are an effective antianginal agent and are considered to be the first choice in post-MI patients with a contraindication to [[Chronic stable angina treatment beta blockers|beta-blocker]].<ref name="pmid1884725">Karlson BW, Emanuelsson H, Herlitz J, Nilsson JE, Olsson G (1991) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=1884725 Evaluation of the antianginal effect of nifedipine: influence of formulation dependent pharmacokinetics.] ''Eur J Clin Pharmacol'' 40 (5):501-6. PMID: [http://pubmed.gov/1884725 1884725]</ref> Long-acting CCBs are also specifically used to control symptoms in patients with [[Coronary Vasospasm|vasospastic angina]].<ref name="pmid1959210">Waters D (1991) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=1959210 Proischemic complications of dihydropyridine calcium channel blockers.] ''Circulation'' 84 (6):2598-600. PMID: [http://pubmed.gov/1959210 1959210]</ref> However [[dihydropyridines|short-acting CCBs]], such as [[nifedipine]], are avoided due to an increased risk of myocardial infarction and mortality.<ref name="pmid15536108">Nissen SE, Tuzcu EM, Libby P, Thompson PD, Ghali M, Garza D et al. (2004) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=15536108 Effect of antihypertensive agents on cardiovascular events in patients with coronary disease and normal blood pressure: the CAMELOT study: a randomized controlled trial.] ''JAMA'' 292 (18):2217-25. [http://dx.doi.org/10.1001/jama.292.18.2217 DOI:10.1001/jama.292.18.2217] PMID: [http://pubmed.gov/15536108 15536108]</ref><ref name="pmid9652879">Savonitto S, Ardissino D (1998) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=9652879 Selection of drug therapy in stable angina pectoris.] ''Cardiovasc Drugs Ther'' 12 (2):197-210. PMID: [http://pubmed.gov/9652879 9652879]</ref><ref name="pmid10448616">Thadani U (1999) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=10448616 Treatment of stable angina.] ''Curr Opin Cardiol'' 14 (4):349-58. PMID: [http://pubmed.gov/10448616 10448616]</ref>
+=====Potassium Channel Openers=====
+[[Nicorandil]] has both, anti-anginal effects due to [[Chronic stable angina treatment nitrates#Mechanisms of benefit|nitrate-like]] and ATP-sensitive potassium channel activating properties and provides cardio-protective effects as well. Therefore, nicorandil usage in addition to standard [[Chronic stable angina medical therapy| anti-anginal therapy]] may be indicated in patients who are intolerant to [[Chronic stable angina treatment beta blockers|beta-blocker]] therapy or in whom [[Chronic stable angina treatment calcium channel blockers|CCB]] monotherapy or combination therapy [[Chronic stable angina treatment calcium channel blockers|CCB]] is unsuccessful.<ref name="pmid11085202">Markham A, Plosker GL, Goa KL (2000) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11085202 Nicorandil. An updated review of its use in ischaemic heart disease with emphasis on its cardioprotective effects.] ''Drugs'' 60 (4):955-74. PMID: [http://pubmed.gov/11085202 11085202]</ref><ref name="pmid14658416"> (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=14658416 Nicorandil for angina--an update.] ''Drug Ther Bull'' 41 (11):86-8. PMID: [http://pubmed.gov/14658416 14658416]</ref><ref name="pmid16735367">{{cite journal| author=Fox K, Garcia MA, Ardissino D, Buszman P, Camici PG, Crea F et al.| title=Guidelines on the management of stable angina pectoris: executive summary: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology. | journal=Eur Heart J | year= 2006 | volume= 27 | issue= 11 | pages= 1341-81 | pmid=16735367 | doi=10.1093/eurheartj/ehl001 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16735367}}</ref>
+=====Newer Anti-anginal Agents=====
+[[Ranolazine]] is a one of the newer FDA approved anti-anginal medication for management of chronic stable angina. [[Perhexiline]] is another anti-anginal, primarily used in Australia and New Zealand, being studied for use in the United States and UK. In patients with chronic stable angina, other effective agents with anti-anginal and anti-ischemic properties are [[ivabradine]], [[trimetazidine]] and [[molsidomine]].
+====ACEI/RAAS Blockers====
+Patients diagnosed with [[syndrome X]] and [[hypertension]] may have microvascular angina characterized by a reduced coronary vasodilator reserve and increased sympathetic drive. [[ACE inhibitors|ACE inhibition]] in such patients may attenuate sympathetic coronary vasoconstriction, normalize [[Chronic stable angina myocardial perfusion scintigraphy|thallium perfusion defects]] and reduce [[Chronic stable angina exercise electrocardiography|exercise-induced ischemia]] with subsequent increased myocardial oxygen supply.<ref name="pmid8113548">Kaski JC, Rosano G, Gavrielides S, Chen L (1994) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=8113548 Effects of angiotensin-converting enzyme inhibition on exercise-induced angina and ST segment depression in patients with microvascular angina.] ''J Am Coll Cardiol'' 23 (3):652-7. PMID: [http://pubmed.gov/8113548 8113548]</ref><ref name="pmid11216965">van den Heuvel AF, Dunselman PH, Kingma T, Verhorst P, Boomsma F, van Gilst WH et al. (2001) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11216965 Reduction of exercise-induced myocardial ischemia during add-on treatment with the angiotensin-converting enzyme inhibitor enalapril in patients with normal left ventricular function and optimal beta blockade.] ''J Am Coll Cardiol'' 37 (2):470-4. PMID: [http://pubmed.gov/11216965 11216965]</ref> Based on the recent [[ACC AHA guidelines classification scheme|AHA]] and [[European society of cardiology|ESC]] guidelines, the recommended goal [[blood pressure]] in patients with [[CAD|atherosclerotic coronary vascular disease]] is less than 130/80 mm Hg.<ref name="pmid17998462">Fraker TD, Fihn SD, Gibbons RJ, Abrams J, Chatterjee K, Daley J et al. (2007)[http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=17998462 2007 chronic angina focused update of the ACC/AHA 2002 Guidelines for the management of patients with chronic stable angina: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Writing Group to develop the focused update of the 2002 Guidelines for the management of patients with chronic stable angina.] ''Circulation'' 116 (23):2762-72.[http://content.onlinejacc.org/cgi/reprint/50/23/2264.pdf] PMID: [http://pubmed.gov/17998462 17998462]</ref><ref name="pmid16735367">{{cite journal| author=Fox K, Garcia MA, Ardissino D, Buszman P, Camici PG, Crea F et al.| title=Guidelines on the management of stable angina pectoris: executive summary: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology. | journal=Eur Heart J | year= 2006 | volume= 27 | issue= 11 | pages= 1341-81 | pmid=16735367 | doi=10.1093/eurheartj/ehl001 | pmc= |url=url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16735367 [http://www.escardio.org/guidelines-surveys/esc-guidelines/GuidelinesDocuments/guidelines-angina-FT.pdf]}} </ref><ref name="pmid17502569">Rosendorff C, Black HR, Cannon CP, Gersh BJ, Gore J, Izzo JL et al. (2007) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=17502569 Treatment of hypertension in the prevention and management of ischemic heart disease: a scientific statement from the American Heart Association Council for High Blood Pressure Research and the Councils on Clinical Cardiology and Epidemiology and Prevention.] ''Circulation'' 115 (21):2761-88. [http://dx.doi.org/10.1161/CIRCULATIONAHA.107.183885 DOI:10.1161/CIRCULATIONAHA.107.183885] PMID: [http://pubmed.gov/17502569 17502569]</ref>
+====Anti-lipid Agents====
+[[Statins]] by inhibiting [[HMG-CoA reductase]] subsequently reduce serum cholesterol levels and have been shown to be effective in the primary prevention of various [[Hyperlipidemia|hyperlipidemias]] and secondary prevention of [[ischemic heart disease]].<ref name="pmid7968073"> (1994) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=7968073 Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S)] ''Lancet'' 344 (8934):1383-9. PMID: [http://pubmed.gov/7968073 7968073]</ref><ref name="pmid16214597">Baigent C, Keech A, Kearney PM, Blackwell L, Buck G, Pollicino C et al. (2005) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=16214597 Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins.] ''Lancet'' 366 (9493):1267-78. [http://dx.doi.org/10.1016/S0140-6736(05)67394-1 DOI:10.1016/S0140-6736(05)67394-1] PMID: [http://pubmed.gov/16214597 16214597]</ref> The most commonly used statins are [[simvastatin]], [[atorvastatin]], [[pravastatin]] and [[rosuvastatin]]. The incidence of major cardiovascular mortality was reduced by 30% with the use of [[simvastatin]]<ref name="pmid7968073"> (1994) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=7968073 Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S)] ''Lancet'' 344 (8934):1383-9. PMID: [http://pubmed.gov/7968073 7968073]</ref> and [[pravastatin]]<ref name="pmid11034935">Sacks FM, Tonkin AM, Shepherd J, Braunwald E, Cobbe S, Hawkins CM et al. (2000) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11034935 Effect of pravastatin on coronary disease events in subgroups defined by coronary risk factors: the Prospective Pravastatin Pooling Project.] ''Circulation'' 102 (16):1893-900. PMID: [http://pubmed.gov/11034935 11034935]</ref><ref name="pmid9841303"> (1998) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=9841303 Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group.] ''N Engl J Med'' 339 (19):1349-57. [http://dx.doi.org/10.1056/NEJM199811053391902 DOI:10.1056/NEJM199811053391902] PMID: [http://pubmed.gov/9841303 9841303]</ref> in patients with [[coronary artery disease]] and therefore may be used for both primary and secondary prevention.<ref name="pmid15358046">Grundy SM, Cleeman JI, Merz CN, Brewer HB, Clark LT, Hunninghake DB et al. (2004) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=15358046 Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines.] ''J Am Coll Cardiol'' 44 (3):720-32. [http://dx.doi.org/10.1016/j.jacc.2004.07.001 DOI:10.1016/j.jacc.2004.07.001] PMID: [http://pubmed.gov/15358046 15358046]</ref><ref name="pmid11277825">Schwartz GG, Olsson AG, Ezekowitz MD, Ganz P, Oliver MF, Waters D et al. (2001) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11277825 Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes: the MIRACL study: a randomized controlled trial.] ''JAMA'' 285 (13):1711-8. PMID: [http://pubmed.gov/11277825 11277825]</ref><ref name="pmid12686036">Sever PS, Dahlöf B, Poulter NR, Wedel H, Beevers G, Caulfield M et al. (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=12686036 Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial--Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial.] ''Lancet'' 361 (9364):1149-58. [http://dx.doi.org/10.1016/S0140-6736(03)12948-0 DOI:10.1016/S0140-6736(03)12948-0] PMID: [http://pubmed.gov/12686036 12686036]</ref><ref name="pmid15755765">LaRosa JC, Grundy SM, Waters DD, Shear C, Barter P, Fruchart JC et al. (2005) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=15755765 Intensive lipid lowering with atorvastatin in patients with stable coronary disease.] ''N Engl J Med'' 352 (14):1425-35. [http://dx.doi.org/10.1056/NEJMoa050461 DOI:10.1056/NEJMoa050461] PMID: [http://pubmed.gov/15755765 15755765]</ref> However, there are no trials specifically performed on patients with stable angina but they form a significant portion in other major trials studying the efficacy of lipid-lowering drugs on the overall mortality from cardiovascular events.<ref name="pmid12114036">Heart Protection Study Collaborative Group (2002) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=12114036 MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial.] ''Lancet'' 360 (9326):7-22. [http://dx.doi.org/10.1016/S0140-6736(02)09327-3 DOI:10.1016/S0140-6736(02)09327-3] PMID: [http://pubmed.gov/12114036 12114036]</ref> In patients with [[HDL|low HDL]] and [[triglyceride|high triglycerides]] as an adjunctive to [[statin|statin therapy]], [[Fibrate|fibrates]] or [[niacin]] may be used.<ref name="pmid12716814">Robins SJ, Rubins HB, Faas FH, Schaefer EJ, Elam MB, Anderson JW et al. (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=12716814 Insulin resistance and cardiovascular events with low HDL cholesterol: the Veterans Affairs HDL Intervention Trial (VA-HIT).] ''Diabetes Care'' 26 (5):1513-7. PMID: [http://pubmed.gov/12716814 12716814]</ref>
+===Revasularization===
+The goal of the treatment of [[chronic stable angina]] is to reduce the symptoms, delay the progression of [[atherosclerosis]], and prevent cardiovascular events. In order to achieve these goals, lifestyle modifications and medical therapy are the first line treatment. Revascularization is done to increase survival in specific conditions where the stenosis of the coronary arteries is anatomically and functionally significant and the symptoms are refractory to medical therapy. There are currently two well-established revascularization approaches for the treatment of chronic stable angina caused by coronary [[atherosclerosis]]: [[CABG]] and [[PCI]]. Since the introduction of [[bypass|coronary artery bypass surgery]] in 1967 and [[angioplasty|percutaneous transluminal coronary angioplasty (PTCA)]] in 1977, research has supported the effective usage of both strategies for treatment of patients with chronic stable angina. However, as with any treatment method, both methodologies have weaknesses. The choice between PCI and CABG is based upon anatomy and other factors such as left ventricular function and the presence or absence of [[diabetes]]. In general, PTCA is reserved for single or some cases of two vessel disease, while CABG is reserved for patients with two or three vessel disease or left main disease. With the availability of drug-eluting [[stents]], PCI is increasingly being performed for many lesions including more complex ones.
+====PCI====
+Percutaneous coronary intervention for [[coronary artery disease]] first began in 1977, as a valuable mode of revascularization, wherein at the point of [[stenosis|coronary stenosis]] a catheter-borne balloon is inflated to relieve the stenosis.
+====CABG====
+Coronary artery bypass surgery, also coronary artery bypass graft (CABG, pronounced "cabbage") surgery, and colloquially heart bypass or bypass surgery is a surgical procedure performed to relieve [[angina]] and reduce the risk of death from [[Coronary heart disease|coronary artery disease]]. [[artery|Arteries]] or [[vein]]s from elsewhere in the patient's body are [[medical grafting|grafted]] to the [[coronary artery|coronary arteries]] to bypass [[atherosclerosis|atherosclerotic]] [[stenosis|narrowings]] and improve the [[blood]] supply to the [[coronary circulation]] supplying the [[myocardium]] (heart muscle). This surgery is usually performed with the heart stopped, necessitating the usage of [[cardiopulmonary bypass]]; techniques are available to perform CABG on a beating heart, so-called "off-pump" surgery.
+====PCI vs Medical Therapy====
+An increased risk of mortality and morbidity is associated with untreated [[coronary artery disease]].<ref name="pmid7600846">Moliterno DJ, Elliott JM (1995) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=7600846 Randomized trials of myocardial revascularization.] ''Curr Probl Cardiol'' 20 (3):125-90. PMID: [http://pubmed.gov/7600846 7600846]</ref> The main aim of therapy in patients with [[Chronic stable angina definition|chronic stable angina]] is to alleviate [[Chronic stable angina symptoms|symptoms]], delay the progression of [[atherosclerosis]], reduce the incidence of adverse coronary events and improve [[Chronic stable angina prognosis|prognosis]]. This may be achieved with either initial [[Chronic stable angina medical therapy|medical therapy]] or with initial revascularization that includes [[Chronic stable angina revascularization percutaneous coronary intervention|percutaneous coronary intervention]] or [[Chronic stable angina revascularization coronary artery bypass grafting|coronary artery bypass grafting]]. Medical therapy alleviates symptom and improves prognosis; however, on the contrary, revascularization procedures provide symptomatic relief but generally does not improve mortality.
+====CABG vs Medical Therapy====
+It is well established that revascularization with [[Chronic stable angina revascularization coronary artery bypass grafting|CABG]] has shown to provide better symptomatic relief and improved survival rates in comparison to [[Chronic stable angina medical therapy|medical therapy]] in some patients with [[chronic stable angina definition|stable angina]].<ref name="pmid16386656">Smith SC, Feldman TE, Hirshfeld JW, Jacobs AK, Kern MJ, King SB et al. (2006) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=16386656 ACC/AHA/SCAI 2005 guideline update for percutaneous coronary intervention: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/SCAI Writing Committee to Update the 2001 Guidelines for Percutaneous Coronary Intervention).] ''J Am Coll Cardiol'' 47 (1):e1-121. [http://dx.doi.org/10.1016/j.jacc.2005.12.001 DOI:10.1016/j.jacc.2005.12.001] PMID: [http://pubmed.gov/16386656 16386656]</ref> However, the long term benefit of CABG is limited by the progression of [[atherosclerosis]] in other unbypassed vessels and stenosis of the graft itself.
+====PCI and CABG vs Medical Therapy====
+The ''Mass'' and ''Mass-II'' trials directly compared the effect of [[Chronic stable angina medical therapy|medical therapy]], [[Chronic stable angina revascularization coronary artery bypass grafting|CABG]] and [[Chronic stable angina revascularization percutaneous coronary intervention|PCI]] for the management of chronic stable angina.<ref name="pmid7594092">Hueb WA, Bellotti G, de Oliveira SA, Arie S, de Albuquerque CP, Jatene AD et al. (1995) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=7594092 The Medicine, Angioplasty or Surgery Study (MASS): a prospective, randomized trial of medical therapy, balloon angioplasty or bypass surgery for single proximal left anterior descending artery stenoses.] ''J Am Coll Cardiol'' 26 (7):1600-5. [http://dx.doi.org/10.1016/0735-1097(95)00384-3 DOI:10.1016/0735-1097(95)00384-3] PMID: [http://pubmed.gov/7594092 7594092]</ref><ref name="pmid15145093">Hueb W, Soares PR, Gersh BJ, César LA, Luz PL, Puig LB et al. (2004) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=15145093 The medicine, angioplasty, or surgery study (MASS-II): a randomized, controlled clinical trial of three therapeutic strategies for multivessel coronary artery disease: one-year results.] ''J Am Coll Cardiol'' 43 (10):1743-51. [http://dx.doi.org/10.1016/j.jacc.2003.08.065 DOI:10.1016/j.jacc.2003.08.065] PMID: [http://pubmed.gov/15145093 15145093]</ref> However, there are a few reservations to the application of results from these studies as they did not include the current optimal strategies of therapy.
+====PCI vs CABG====
+[[Chronic stable angina revascularization percutaneous coronary intervention|PCI]] and [[Chronic stable angina revascularization coronary artery bypass grafting|CABG]] have become the standard of care in the management of patients with [[CAD|symptomatic coronary artery disease]]. Patients with multi-vessel disease, the overall mortality and freedom from [[myocardial infarction]] appear to be similar in both the treatment strategies; however, the need for repeat [[Chronic stable angina revascularization|revascularization]] is significantly higher in patients who initially underwent [[Chronic stable angina revascularization percutaneous coronary intervention|PCI]] secondary to a higher incidence of [[restenosis]].
+===Alternative Therapies for Refractory Angina===
+====Transmyocardial Revascularization (TMR)====
+As the survival of patients with primary coronary events continue to increase, the number of patients presenting with [[Ischemia|refractory ischemia]] despite maximal [[Chronic stable angina medical therapy|medical therapy]] and unsuitable for further traditional [[Chronic stable angina revascularization|revascularization techniques]] also continues to rise.<ref name="pmid11897431">Kim MC, Kini A, Sharma SK (2002) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11897431 Refractory angina pectoris: mechanism and therapeutic options.] ''J Am Coll Cardiol'' 39 (6):923-34. PMID: [http://pubmed.gov/11897431 11897431]</ref> Transmyocardial revascularization (TMR) is one of the emerging techniques that has been studied in many randomized trials and has shown to reduce the incidence of recurrent angina, increase exercise tolerance time and improve quality of life.<ref name="pmid11897431">Kim MC, Kini A, Sharma SK (2002) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11897431 Refractory angina pectoris: mechanism and therapeutic options.] ''J Am Coll Cardiol'' 39 (6):923-34. PMID: [http://pubmed.gov/11897431 11897431]</ref><ref name="pmid10489946">Burkhoff D, Schmidt S, Schulman SP, Myers J, Resar J, Becker LC et al. (1999) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=10489946 Transmyocardial laser revascularisation compared with continued medical therapy for treatment of refractory angina pectoris: a prospective randomised trial. ATLANTIC Investigators. Angina Treatments-Lasers and Normal Therapies in Comparison.] ''Lancet'' 354 (9182):885-90. PMID: [http://pubmed.gov/10489946 10489946]</ref> TMR can be performed using either a laser beam or a percutaneous approach. However, only laser TMR is currently FDA approved.
+====Spinal Cord Stimulation (SCS)====
+In patients with refractory angina, spinal cord stimulation (SCS) is used to provide [[analgesia]] in the region of radiation of anginal-pain with the help an implanted device consisting of a stimulating electrode tip that extends into the dorsal epidural space, usually at the C7-T1 level.
+====Enhanced External Counter Pulsation (EECP)====
+Enhanced external counter pulsation (EECP) is another alternative therapy in the management of refractory angina. Most data from observational studies have demonstrated significant improvement in the exercise tolerance and reduction in the frequency of [[Chronic stable angina symptoms|anginal symptoms]] as well as the use of [[Chronic stable angina treatment nitrates|nitroglycerin]] among patients treated with EECP.<ref name="pmid11153780">Urano H, Ikeda H, Ueno T, Matsumoto T, Murohara T, Imaizumi T (2001) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11153780 Enhanced external counterpulsation improves exercise tolerance, reduces exercise-induced myocardial ischemia and improves left ventricular diastolic filling in patients with coronary artery disease.] ''J Am Coll Cardiol'' 37 (1):93-9. PMID: [http://pubmed.gov/11153780 11153780]</ref>
+===Discharge Care===
-Angina pectoris is a sign of [[coronary heart disease]]. If it occurs chronically this is called [[stable angina]]. If it occurs at rest or in an accelerating pattern this is called an [[acute coronary syndrome]] and can be a symptom of either:
+====Patient Follow-Up====
-#[[Unstable angina]]: An open artery with insufficient blood flow to the heart but without irreversible damage
+Ongoing follow-up of the patient with chronic stable angina is necessary to monitor symptoms and to optimize antianginal therapy. It is generally recommended that these patients be evaluated every 4-6 months during first year of diagnosis/initiation of therapy and annually thereafter.  Based upon clinical judgement, if the patient is poorly responsive to therapy, if the episodes are severe or frequent, or if the patient is fragile with multiple co-morbidities, they may need to be seen more frequently.
-#[[Non ST elevation MI]]: An open artery with insufficient blood flow to the heart with irreversible damage
-#[[ST elevation MI]]: A closed artery with insufficient blood flow to the heart and irreversible damage
-===Pathophysiology===
+During a follow-up visit, the patient should be asked about the frequency and severity of their anginal symptoms, their level of exercise capacity, whether they have been able to modify his/her risk factors, how well they are tolerating and complying with the therapy and whether he/she has developed new illnesses or co-morbidities.
-Whenever there is limitation in the flow through one or more coronary arteries, there occurs a mismatch between the oxygen supply and demand to the myocardium. This activates the molecular cascade and release of [[bradykinin]], [[adenosine]] which stimulate the sympathetic and vagal afferent fibers, causing the anginal pain. Certain conditions can increase the myocardial oxygen demand secondary to increase cardiac output(like fever, thyrotoxicosis, stress, tachyarrythmias)
-===Clinical presentation===
+====Rehabilitation====
-Most of the patients will present with pain or discomfort which may be typical, but commonly is atypical. Some patients also present with dyspnea instead of pain and this is termed as angina equivalent. History is extremely helpful and should include an assessment of risk factors as well. Physical examination may be normal or reveal findings of heart failure. Other findings to look for are peripheral vascular disease which is considered to be risk factor for [[CAD]].
+Cardiac rehabilitation, also called cardiac rehab (CR), is a medically supervised program to help cardiac patients recover quickly and improve their overall well being. The main goal of rehabilitation is to help patients understand their disease and inculcate a regimen to stabilize and reduce, or even reverse the progression of cardiovascular disease. Cardiac rehab is often divided into phases that involve monitored exercise, counseling, emotional support, and education about lifestyle changes to reduce the risks of heart problems. It also helps reverse limitations experienced by patients who have suffered the adverse patho-physiologic and psychological consequences of cardiac events, thus, also helping patients to return to work early. Traditionally, cardiac rehabilitation has been provided to lower-risk patients who could exercise without physical limitations. However, rapid evolution in the management of [[CAD]] has now changed the demographics of the patients, so that, even patients with recent revascularization can be candidates for rehabilitation training.
-===Calculating pretest probability for CAD===
+===Secondary Prevention===
-Pretest probability tells the probability of a target disorder before the result of the diagnostic test(s) are known. In case of angina, initial history and physical examination can help categorize the patient into low, intermediate or high probability group. This will then help in deciding the type of testing, interpreting result of the test and timing for starting the treatment.
-===Diagnostic tests===
+====Smoking Cessation====
-This includes lab tests like lipid profile, hemoglobin and hematocrit, blood glucose, TSH. ECG should be done but one shuld remember that it may be normal in majority of cases. Some findings to look for are evidence of active ischemia like ST-T wave depression, left ventricular hypertrophy, Q waves in multiple leads suggestive of old MI, bundle branch blocks, arrythmias. These findings will also help in choosing the next diagnostic test. Chest X-ray may be normal or show cardiomegaly or pulmonary vascular congestion. Specific cardiac tests for angina include exercise [[ECG]] testing, [[myocardial perfusion imaging]], [[echocardiography]], [[stress echocardiography]] and [[coronary angiography]]. Choice of these tests is based largely on initial history and physical examination as well as resting [[ECG]] findings.
+The 1989 Surgeon General’s report, which assessed numerous case-control and cohort studies, reported that smoking increased cardiovascular disease mortality by 50%.<ref name="pmid2494426">Centers for Disease Control (CDC) (1989) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=2494426 The Surgeon General's 1989 Report on Reducing the Health Consequences of Smoking: 25 Years of Progress.] ''MMWR Morb Mortal Wkly Rep'' 38 Suppl 2 ():1-32. PMID: [http://pubmed.gov/2494426 2494426]</ref> Cigarette smoking, likely due to the hemodynamic consequences of sympathetic neural stimulation and systemic [[catecholamine]] release, plays an important role in the pathogenesis of [[coronary artery disease]]. Cigarette smoking also forms a major risk factor for acute cardiovascular events as it relates to an associated increase in [[Coagulopathy|blood coagulability]].<ref name="pmid9180099">Benowitz NL, Gourlay SG (1997) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=9180099 Cardiovascular toxicity of nicotine: implications for nicotine replacement therapy.] ''J Am Coll Cardiol'' 29 (7):1422-31. PMID: [http://pubmed.gov/9180099 9180099]</ref> Hence, cigarette smoking is an important reversible risk factor in the pathogenesis of [[CAD]] and cessation of which improves [[Chronic stable angina prognosis|prognosis]] and is associated with a substantial decrease in the risk of mortality.<ref name="pmid8114863">Bartecchi CE, MacKenzie TD, Schrier RW (1994) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=8114863 The human costs of tobacco use (1)] ''N Engl J Med'' 330 (13):907-12. [http://dx.doi.org/10.1056/NEJM199403313301307 DOI:10.1056/NEJM199403313301307] PMID: [http://pubmed.gov/8114863 8114863]</ref><ref name="pmid8121461">MacKenzie TD, Bartecchi CE, Schrier RW (1994) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=8121461 The human costs of tobacco use (2)] ''N Engl J Med'' 330 (14):975-80. [http://dx.doi.org/10.1056/NEJM199404073301406 DOI:10.1056/NEJM199404073301406] PMID: [http://pubmed.gov/8121461 8121461]</ref><ref name="pmid14583958">Critchley J, Capewell S (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=14583958 Smoking cessation for the secondary prevention of coronary heart disease.] ''Cochrane Database Syst Rev''  (4):CD003041. [http://dx.doi.org/10.1002/14651858.CD003041 DOI:10.1002/14651858.CD003041] PMID: [http://pubmed.gov/14583958 14583958]</ref> In patients with [[Chronic stable angina definition|stable angina pectoris]], nicotine replacement therapy has shown to be potentially beneficial despite the associated cardiovascular risks of [[nicotine]], such as increase in [[heart rate]] with a small rise in [[blood pressure]]. Nicotine replacement therapy may be initiated as early as 2–3 days after [[MI|acute myocardial infarction]] or [[arrhythmias|cardiac arrhythmias]].<ref name="pmid9180099">Benowitz NL, Gourlay SG (1997) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=9180099 Cardiovascular toxicity of nicotine: implications for nicotine replacement therapy.] ''J Am Coll Cardiol'' 29 (7):1422-31. PMID: [http://pubmed.gov/9180099 9180099]</ref>  Additionally, nicotine patches have been used successfully in [[Chronic stable angina risk assessment in patients with an intermediate or high probability of coronary artery disease|high-risk patients]] without any adverse effects such as aggravation of [[MI]] or [[arrhythmia]].<ref name="pmid9784902">Tzivoni D, Keren A, Meyler S, Khoury Z, Lerer T, Brunel P (1998) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=9784902 Cardiovascular safety of transdermal nicotine patches in patients with coronary artery disease who try to quit smoking.] ''Cardiovasc Drugs Ther'' 12 (3):239-44. PMID: [http://pubmed.gov/9784902 9784902]</ref><ref name="pmid8179456"> (1994) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=8179456 Nicotine replacement therapy for patients with coronary artery disease. Working Group for the Study of Transdermal Nicotine in Patients with Coronary artery disease.] ''Arch Intern Med'' 154 (9):989-95. PMID: [http://pubmed.gov/8179456 8179456]</ref>
-===Treatment===
+====Weight Management====
-Treatment for chronic stable angina includes lifestyle modification, pharmacotherapy and revascularization procedures([[PCI]], [[CABG]]). It is also important to identify any exacerbating factors like anemia, thyrotoxicosis, valvular heart disease or decompensated heart failure and treat them first, when possible. Smoking cessation counselling, diet and weight management, promoting physical exercise, BP and diabetes control are all part of risk factor modification and should be stressed at each clinic visit. Specific medical therapy includes antiplatelets(like [[ASA]], clopidogrel), antianginals(like nitrates, beta blockers, calcium channel blockers, antilipid agents, [[ACE]] inhibitors and angiotensin receptor blocking agents.
+Obesity is directly associated with the development of [[coronary artery disease|coronary artery disease (CAD)]] risk factors such as: [[hypertension]], [[diabetes]], reduced levels of [[HDL|HDL-C]] and elevated levels of [[triglyceride]]. Research has demonstrated that CAD risk factors contribute to a strong, graded, J-shaped univariable relationship between BMI and cardiovascular disease mortality. This increased mortality, when adjusted for age, self-reported smoking status, total cholesterol, and systolic blood pressure, maintained significant hazard ratios.<ref name="pmid21642320">Dudina A, Cooney MT, De Bacquer D, De Backer G, Ducimetière P, Jousilahti P et al. (2011) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=21642320 Relationships between body mass index, cardiovascular mortality, and risk factors: a report from the SCORE investigators.] ''Eur J Cardiovasc Prev Rehabil''  ():. [http://dx.doi.org/10.1177/1741826711412039 DOI:10.1177/1741826711412039] PMID: [http://pubmed.gov/21642320 21642320]</ref> Hence, in obese patients with [[CAD]], weight reduction and/or dietary interventions may be warranted to reduce the incidence of above-mentioned risk factors and prevent future coronary events. Weight reduction is strongly recommended in patients with a [[BMI]] greater than 30 kg/m<sup>2</sup> and in patients with increased waist circumference (greater than 102 cms for men and 89 cms for women), characteristic of truncal obesity.<ref name="pmid17998462">Fraker TD, Fihn SD, Gibbons RJ, Abrams J, Chatterjee K, Daley J et al. (2007)[http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=17998462 2007 chronic angina focused update of the ACC/AHA 2002 Guidelines for the management of patients with chronic stable angina: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Writing Group to develop the focused update of the 2002 Guidelines for the management of patients with chronic stable angina.] ''Circulation'' 116 (23):2762-72.[http://content.onlinejacc.org/cgi/reprint/50/23/2264.pdf] PMID: [http://pubmed.gov/17998462 17998462]</ref> Based on the plasma lipid abnormalities, adequate dietary modification may also be indicated.<ref name="pmid1727199">Smith GD, Shipley MJ, Marmot MG, Rose G (1992) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=1727199 Plasma cholesterol concentration and mortality. The Whitehall Study.] ''JAMA'' 267 (1):70-6. PMID: [http://pubmed.gov/1727199 1727199]</ref>
-Coronary revascularization is recommended when optimal medical therapy has failed to reduce symptoms or severe atherosclerotic disease or high risk criteria on noninvasive testing. Options available for revascularization are Percutaneous coronary intervention[[PCI]] and coronary artery bypass grafting[[CABG]].
-In patients with chronic stable angina, the factors influencing the choice of coronary revascularization therapy (percutaneous coronary intervention or coronary artery bypass surgery) are varied and complex.
-The severity of symptoms, lifestyle, extent of objective ischemia, and underlying risks must be weighed against the benefits of revascularization and the patient’s preference, as well as local availability and expertise. Evidence from randomized trials and large revascularization registers can guide these decisions, but the past decade has seen rapid change in medical treatment, bypass surgery and percutaneous coronary intervention.
-===Prognosis and risk stratification===
+====Physical Activity====
-Ischemic heart disease remains number one cause of mortality in developed countries. Prognosis of stable angina varies widely depending on severity of symptoms, extent of atherosclerosis and presence of other risk factors and co-morbidities. For this reason, it is important to risk stratify every patient. This can be done with the help of history, physical exam and use of one or more of diagnostic tests like [[ECG]], [[Echocardiography]], exercise ECG testing, myocaridal perfusion imaging or coronary angiography.
+Based on an individual's ability to exercise and severity of the symptoms, physical activity may be indicated as a treatment. As a treatment, increased physical activity has demonstrated improvements in an individual's sustained exercise duration, reduced the frequency of symptoms and also provided beneficial effects on [[blood pressure]], [[diabetes]] and the overall lipid profile. Before the initiation of an exercise regimen, an [[Chronic stable angina risk assessment in patients with an intermediate or high probability of coronary artery disease|exercise test]] is indicated as a useful guide to assess the level of tolerance.<ref name="pmid1639095"> (1992) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=1639095 Long-term comprehensive care of cardiac patients. Recommendations by the Working Group on Rehabilitation of the European Society of Cardiology.] ''Eur Heart J'' 13 Suppl C ():1-45. PMID: [http://pubmed.gov/1639095 1639095]</ref>
-==References==
+====Lipid Management====
-{{Reflist|2}}
+In patients with established [[coronary artery disease]], the recommended goal for [[cholesterol|total cholesterol]] is 130 mg/dl and [[LDL|LDL-C]] is 100 mg/dl, while the [[HDL|HDL-C]] and [[triglyceride]] concentrations serve as preferred markers for [[Chronic stable angina risk stratification|risk assessment]].<ref name="pmid17998462">Fraker TD, Fihn SD, Gibbons RJ, Abrams J, Chatterjee K, Daley J et al. (2007)[http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=17998462 2007 chronic angina focused update of the ACC/AHA 2002 Guidelines for the management of patients with chronic stable angina: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Writing Group to develop the focused update of the 2002 Guidelines for the management of patients with chronic stable angina.] ''Circulation'' 116 (23):2762-72.[http://content.onlinejacc.org/cgi/reprints/50/23/2264.pdf] PMID: [http://pubmed.gov/17998462 17998462]</ref> In patients with [[CAD]], a fasting lipid-profile may be repeated at 5 year intervals to assess the overall risk of cardiovascular mortality and morbidity.<ref name="pmid12964575">De Backer G, Ambrosioni E, Borch-Johnsen K, Brotons C, Cifkova R, Dallongeville J et al. (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=12964575 European guidelines on cardiovascular disease prevention in clinical practice. Third Joint Task Force of European and Other Societies on Cardiovascular Disease Prevention in Clinical Practice.] ''Eur Heart J'' 24 (17):1601-10. PMID: [http://pubmed.gov/12964575 12964575]</ref> Based on the individual’s lipid abnormalities, necessary dietary interventions and/or [[Chronic stable angina treatment anti-lipid agents|lipid-lowering agents]] are suggested to prevent the risk of future coronary events.<ref name="pmid1727199">Smith GD, Shipley MJ, Marmot MG, Rose G (1992) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=1727199 Plasma cholesterol concentration and mortality. The Whitehall Study.] ''JAMA'' 267 (1):70-6. PMID: [http://pubmed.gov/1727199 1727199]</ref> A Mediterranean diet consisting of fruits, vegetables, lean meat and fish has also been shown to be beneficial. Omega-3 fatty acid supplementation may be indicated in patients with [[Chronic stable angina definition|stable angina]] for secondary prevention, as it has been shown to reduce elevated [[triglycerides]] and also reduce the risk of [[sudden cardiac arrest|sudden cardiac death]].<ref name="pmid10465168"> (1999) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=10465168 Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto miocardico.] ''Lancet'' 354 (9177):447-55. PMID: [http://pubmed.gov/10465168 10465168]</ref><ref name="pmid11997274">Marchioli R, Barzi F, Bomba E, Chieffo C, Di Gregorio D, Di Mascio R et al. (2002) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11997274 Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI)-Prevenzione.] ''Circulation'' 105 (16):1897-903. PMID: [http://pubmed.gov/11997274 11997274]</ref><ref name="pmid11893369">Bucher HC, Hengstler P, Schindler C, Meier G (2002) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11893369 N-3 polyunsaturated fatty acids in coronary heart disease: a meta-analysis of randomized controlled trials.] ''Am J Med'' 112 (4):298-304. PMID: [http://pubmed.gov/11893369 11893369]</ref><ref name="pmid15824290">Studer M, Briel M, Leimenstoll B, Glass TR, Bucher HC (2005) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=15824290 Effect of different antilipidemic agents and diets on mortality: a systematic review.] ''Arch Intern Med'' 165 (7):725-30. [http://dx.doi.org/10.1001/archinte.165.7.725 DOI:10.1001/archinte.165.7.725] PMID: [http://pubmed.gov/15824290 15824290]</ref> Fish consumption once a week has also been associated with reduced risk of mortality from [[coronary artery disease]] and, for this reason, is strongly recommended.<ref name="pmid12588785">Kris-Etherton PM, Harris WS, Appel LJ, Nutrition Committee (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=12588785 Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease.] ''Arterioscler Thromb Vasc Biol'' 23 (2):e20-30. PMID: [http://pubmed.gov/12588785 12588785]</ref><ref name="pmid15184295">He K, Song Y, Daviglus ML, Liu K, Van Horn L, Dyer AR et al. (2004) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=15184295 Accumulated evidence on fish consumption and coronary heart disease mortality: a meta-analysis of cohort studies.] ''Circulation'' 109 (22):2705-11. [http://dx.doi.org/10.1161/01.CIR.0000132503.19410.6B DOI:10.1161/01.CIR.0000132503.19410.6B] PMID: [http://pubmed.gov/15184295 15184295]</ref>
+====BP Control====
+The risk of progression of [[atherosclerosis]] is proportional to the increase in [[hypertension|elevated blood pressure]], [[hyperglycemia]] and [[dyslipidemia]]. Therefore, the control of [[hypertension]], [[hyperglycemia]] and other features of [[metabolic syndrome]] deserves special attention in the prevention of mortality and morbidity due to [[coronary artery disease]]. In patients with established [[CAD]], concomitant [[diabetes]] and/or [[renal dysfunction]], the blood pressure goal is 130/80-85 and the decision to lower blood pressure depends on the total cardiovascular risk and the extent of target organ damage.<ref name="pmid12964575">De Backer G, Ambrosioni E, Borch-Johnsen K, Brotons C, Cifkova R, Dallongeville J et al. (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=12964575 European guidelines on cardiovascular disease prevention in clinical practice. Third Joint Task Force of European and Other Societies on Cardiovascular Disease Prevention in Clinical Practice.] ''Eur Heart J'' 24 (17):1601-10. PMID: [http://pubmed.gov/12964575 12964575]</ref><ref name="pmid12777938">European Society of Hypertension-European Society of Cardiology Guidelines Committee (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=12777938 2003 European Society of Hypertension-European Society of Cardiology guidelines for the management of arterial hypertension.] ''J Hypertens'' 21 (6):1011-53. [http://dx.doi.org/10.1097/01.hjh.0000059051.65882.32 DOI:10.1097/01.hjh.0000059051.65882.32] PMID: [http://pubmed.gov/12777938 12777938]</ref> Close monitoring and [[Chronic stable angina risk factor modifications|lifestyle changes]] may be indicated in [[Chronic stable angina assessing the pretest probability of coronary artery disease#Calculating the pretest probability for coronary artery disease|low-risk patients]] without documented target organ damage. However, in [[Chronic stable angina assessing the pretest probability of coronary artery disease#Calculating the pretest probability for coronary artery disease|high-risk patients]] with a sustained [[Systolic blood pressure|SBP]] of ≥140 mm Hg and/or [[diastolic blood pressure|DBP]] ≥90 mm Hg, the goal is to lower blood pressure less than 140/90 with the help of combined [[Chronic stable angina medical therapy|drug therapy]] and [[Chronic stable angina risk factor modifications|life style modification]]. Anti-hypertensive therapies that have shown to significantly reduce cardiovascular mortality and morbidity in patients with [[coronary artery disease]] include [[diuretics]], [[Chronic stable angina treatment beta blockers|beta-blockers]], [[Chronic stable angina treatment angiotensin converting enzyme inhibitors (ACEI) and renin angiotensin aldosterone system blockers (RAAS blockers)|ACEIs, ARBs]] and [[Chronic stable angina treatment calcium channel blockers|calcium channel blockers]].
-[[{{PAGENAME}}#Overview|''Return to top'']]
+====Diabetes Control====
+[[Diabetes]] is one of the major modifiable risk factors for [[coronary artery disease]]. Maintaining a good glycemic control has been demonstrated to delay the disease progression in patients with impaired glycemic control and further prevent microvascular complications.<ref name="pmid12777938">European Society of Hypertension-European Society of Cardiology Guidelines Committee (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=12777938 2003 European Society of Hypertension-European Society of Cardiology guidelines for the management of arterial hypertension.] ''J Hypertens'' 21 (6):1011-53. [http://dx.doi.org/10.1097/01.hjh.0000059051.65882.32 DOI:10.1097/01.hjh.0000059051.65882.32] PMID: [http://pubmed.gov/12777938 12777938]</ref><ref name="pmid12502618">American Diabetes Association (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=12502618 Standards of medical care for patients with diabetes mellitus.] ''Diabetes Care'' 26 Suppl 1 ():S33-50. PMID: [http://pubmed.gov/12502618 12502618]</ref><ref name="pmid12663615">Inzucchi SE, Amatruda JM (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=12663615 Lipid management in patients with diabetes: translating guidelines into action.] ''Diabetes Care'' 26 (4):1309-11. PMID: [http://pubmed.gov/12663615 12663615]</ref> In [[Diabetes mellitus type 1|type 1 diabetics]], appropriate insulin therapy and concomitant dietary modification may be required. However, in patients with [[Diabetes mellitus type 2|type 2 diabetes]], a multi-factorial intervention involving increased [[Chronic stable angina treatment physical activity|physical activity]], [[Chronic stable angina treatment weight management|weight reduction]], dietary modification and/or drug therapy has shown to reduce the risk of overall cardiovascular and microvascular events by approximately 50%.<ref name="pmid12964575">De Backer G, Ambrosioni E, Borch-Johnsen K, Brotons C, Cifkova R, Dallongeville J et al. (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=12964575 European guidelines on cardiovascular disease prevention in clinical practice. Third Joint Task Force of European and Other Societies on Cardiovascular Disease Prevention in Clinical Practice.] ''Eur Heart J'' 24 (17):1601-10. PMID: [http://pubmed.gov/12964575 12964575]</ref><ref name="pmid12556541">Gaede P, Vedel P, Larsen N, Jensen GV, Parving HH, Pedersen O (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=12556541 Multifactorial intervention and cardiovascular disease in patients with type 2 diabetes.] ''N Engl J Med'' 348 (5):383-93. [http://dx.doi.org/10.1056/NEJMoa021778 DOI:10.1056/NEJMoa021778] PMID: [http://pubmed.gov/12556541 12556541]</ref>
-{{Circulatory system pathology}}
+==References==
-{{SIB}}
+{{Reflist|2}}
-[[Category:Cardiology]]
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+[[Category:Disease]]
+[[Category:Ischemic heart diseases]]
+[[Category:Cardiology]]
+[[Category:Emergency medicine]]
+[[Category:Intensive care medicine]]
+[[Category:Up-To-Date]]
+[[Category:Up-To-Date cardiology]]


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