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==Pathophysiology== | ==Pathophysiology== | ||
*Most commonly, chronic stable angina is due to '''fixed obstructive disease or [[atherosclerosis]]''' which narrows the coronary arteries. | *Most commonly, chronic stable angina is due to '''fixed obstructive disease or [[atherosclerosis]]''' which narrows the coronary arteries. | ||
:*This results in inadequate supply of blood and oxygen to meet the demands of myocardial | :*This results in inadequate supply of blood and oxygen to meet the demands of myocardial metabolism. This supply / demand mismatch activates a molecular cascade of events that causes the release of molecules such as [[bradykinin]] and [[adenosine]] which in turn stimulate the sympathetic and [[vagal]] afferent fibers, causing the anginal pain. | ||
:*Certain conditions can increase the myocardial oxygen demand secondary to an increase cardiac output and can exacerbate chronic stable angina. These conditions include [[fever]], [[thyrotoxicosis]], [[anemia]], emotional stress, and [[tachyarrythmias]]. | :*Certain conditions can increase the myocardial oxygen demand secondary to an increase in [[cardiac output]] and can exacerbate chronic stable angina. These conditions include but are not limited to [[fever]], [[thyrotoxicosis]], [[anemia]], emotional stress, and [[tachyarrythmias]]. | ||
*While fixed obstructive epicardial disease is the most common cause of chronic stable angina, '''vasospasm of the epicardial artery''' can also cause angina. Angina due to spasm of an epicardial artery is known as [[Prinzmetal's angina]] or [[variant angina]]. | *While fixed obstructive epicardial disease is the most common cause of chronic stable angina, '''vasospasm of the epicardial artery''' can also cause angina. Angina due to spasm of an epicardial artery is known as [[Prinzmetal's angina]] or [[variant angina]]. | ||
Revision as of 01:12, 18 July 2011
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Chronic stable angina Microchapters | ||
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Classification | ||
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Differentiating Chronic Stable Angina from Acute Coronary Syndromes | ||
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Diagnosis | ||
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Alternative Therapies for Refractory Angina | ||
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Discharge Care | ||
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Guidelines for Asymptomatic Patients | ||
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Case Studies | ||
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Chronic stable angina overview On the Web | ||
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Risk calculators and risk factors for Chronic stable angina overview | ||
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
- Angina pectoris, commonly known as angina is chest pain [1] due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle, generally due to obstruction or spasm of the coronary arteries (the heart's blood vessels).
- Coronary artery disease or 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"), 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.
Pathophysiology
- Most commonly, chronic stable angina is due to fixed obstructive disease or atherosclerosis which narrows the coronary arteries.
- This results in inadequate supply of blood and oxygen to meet the demands of myocardial metabolism. This supply / demand mismatch activates a molecular cascade of events that causes the release of molecules such as bradykinin and adenosine which in turn stimulate the sympathetic and vagal afferent fibers, causing the anginal pain.
- Certain conditions can increase the myocardial oxygen demand secondary to an increase in cardiac output and can exacerbate chronic stable angina. These conditions include but are not limited to fever, thyrotoxicosis, anemia, emotional stress, and tachyarrythmias.
- While fixed obstructive epicardial disease is the most common cause of chronic stable angina, vasospasm of the epicardial artery can also cause angina. Angina due to spasm of an epicardial artery is known as Prinzmetal's angina or variant angina.
- Chronic stable angina can also result from microvascular disease as well. This is known as microvascular angina or Syndrome X.
Clinical presentation
The majority of patients present with a history of either chest pain or chest discomfort which may be typical (occurs in the epicardial region).
The presentation may also be atypical. For instance, some patients may present with dyspnea instead of chest pain and this is termed an angina equivalent.
The history should include an assessment of cardiovascular risk factors as well.
Physical examination may be normal or may reveal findings of heart failure. The presence of peripheral vascular disease may be associated with an increased risk of coronary artery disease CAD.
Pretest probability for CAD
Pretest probability is the probability of a given disorder before the result of the diagnostic test(s) are known.
In the case of angina, the initial history and physical examination can help categorize the patient into a low, intermediate or high probability group.
Assessment of the pretest probability of disease aids in the selection of diagnostic studies and in the initiation of treatment.
Diagnostic tests
Initial Studies:
- The goal of initial testing is to exclude the presence of an acute coronary syndrome such as ST elevation MI, non ST elevation MI and unstable angina. Therefore, an electrocardiogram is performed in the patient who first presents with chronic stable angina.
- The EKG may be normal in the majority of cases if ischemia is not present at the time the EKG is obtained.
- Other relevant findings would include evidence of left ventricular hypertrophy, or Q waves in multiple leads suggestive of old MI.
Exclusion of Factors That Would Exacerbate A Supply Demand Mismatch:
In the patient who first presents with unstable angina a hemoglobin, hematocrit, and TSH should be obtained to exclude factors that would exacerbate a supply demand mismatch.
Studies to aid in the Management of Chronic Risk Factors:
This includes lab tests like lipid profile and the assessment of the Hb a1C and glucose.
Imaging Studies and Studies to Assess the Magnitude of Ischemia:
- A chest x ray is often performed to assess for the presence of cardiomegaly and congestive heart failure.
- Specific cardiac tests for angina include exercise ECG testing, myocardial perfusion imaging, echocardiography, stress echocardiography and coronary angiography[2].
- To confirm or qualify for the diagnosis of chronic stable angina, at least one of the following additional criteria for coronary artery disease and / or ischemia must be present:
- New and/or dynamic ST-depression >0.05 mV, ST-elevation >0.1 mV, or symmetric T wave inversion >0.2 mV on a resting ECG
- Definite evidence of ischemia on stress echocardiography, myocardial scintigraphy (e.g. an area of clear reversible ischemia), or ECG-only stress test (e.g., significant dynamic ST shift, horizontal or downsloping)
- Angiographic evidence of epicardial coronary artery stenosis of >70% diameter reduction and/or evidence for intraluminal arterial thrombus.
Treatment
- Treatment for chronic stable angina includes:
- 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.
- Coronary revascularization is recommended when optimal medical therapy has failed to reduce symptoms or severe atherosclerotic disease or high risk criteria on noninvasive testing [3].
- Options available for revascularization are Percutaneous coronary interventionPCI and coronary artery bypass graftingCABG.
- 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 of Chronic Stable Angina
Ischemic heart disease remains 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.
References
- ↑ "MerckMedicus : Dorland's Medical Dictionary". Retrieved 2009-01-09.
- ↑ 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). Gibbons RJ, Abrams J, Chatterjee K, Daley J, Deedwania PC, Douglas JS, Ferguson TB Jr, Fihn SD, Fraker TD Jr, Gardin JM, O'Rourke RA, Pasternak RC, Williams SV; American College of Cardiology; American Heart Association Task Force on practice guidelines (Committee on the Management of Patients With Chronic Stable Angina). J Am Coll Cardiol. 2003 Jan 1;41(1):159-68. No abstract available. PMID: 12570960
- ↑ 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. Fraker TD Jr, Fihn SD; 2002 Chronic Stable Angina Writing Committee; American College of Cardiology; American Heart Association, Gibbons RJ, Abrams J, Chatterjee K, Daley J, Deedwania PC, Douglas JS, Ferguson TB Jr, Gardin JM, O'Rourke RA, Williams SV, Smith SC Jr, Jacobs AK, Adams CD, Anderson JL, Buller CE, Creager MA, Ettinger SM, Halperin JL, Hunt SA, Krumholz HM, Kushner FG, Lytle BW, Nishimura R, Page RL, Riegel B, Tarkington LG, Yancy CW. J Am Coll Cardiol. 2007 Dec 4;50(23):2264-74. No abstract available. Erratum in: J Am Coll Cardiol. 2007 Dec 4;50(23):e1. Pasternak, Richard C [removed]. PMID: 18061078