Sandbox:Mitra

 | |  |  | Ca Channel Blockers | Nitrates | Hydralazine | Positive Inotropics | Anticoagulants |  | Antiarrhythmic Drugs | Nutritional Supplements | Hormonal Therapies | Lifestyle modification

Device therapy for heart failure with reduced ejection fraction: Implantable cardioverter-defibrillator | Cardiac resynchronization therapy | Devices under evaluation

• Efficacy: Low
  • Sinus rhythm is maintained in <20% of patients
  • Symtoms are reduced in >=20%.

Adverse effects

• Bradycardia
• Hypotension
• Edema

Contraindications

• Bradycardia
• Hypotension
• Heart failure with depressed ejection fraction

Contraindications

• Bradycardia
• Hypotension

Precautions during treatment

• Monitor for bradycardia

Books by Psychologists and Psychiatrists

• Beck, A. T., Rush, A. J., Shaw, B. F., Emery, G. (1987). Cognitive therapy of depression. New York: Guilford.
• Burns, David D. (1999). Feeling Good : The New Mood Therapy. Avon.
• Griffin, J., Tyrrell, I. (2004) How to lift Depression – Fast. HG Publishing. ISBN 1-899398-41-4
• Jacobson, Edith: "Depression; Comparative Studies of Normal, Neurotic, and Psychotic Conditions", International Universities Press, 1976, ISBN 0-8236-1195-7
• Klein, D. F., & Wender, P. H. (1993). Understanding depression: A complete guide to its diagnosis and treatment. New York: Oxford University Press.
• Kramer, Peter D. (2005). Against Depression. New York: Viking Adult.
• Plesman, J. (1986). Getting off the Hook, Sydney Australia. A self-help book available on the internet.
• Rowe, Dorothy (2003). Depression: The way out of your prison. London: Brunner-Routledge.
• Sarbadhikari, S. N. (ed.) (2005) Depression and Dementia: Progress in Brain Research, Clinical Applications and Future Trends. Hauppauge, Nova Science Publishers. ISBN 1-59454-114-0.
• Weissman, M. M., Markowitz, J. C., & Klerman, G. L. (2000). Comprehensive guide to interpersonal psychotherapy. New York: Basic Books.
• Bieling, Peter J. & Anthony, Martin M. (2003) Ending The Depression Cycle. New Harbinger Publications. ISBN 1572243333
• For books on male depression, see Terrence Real

Historical Account

• Healy, David. (1999). The Antidepressant Era, Paperback Edition, Harvard University Press. ISBN 0-674-03958-0

Medical Therapy

Antidepressant drugs include selective serotonin reuptake inhibitors, such as escitalopram oxalate (Lexapro), citalopram (Celexa), fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft), are the primary medications considered for patients, having fewer side effects than the older monoamine oxidase inhibitors (MAOIs).

The effect size is very small for moderate depression but increased with severity reaching the NICE criteria for 'clinical significance' for very severe depression. This result is consistent with the earlier clinical studies where only patients with severe depression benefited from the treatment with a tricyclic antidepressant imipramine or from psychotherapy more than from the placebo treatment. According to the STAR*D randomized controlled trial, about 50% of patients with major depression have a response and about 30% of have remission of symptoms with usage of citalopram.

Bupropion (Wellbutrin, Zyban), an atypical antidepressant that acts as a norepinephrine and dopamine reuptake inhibitor, is also considered to be effective in the treatment of depression, without sexual dysfunction or sexual side effects and without weight gain. Bupropion has also been shown to be more effective than SSRIs at improving symptoms such as hypersomnia and fatigue in depressed patients.

Measurement-based care, which guides mediation based on serial measurement of psychometric testing, improves outcomes according to randomized controlled trials.

Predictors of a response to treatment

Severity of depression

The effectiveness is antidepressants may or may not depend on the severity of a patient's depression. This relationship may be due to the declining effect of placebo among more severely depressed patients.

The effectiveness of antidepressants depending on severity of depression

American Psychiatric Association classification of severity	Hamilton Depression Rating Scale (HDRS)	Number needed to treat	Clinical significance (NICE)
Mild to moderate	< 19	16	No
Severe	19 - 22	11	No
Very severe	> 22	4	Yes

Genetic variations

Variations in the GRIK4 (glutamate receptor, ionotropic, kainate 4 protein) and HTR2A (5-hydroxytryptamine receptor) genes predict response to citalopram.

Treatment failure

Treatment after monotherapy failure
(VAST-D Study)

Intervention		Outcome
Medication	Mode final dose	Remission %	Quit 2˚ ADRs (%)
Switch medications
Bupropion SR	200 mg twice daily	22.3%	10%
Augment medications
Aripiprazole	10 mg	29%	5%
Bupropion SR	300 mg daily	27%	7%

After starting medications, treatment should be switched if there is no response within one month.

When treated with monotherapy for depression, approximately 30% of patients have remission of symptoms while 50% have a response to medications.

For patients with inadequate response, randomized controlled trials provide guidance.

• The original VAST-D trial, that did not include aripiprazole, confirms that augmenting with bupropion is the most effective of options other than augmentation with aripiprazole. In this trial, either adding sustained-release bupropion ("bupropion was 200 mg per day during weeks 1 and 2, increasing to 300 mg per day by week 4 and to 400 mg per day (the final dose) during week 6") or buspirone (up to 60 mg per day) for augmentation as a second drug can cause remission in approximately 30% of patients (bupropion may be more effective than buspirone), while switching medications can achieve remission in about 25% of patients. Alternatively, "extended-release venlafaxine, the starting daily dose of 37.5 mg for 7 days was increased to 75 mg from day 8 to 14, to 150 mg from day 15 to 27, to 225 mg from day 28 to 41, to 300 mg from day 42 to 62, and to 375 mg from day 63 onward."
• The PReDICT trial found that among patients who initially were treated with either an SSRI or CBT, remission was increased when the opposite treatment (CBT or SSRI) was added to non-remitters.
• The newer VAST-D trial found that augmentation with aripiprazole is effective. The dose of aripiprazole was 2 mg of with titration to 5, 10, or 15 mg daily as guided by measurement-based care using the PHQ-9. However, aripiprazole led to more adverse drug reactions including somnolence, akathisia, and weight gain. The second most effective was augmentation with buproprion starting at 150 mg sustained release to 300 mg or 400 mg daily as guided by measurement-based care using the PHQ-9.

• More recently, mirtazapine, was found not to add to SSRIs.

Treatment after SSRI (citalopram) failure
(STAR*D Studies)

Intervention		Outcome
Medication	Mean final dose	Remission %	Quit 2˚ ADRs (%)
Switch meds (NEJM 2006; PMID: 16554525)
Bupropion SR	283 mg	21%	27%
Sertraline (SSR)	136 mg	18%	21%
Venlafaxine ER (SNRI)	194 mg	25%	21%
Augment meds (NEJM 2006; PMID: 16554526)
Bupropion SR	268 mg	30%	13%
Buspirone	41 mg	30%	21%

The STAR*D trial has reported the frequency of re-emergence of suicidality for different second levels of treatment.

In level 3 of the STAR*D trials, patients who had failed two trials of a second-generation antidepressant, tended to better with nortriptyline than mirtazapine.

Aripiprazole, originally introduced as an atypical antipsychotic agent, is approved as an adjunct to other antidepressants.

Stopping medications

Patients are generally advised not to stop taking an antidepressant suddenly and to continue its use for at least four to months to prevent the chance of recurrence. For patients that have chronic depression, medication may need to be continued for the remainder of their life.

Patients should be treated indefinitely if they have "three or more prior major depressive episodes or who have chronic major depressive disorder should proceed to the maintenance phase of treatment after completing the continuation phase."

Table

American College of Cardiology Foundation/American Heart Association (ACCF/AHA) heart failure staging system
Stages	Definition	Example	Corresponding NYHA class
A	Patient at high risk for developing HF but without structural heart disease or symptoms of heart failure	coronary artery disease, hypertension, diabetes mellitus without impaired left ventricular (LV) function	None
B	Patient with structural heart disease who has never developed signs/symptoms of HF	LVH, impaired LV function	NYHA class I
C	Patient with past or current symptoms of HF associated with structural heart disease	Patients with known structural heart disease and symptoms of dyspnea, fatigue, reduced exercise tolerance	NYHA classes I, II, III, and IV
D	Patient with refractory (end-stage) disease who requires specialized treatment strategies such as mechanical circulatory support, continuous inotropic infusions, cardiac transplantation, or hospice care	Patients who have marked symptoms at rest despite maximal medical therapy	NYHA class IV

tABLE 2

Distinguishing the Jugular Venous Pulse frm the Carotid Pulse
Feaure	Internal Jugular Vein	Carotid Artery
Appearance of pulse	Biphasic	Monophasic
Response to inspiration	Inspiration generally decreases the pressure (the height of column decrease and troughs become more prominent)	No respiratory change
Pulpabillity	Not palpable (exception: severe TR)	Palpable
Effect of pressure

Table

Therapies to maintain sinus rhythm
Treatment	Efficacy	Adverse effects	Contraindications	Precausions
Drug therapy
Beta-blockers	Low Sinus rhythm is maintained in <20% of patients Symptoms are reduced in >=20% of patients	Fatigue Bradycardia Monitor for bradycardia	Bradycardia Hypotension	Monitor for bradycardia
Nondihydropyridine Calcium Channel Blockers: Verapamil Diltiazem	Low Sinus rhythm is maintained in <20% of patients Symptoms are reduced in >=20% of patients	Edema Bradycardia Hypotension	Bradycardia [[Hypotension Heart failure with reduced ejection fraction
Flecainide	Moderate AF is prevented or reduced in 50-70% of patients	Uncommon Proarrhythmia risk in patients with structural heart disease	Structural heart disease (proarrhythmia risk)	Evaluate for ischemic heart disease before initiation of therapy
Propafenone	Moderate AF is prevented or reduced in 50-70% of patients	Dysgeusia	Structural heart disease (proarrhythmia risk)	Evaluate for ischemic heart disease before initiation of therapy
Quinidine	Moderate AF is prevented or reduced in 50-70% of patients	Gastrointestinal side effects	QT prolongation	Monitor for QT prolongation, polymorphic ventricular tachycardia
Disopyramide	Moderate AF is prevented or reduced in 50-70% of patients	Antimuscarinic effects Urinary retention	QT prolongation Heart failure	Monitor for QT prolongation,
Dronendrone	Moderate AF is prevented or reduced in 50-70% of patients	Uncommon	Heart failure	Monitor for: Fluid retention Hepatitis
Dofetilide	Moderate AF is prevented or reduced in 50-70% of patients	QT prolongation	QT prolongation Advanced renal disease	Monitor for QT prolongation (should be initiated in hospital)
Sotalol	Moderate AF is prevented or reduced in 50-70% of patients	QT prolongation Fatigue Bradycardia Hypotension	QT prolongation Advanced renal disease Bradycardia	Monitor for QT prolongation
Amiodarone	High AF is prevented or reduced in 80% of patients	Bradycardia Thyroid diseases Hepatitis Interstitial lung disease (pulmonary fibrosis) Neurologic dysfunction Photosensitivity	Bradycardia Hyperthyroidism	Monitor for systemic toxicities involving the thyroid, liver, lungs, and nervous system Monitor for druginteractions
Interventional procedures
Catheter ablation	High 60-80% of patients with paroxysmal AF are free from AF at 1 year 50% of patients with persistent AF are free from AF at 1 year Reduced AF burden	Procedure-related adverse effects Risks associated with sedation and anesthesia Transient arrhythmia (for 3 months) For patients with persistent AF, a second procedure s often needed
Surgery (Maze procedure)	High AF is prevented in 80% patients	Risks associated with anesthesia and surgery	Surgical contraindications	Monitor for complications of surgery

Resident Survival Guide

Acute Coronary Syndrome Chapters
Heart Attack Patient Information
Unstable Angina Patient Information
Overview
Classification Unstable Angina Non-ST Elevation Myocardial Infarction ST Elevation Myocardial Infarction
Causes
Differential Diagnosis
Treatment
AHA/ACC Guidelines for Acute Coronary Syndrome
Guideline for Risk Stratification in ACS
Guideline for Pre-Hospital Evaluation and Care
Guidelines for Initial Management of ACS
Guidelines for Patients with Atrial Fibrillation Complicating ACS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]; Tarek Nafee, M.D. [3]; Sabawoon Mirwais, M.B.B.S, M.D.[4]

Synonyms and keywords: ACS

Diseases	Symptoms			Physical Examination			Diagnostic tests				Other Findings
	Dyspnea on Exertion	Chest Pain	Hemoptysis	Fever	Tachypnea	Tachycardia	Chest X-ray	ECG	Echocardiography>	CT scan and CMRI
COVID-19-associated heart failure	✔	-	✔	-	✔	✔	Cardiomegaly Pulmonary edema (interstitial, alveolar)	Left ventricular hypertrophy Low-voltage QRS Non-specific ST-T change	Systoloic dysfunction (in HFrEF) Diastoic dysfunction (in HFpEF) COVID-19-associated stress cardiomyopathy (apical ballooning)	CT: Cardiomegaly, Pulmonary edema CMR: Signs of underlying myocarditis may be seen.	Increased NT-proBNP and cardiac troponins levels
COVID-19-associated pneumonia	✔ (Usually high)	✔ (Pleuritic)	✔	✔	✔	✔	Lobar Consalidation	Prolonged PR interval Transient T wave inversions	-	CT: Lobar Consalidation	Increased inflammatory markers, including ESR, hs-CRP
COVID-19-associated acute respiratory distress syndrome	✔	-	✔	✔	✔	✔	Bilateral ground-glass opacities	-	Signs of RV dysfunction/RV dilatation may be seen.	CT: Bilateral ground-glass opacities	-
COVID-19-associated myocarditis	✔	✔	-	✔	✔	✔	Pericardial effusion may be detectable	Non-specific:may show nonspecific ST-T abnormalities, sinus tachycardia and conduction abnormalities (such as bundle-branch blocks or atrioventricular conduction delays)	Non-specific: In fulminant myocarditis, cardiac chamber sizes are usually normal with an increased septal thickness (secondary to acute myocardial edema), whereas in acute myocarditis marked left ventricular dilation and normal wall thickness might be seen. Pericardial effusion may be be seen.	CMR: T2-weighted edema imaging shows the presence of “acute myocardial inflammation”. "Late gadolinium enhancement (LGE) imaging” can demonstrate myocardial damage.	Increased cardiac troponins level
COVID-19-associated pulmonary embolism	✔ (Usually sudden-onset)	✔ (Pleauritic)	✔ (If massive PE)	✔ (Low-grade)	✔	✔	May show Fleischner sign (enlarged pulmonary artery), Hampton hump, Westermark's sign	Non-specific:may show S1Q3T3 pattern	May show signs of RV strain, Rv dilatation, Rv dysfunction (if large PE)	On CT angiography: Intra-luminal filling defect On MRI: Narrowing of involved vessel No contrast seen distal to obstruction Polo-mint sign (partial filling defect surrounded by contrast)	Increased D-dimer, fibrinogen, and fibrin degradation products levels May have symptoms and/or signs of accompanying DVT Classification Acute coronary syndrome may be classified as follows: Unstable Angina Non ST Elevation Myocardial Infarction ST Elevation Myocardial Infarction Symptoms The signs and symptoms of acute coronary syndrome include: Chest pain Substernal chest pain Occurs at rest or exertion Radiation to neck, jaw, left shoulder and left arm Aggravated by physical activity and emotional stress Relieved by rest, nitroglycerin or both Chest discomfort described crushing, squeezing, burning, choking, tightness or aching Dyspnea Diaphoresis Nausea and vomiting Fatigue Syncope Pathophysiology For more information on atherosclerotic plaque, click here. The pathophysiology of acute coronary syndromes depends on coronary atherosclerotic plaque which includes: Initiation and Progression of Coronary Atherosclerotic Plaque The endothelium of coronary arteries are damaged by the risk factors resulting in endothelial dysfunction, leading to the formation of atherosclerotic plaque. The macrophages in the atherosclerotic plaque release matrix metalloproteinases, leading to plaque disruption. The balance between smooth muscle cells and macrophages in the plaque plays a major role in plaque vulnerability and the propensity to rupture. Plaque Vulnerability The plaque vulnerability depends on the following factors: Inflammation (A high density of macrophages and T-lymphocytes are marker of unstable atherosclerotic plaque) Large lipid core Locally increased matrix metalloproteinases that degrade collagen Thin fibrous cap Relative paucity of smooth muscle cells Increase in plaque neovascularity and plaque hemorrhage Eccentric outward remodelling Pathogenesis The pathogenesis of acute coronary syndrome depends on: Endothelial integrity Inflammation Thrombogenicity of the blood Following plaque rupture or endothelial erosion, the subendothelial matrix is exposed to the circulating platelets, which get activated leading to thrombus formation. Two types of thrombi can form: White clots: Platelet-rich clots which partially occludes the artery Red clots: Fibrin rich clots superimposed on white clots and cause total occlusion of the artery Risk Factors Common risk factors in the development of acute coronary syndrome are: Age (men >45 and women >55) Diabetes mellitus Hypercholesterolemia Hypertension Smoking Obesity Lack of physical activity Family history of heart disease History of HTN, DM and pre-eclampsia during pregnancy Diagnosis High-sensitivity Cardiac Troponin (hs-cTn) 99th percentile of a healthy reference population (recommended cut-off) Turnaround time Name and manufacturer FDA Approval? Troponin T hs-cTnT 14 ng/L 18 minutes Elecsys (Roche Diagnostics) Troponin I hs-cTnI 26.2 ng/L ARCHITECTSTAT (Abbott Laboratories) Clinical Implications of High-sensitivity Cardiac Troponin Assays Compared with standard cardiac troponin assays, high-sensitivity assays: Have higher negative predictive value for acute MI. Reduce the “troponin-blind” interval leading to earlier detection of acute MI. Reduce the “troponin-blind” interval leading to earlier detection of acute MI. Are associated with a 2-fold increase in the detection of type 2 MI. Levels of high-sensitivity cardiac troponin should be interpreted as quantitative markers of cardiomyocyte damage (i.e. the higher the level, the greater the likelihood of MI): Elevations beyond 5-fold the upper reference limit have high (>90%) positive predictive value for acute type 1 MI. Elevations up to 3-fold the upper reference limit have only limited (50–60%) positive predictive value for acute MI and may be associated with a broad spectrum of conditions. It is common to detect circulating levels of cardiac troponin in healthy individuals. Rising and/or falling cardiac troponin levels differentiate acute from chronic cardiomyocyte damage (the more pronounced the change, the higher the likelihood of acute MI). Adapted from European Heart Journal (2016) 37, 267–315 Available high sensitivity troponin assays: Troponin T: Elecsys by Roche Diagnostics Troponin I: ARCHITECTSTAT by Abbott Laboratories When both tests have sensitivity of > 99%, cTnT can exclude infarction in more patients with a sensitivity of 90% according to meta-analysis. The agreement between hscTnT and hscTnI measurements is excellent (Cohen's kappa =0.9). High sensitivity troponin levels have reduced predictive value when prevalence is low. Clinical Prediction Rules Clinical prediction rules can help diagnose: HEART risk score (History, EKG, Age, Risk factors, and troponin) is the only one of these three prediction rules designed for use prior to diagnosis GRACE risk score incorporates 8 findings TIMI risk score Regarding the comparative performance of the prediction rules: In the setting of acute chest pain, the HEART score may best predict complications according to a cohort study. In the setting of NSTEMI, the GRACE risk score may best predict complications according to a cohort study. However, the HEART risk score was not assessed in this cohort. Diagnostic Pathways Clinical diagnostic pathways may help. The European Society of Cardiology recommends two pathways: 0 h/3 h 0 h/1 h The last American Health Association guidelines were prepared prior to approval of hs-cTn tests by the FDA. More recent strategies include: Single cTnT measurement, combined with a non-ischemic EKG, that reports troponin is below the limits of detection. Single cTnI measurement, combined with low-risk clinical prediction rule Differential Diagnosis Diagnosis of ACS is initiated by a clinical suspicion based on a thorough history of the patient's symptoms. Subsequently, confirmatory tests should be ordered to confirm the diagnosis, identify the specific cause of ACS, or to rule out other possible differentials. In some circumstances, utilizing a clinical prediction tool may be beneficial in guiding the clinician's diagnosis. View the page on diagnosis using the clinical prediction rule for ACS for more detail. Acute Coronary Syndrome (ACS) may be differentiated from other diseases as follows: Organ System Diseases Presentation Diagnostic Tests Past Medical History Other Findings Chest Pain GI Symptoms Pulmonary Neck On Palpation On inspiration Radiating to Extremeties Radiating to Back With Movement Nausea or Vomitting Epigastric Pain Odynophagia or Dysphagia Shortness of Breath Jugular Distention Cardiac Biomarkers CBC Findings ESR D-Dimer EKG Findings CXR Findings DM Hyperlipidemia Obesity Trauma Inxn* Htn Cardiovascular Acute Coronary Syndrome + + + + + + + + + + + •Palpitations •Sweating Aortic Dissection + + + - + + - + •Pain maximal upon onset •Pain difficult to treat with opiates •Weak pulse in one arm compared to other •Syncope •Symptoms similar to stroke •Smoking Brugada Syndrome No chest pain + •Syncope •Cardiac arrest •ST-segment elevation •F/H of sudden cardiac death Takotsubo carditis Sudden onset of chest pain mimicking myocardial infarction + + + + + - •Extreme emotional or physical stress•syncope •Women>men •ST segment elevation •Left ventricular apical ballooning on echo •Normal coronary arteries Pericarditis + + + •Relieving factor: Sitting up and leaning forward •Aggravating factor: Lying down and breathing deep + + + + + + + •Other causes:Malignancy, autoimmune disorders, chest trauma •Pericardial friction rub Organ System Diseases Presentation Diagnostic Tests Past Medical History Other Findings Chest Pain GI Symptoms Pulmonary Neck On Palpation On inspiration Radiating to Extremeties Radiating to Back With Movement Nausea or Vomitting Epigastric Pain Odynophagia or Dysphagia Shortness of Breath Jugular Distention Cardiac Biomarkers CBC Findings ESR D-Dimer EKG Findings CXR Findings DM Hyperlipidemia Obesity Trauma Inxn* Htn Pulmonary Pleuritis (pleurisy) + + + + •Aggravating factor: Deep breathing + + + + + + •Other causesPulmonary embolism, malignancy, autoimmune diseases Pulmonary Embolism + •Aggravating factors: Deep breathing, coughing, eating, bending and stooping + + + •Other causes: Immobility, pregnancy, oral contraceptive pills Pneumonia + + + + + + •Complications: Sepsis, ARDS, Lung abscess Gastrointestinal GERD + + + •Other symptoms: Hoarseness, Dry cough at night, Sensation of lump in throat etc Esophageal Spasms + + + + + + + • Risk factors: Anxiety or depression and drinking wine, very hot or cold foods Esophagitis + + + + + + + • Causes: Hiatal hernia, infection, medications, radiation therapy Gastritis + + + + + + + • Causes: H.pylori infection, bile reflux, alcohol use, alcohol use Organ System Diseases Presentation Diagnostic Tests Past Medical History Other Findings Chest Pain GI Symptoms Pulmonary Neck On Palpation On inspiration Radiating to Extremeties Radiating to Back With Movement Nausea or Vomitting Epigastric Pain Odynophagia or Dysphagia Shortness of Breath Jugular Distention Cardiac Biomarkers CBC Findings ESR D-Dimer EKG Findings CXR Findings DM Hyperlipidemia Obesity Trauma Inxn* Htn Musculoskeletal Muscle sprain/Spasm + + + + • Causes: Over use, dehydration, electrolyte abnormalities Costochondritis + + + + + + + + + + + • Risk factors: Rheumatoid arthritis, ankylosing spondylitis, Reiter's syndrome Rib fracture/Trauma + + + + + + + + + + • Complications: Pneumothorax, hemothorax, surgical emphysema Psychiatry Anxiety (Panic Attack) Chest tightness + + • Other symptoms: Palpitations, trembling, sweating, choking, light headed, hot or cold flashes. The following table summarizes the significant history, and diagnostic test findings that will help differentiate the acute coronary syndromes from one another, as well as from other coronary artery diseases: Acute Coronary Syndromes History and Symptoms Pathology Diagnostic tests Treatment Complications Prognosis Chest pain Duration of Chest pain Coronary Artery Plaque Cardiac Biomarkers (e.g.CK-MB, Troponins) EKG Findings Medical Therapy Reperfusion (e.g. PCI, CABG, or Medical) At Rest Exertion Unstable Angina + + <30 minutes Partial occlusion Erosion or Rupture (39%) Normal •Normal EKG findings (some cases) •Flipped or inverted T waves •ST segment depression •Non-specific ST-T changes + •Arrhythmias •Congestive heart failure •Hypotension •New mitral regurgitation •MI •Sudden death •1 year mortality rate is 1.7% NSTEMI + + >30 minutes Partial or complete occlusion Rupture (56%) or Erosion Elevated •No EKG findings (some cases) •Flipped or inverted T waves •ST segment depression •Non-specific ST-T changes •New left bundle branch block + + •Arrhythmias •Congestive heart failure •Hypotension •New mitral regurgitation •Ventricular aneurysms •Sudden death •1 year mortality rate is 24.4% •30 day mortality rate is about 2% STEMI + + >30 minutes Complete occlusion Rupture (50%-75%) or Erosion Elevated •ST elevation in at least 2 contiguous leads in V2-V3 •ST depression in at least two precordial leads V1-V4 •ST depression in several leads plus ST elevation in lead aVR (suggestive of occlusion of the left main or proximal LAD artery) + + •Reinfarction •Arrhythmias •Left ventricular aneurysm •Pseudoaneurysm •rupture of papillary muscle, interventricular septum and LV free wall •Sudden death •30 day mortality rate is 1.1% in <45 yrs and 20.4% in >75 yrs patients Other Coronary Artery Diseases Chronic stable angina - + ≤ 5 minutes Severely narrowed coronary vessels Stable plaque Normal •Normal EKG in 50% of cases •Down sloping, up sloping or horizontal ST segment depression •T wave inversion + •Heart failure •Estimated annual mortality rate is 0.9%-1.4% •Annual incidence of non-fatal MI between 0.5%-2.6% •1 year mortality rate is 1.3% Prinzmetal's angina •Occur at rest (Mid night to early morning) •Not associated with exertion 5-30 minutes Coronary artery vasospasm - Normal •Transient ST segment elevation + •Arrhythmias •MI •5 year survival is excellent (90%-95%) Differential Diagnoses of Acute Coronary Syndromes in the Setting of Chest Pain Cardiac Pulmonary Vascular Gastrointestinal Orthopedic Other Myopericarditis Cardiomyopathiesa Pulmonary embolism Aortic dissection Esophagitis, reflex or spasm Musculoskeletal disorders Anxiety disorders Tachyarrhythmias (Tension)-Pneumothorax Symptomatic aortic aneurysm Peptic ulcer, gastritis Chest trauma Herpes zoster Acute heart failure Bronchitis, pneumonia Stroke Pancreatitis Muscle injury/inflammation Anemia Hypertensive emergencies Pleuritis Cholecystitis Costochondritis Aortic valve stenosis Cervical spine pathologies Tako-Tsubo cardiomyopathy Coronary spasm Cardiac trauma Bold = Common and/or important differential diagnoses aDilated, hypertrophic and restrictive cardiomyopathies may cause angina or chest discomfort Treatment Coronary Angiography Coronary angiography within 12 hours likely benefits high risk (elevated cardiac biomarkers at baseline or diabetes or a GRACE score more than 140) patients. Recommendations for Anti-ischemic Drugs in the Acute Phase of Non-ST-elevation Acute Coronary Syndromes Recommendations Class of Recommendations Level of Evidence Early initiation of beta-blocker treatment is recommended in patients with ongoing ischemic symptoms and without contraindications. I B It is recommended to continue chronic beta-blocker therapy, unless the patient is in Killip class III or higher. I B Sublingual or i.v. nitrates are recommended to relieve angina;a intravenous treatment is recommended in patients with recurrent angina, uncontrolled hypertension or signs of heart failure. I C In patients with suspected/confirmed vasospastic angina, calcium channel blockers and nitrates should be considered and beta-blockers avoided. IIa B aShould not be administered in patients with recent intake of sildenafil or vardenafil (< 24 h) or tadalafil (< 48 h). Prevention Primary Prevention The primary prevention strategies include: Dietary modifications: Regular consumption of fruits, vegetables, whole grains and lean meats Limit foods high in cholesterol and saturated fats Physical exercise 30 minutes of moderate exercise Weight loss Smoking cessation Regular blood pressure, blood sugar and cholesterol check Secondary Prevention The secondary prevention strategies include: Dietary modifications Regular blood pressure, blood sugar and cholesterol check Compliance with therapy for post acute coronary syndrome event Cardiac rehabilitation programs References