Acute coronary syndromes
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Resident Survival Guide |
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Acute Coronary Syndrome Chapters |
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AHA/ACC Guidelines for Acute Coronary Syndrome |
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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
Overview
Acute coronary syndrome (ACS) refers to any group of symptoms attributed to obstruction of the coronary arteries. The most common symptom prompting diagnosis of ACS is chest pain, often radiating to the left arm or angle of the jaw, pressure-like in character, and associated with nausea and sweating. Acute coronary syndrome usually occurs as a result of one of three problems: ST-elevation myocardial infarction (30%), non ST-elevation myocardial infarction (25%), or unstable angina (38%). These types are named according to the appearance of the electrocardiogram. There can be some variation as to which forms of myocardial infarction (MI) are classified under acute coronary syndrome. ACS should be distinguished from stable angina, which is chest pain that develops during exertion and resolves at rest. New-onset angina however should be considered as a part of acute coronary syndrome, since it suggests a new problem in a coronary artery. Though ACS is usually associated with coronary thrombosis, it can also be associated with cocaine use. Cardiac chest pain can also be precipitated by anemia, bradycardias or tachycardias.
Historical Perspective
Classification
- Traditionally, ACS has been classified into:
- According to this classification, unstable angina was defined as clinical and electrocardiographic (ECG) evidence of myocardial ischemia in the absence of an elevated troponin level.
- However, the widespread use of the high-sensitivity troponin assays made UA and NSTEMI indistinguishable since it was shown that almost all patients previously named UA actually have increased high-sensitivity troponin levels.
- In other words, it is very unlikely that patients with clinical and ECG evidence of myocardial ischemia have normal high-sensitivity troponin levels.
- Consequently, in recent guidelines, acute coronary syndrome is classified into two broad categories:
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:[1]
- 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 remodeling
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
Causes
Differentiating Xyz from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic study of choice | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X-Ray Findings | Echocardiography and Ultrasound | CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies
Treatment
Medical Therapy | Interventions | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
- ↑ Sukhova GK, Schönbeck U, Rabkin E, Schoen FJ, Poole AR, Billinghurst RC; et al. (1999). "Evidence for increased collagenolysis by interstitial collagenases-1 and -3 in vulnerable human atheromatous plaques". Circulation. 99 (19): 2503–9. PMID 10330380.