1 Overview of acute coronary syndrome

Introduction Conditions Evidence References Credits

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Introduction
Acute coronary syndrome (ACS) refers to acute myocardial ischaemia caused by atherosclerotic coronary disease and includes ST-elevation myocardial infarction (STEMI), non ST-elevation MI (NSTEMI), and unstable angina (UA). These terms are used as a framework for guiding management. Patients with STEMI should be considered for immediate reperfusion therapy by thrombolytic agents or percutaneous coronary intervention (PCI). Patients with NSTEMI or UA patients do not benefit from immediate reperfusion therapy. [1] [2]

Background
In the US, coronary heart disease is one of the most common causes of death worldwide and is the leading cause of death among men and women. In 1990, ischaemic heart disease accounted for 6.3 million deaths worldwide. [3] The age-standardised incidence varies among and within countries. There were about 1.6 million hospital discharges for ACS in the US in 2003. [4] About 30% of ACS patients have STEMI. [5] In industrialised countries the annual incidence of UA is in the region of 6 cases per 10,000 people. The incidence of ACS increases with age, with a higher incidence among men until the age of 70. Women who are 15 years postmenopausal are equally likely as men to develop ACS. [6] About 90% of patients with coronary heart disease report at least 1 of the major risk factors, including cigarette smoking, dyslipidaemia, hypertension, diabetes, and abdominal obesity. [7]

Pathophysiology
All 3 of these disease processes involve disruption of vulnerable or high-risk plaques leading to platelet activation and thrombus formation. Blood flow is disrupted and if occlusion is severe it will result in myocardial ischaemia. More than 90% of patients with STEMI have evidence of a coronary thrombus occluding the infarct artery, compared with about 35% to 75% of patients with UA or NSTEMI. [8]

History

History includes chest pain in about 50% of cases. Chest pain is described as substernal pressure, heaviness, squeezing, burning sensation, or tightness. Chest pain may localise or radiate to the arms, shoulders, back, neck, or jaw. Pain is usually reproduced by exertion, eating, exposure to cold, or emotional stress. Other symptoms include abdominal pain, syncope, dyspnoea, diaphoresis, nausea, vomiting, or weakness. Symptoms commonly last 30 minutes or more.

Evaluation
The initial assessment of a patient with ACS should be aimed at determining whether the underlying cause is STEMI, NSTEMI, or UA. Clinical history is most useful but risk factors, ECG, and serum biomarkers all contribute in confirming the diagnosis.

Conditionshide all
Unstable angina see our comprehensive coverage of Unstable angina New ST-segment depression or T-wave inversion in the presence of ischaemic symptoms suggests UA or NSTEMI. If there is no elevation in CK-MB or troponin (cardiac biomarkers) the patient has UA; elevated cardiac biomarkers are consistent with NSTEMI. UA may present with angina at rest, new onset severe angina, or increasing angina. Treatment includes aspirin, beta-blockers, and enoxaparin or heparin. Myocardial infarction, non ST-elevation see our comprehensive coverage of Non-ST-elevation myocardial infarction New ST-segment depression or T-wave inversion with elevated CK-MB or troponin suggests NSTEMI. The distinction from UA is based on cardiac biomarkers, which in NSTEMI may be raised several hours after presentation. CK-MB and troponin have low sensitivity early in acute MI. Treatment includes aspirin, beta-blockers, and enoxaparin or heparin. Once the diagnosis of NSTEMI is confirmed, a glycoprotein IIb/IIIa inhibitor should also be started with percutaneous coronary intervention (PCI) and stenting within 48 hours in selected patients. Myocardial infarction, ST-elevation see our comprehensive coverage of ST-elevation myocardial infarction STEMI is characterised by ST-segment elevation or new left bundle branch block (LBBB). Cardiac biomarkers will be elevated. Over several hours to days, an initial Q wave may evolve and the amplitude of the R wave may diminish. STEMI requires urgent reperfusion therapy with PCI or thrombolytics if PCI is unavailable within 90 minutes. [9]