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Overview of acute coronary syndromeIntroductionConditions
EvidenceReferencesCredits
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IntroductionAcute 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]
PathophysiologyAll 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
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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 allUnstable 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]
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