Key Points
Î ACS has evolved as a useful operational term that refers to a spectrum
of conditions compatible with acute myocardial ischemia and/or
infarction which are usually due to an abrupt reduction in coronary
blood flow (Figure 1).
• A key branch point is ST elevation or new left bundle-branch block on the ECG,
which are considerations for immediate coronary angiography to determine if
there is an indication for reperfusion therapy to open a likely completely occluded
coronary artery.
Î The hallmark of ACS is the sudden imbalance between myocardial
oxygen supply and demand, which is usually the result of coronary
artery obstruction.
• The imbalance may also be caused by other conditions, including excessive
myocardial oxygen demand in the setting of a stable flow-limiting lesion; acute
coronary insufficiency due to other causes (e.g., vasospastic [Prinzmetal] angina,
coronary embolism, coronary arteritis); noncoronary causes of myocardial
oxygen supply-demand mismatch (e.g., hypotension, severe anemia, hypertension,
tachycardia, hypertrophic cardiomyopathy, severe aortic stenosis); nonischemic
myocardial injury (e.g., myocarditis, cardiac contusion, cardiotoxic drugs); and
multifactorial causes that are not mutually exclusive (e.g., stress [Takotsubo]
cardiomyopathy, pulmonary embolism, severe HF, sepsis).
Î The absence of persistent ST elevation is suggestive of NSTE-ACS
(except in patients with true posterior MI). NSTE-ACS can be further
subdivided on the basis of cardiac biomarkers of necrosis (e.g.,
cardiac troponin).
• If cardiac biomarkers are elevated and the clinical context is appropriate, the
patient is considered to have NSTEMI. Otherwise, the patient is deemed to
have UA.
• ST depression, transient ST elevation, and/or prominent T-wave inversions may
be present but are not required for a diagnosis of NSTEMI.
• Abnormalities on the ECG and elevated troponins in isolation are insufficient
to make the diagnosis of ACS but must be interpreted in the appropriate clinical
context.
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