- New or worsening symptoms (angina, pulmonary edema) or
signs (electrocardiographic [ECG] changes) of
- Absence or mild elevation of cardiac enzymes (creatine kinase
and its MB fraction or troponin I or T) without prolonged ST segment
elevation on ECG.
- Unstable angina and non-ST elevation myocardial infarction
are closely related in pathogenesis and clinical presentation and
are therefore discussed as one entity in this chapter.
Unstable angina and non-ST elevation myocardial infarction (USA/NSTEMI)
are a part of the wide spectrum of acute coronary syndrome. They
are closely related in pathogenesis but with different severity
in presentation. Compared with ST elevation myocardial infarction
(STEMI), the incidence of USA/NSTEMI has been increasing.
In the current era, USA/NSTEMI is the admitting diagnosis
for about 40–50% of all admissions to cardiac
Atherosclerotic coronary artery disease comprises a spectrum
of conditions that ranges from a totally asymptomatic state at one
end to sudden cardiac death at the other (Table
4–1). It is clear that coronary artery disease, the
primary cause of mortality and morbidity in much of the industrialized
world, takes its toll through such acute complications (unstable
coronary syndromes) as unstable angina, myocardial infarction, acute
congestive heart failure, and sudden cardiac death. Also known as acute
ischemic syndromes, these are the first clinical expressions of
atherosclerotic coronary artery disease in 40–60% of
patients with coronary artery disease.
Table 4–1. Clinical Spectrum of Atherosclerotic Coronary Artery Disease.
Angina pectoris is the symptomatic equivalent of transient myocardial ischemia,
which results from a temporary imbalance in the myocardial oxygen demand
and supply. Most episodes of myocardial ischemia are generally believed
to result from an absolute reduction in regional myocardial blood flow
below basal levels, with the subendocardium carrying a greater burden
of flow deficit relative to the epicardium, whether triggered by
a primary reduction in coronary blood flow or an increase in oxygen
demand. As shown in Figure 4–1,
the various acute coronary syndromes share a more-or-less common
pathophysiologic substrate. The differences in clinical presentation
result largely from the differences in the magnitude of coronary
occlusion, the duration of the occlusion, the modifying influence
of local and systemic blood flow, and the adequacy of coronary collaterals.
Schematic summarizing the current view of the key pathophysiologic
events in acute coronary syndromes.
In patients with unstable angina, most episodes of resting ischemia
occur without antecedent changes in myocardial oxygen demand but
are triggered by primary and episodic ...