Ischemic Heart Disease

Chapter: Ischemic Heart Disease
McMaster Section Editor(s): P.J. Devereaux
Section Editor(s) in Interna Szczeklika: Andrzej Budaj, Wiktoria Leśniak
McMaster Author(s): P.J. Devereaux
Author(s) in Interna Szczeklika: Andrzej Budaj, Anetta Undas
Additional Information

Ischemic heart disease (IHD) comprises all types of myocardial ischemia (ie, reduced blood supply), regardless of the pathologic mechanism.

Coronary artery disease (CAD) is IHD due to atherosclerosis of a coronary artery.

Classification Top

1. Classification of CAD:

1) Stable CAD:

a) Stable angina pectoris.

b) Microvascular angina (syndrome X).

c) Angina associated with myocardial bridging of coronary arteries.

d) Vasospastic angina (Prinzmetal variant angina).

2) Acute coronary syndromes (ACSs).

2. ACS classification based on initial electrocardiography (ECG) findings:

1) Non–ST-segment elevation ACS.

2) ST-segment elevation ACS.

3. Classification of ACS based on clinical manifestations, biochemical markers of myocardial necrosis, and ECG:

1) Unstable angina (UA).

2) Non–ST-segment elevation myocardial infarction (NSTEMI).

3) ST-segment elevation myocardial infarction (STEMI).

4) Unspecified myocardial infarction (MI). ECG abnormalities that do not allow an unequivocal diagnosis of ST-segment elevation: left bundle branch block (LBBB) (acute or preexisting), pacemaker rhythm, or infarction diagnosed on the basis of clinical and biochemical criteria, where an ECG was performed >24 hours after the onset of symptoms.

5) Sudden cardiac death.

4. Classification of MI based on the evolution of ECG features:

1) Q-wave MI.

2) Non–Q-wave MI.

Etiology and Pathogenesis Top

1. Etiology of IHD:

1) Most commonly, IHD is due to coronary atherosclerosis.

2) Less commonly, IHD is due to coronary artery spasm (Prinzmetal variant angina, illicit drug use [eg, cocaine], or discontinuation of nitrates), coronary artery embolism, vasculitis of the coronary arteries, metabolic disorders affecting the coronary arteries, anatomical defects of the coronary arteries, coronary artery injury, arterial thrombosis due to disorders of hemostasis, reduced oxygen supply in relation to demand (aortic stenosis or regurgitation, hypertrophic cardiomyopathy, carbon monoxide poisoning, decompensated thyrotoxicosis, long-standing hypotension, anemia, myocardial bridging), or aortic dissection.

2. Etiology of stable angina pectoris: Stable angina pectoris is usually due to occlusion of an epicardial coronary artery by an atherosclerotic plaque.

Classification of epicardial coronary artery stenosis:

1) Noncritical stenosis: Approximately 50% focal reduction of the coronary artery luminal diameter and ~75% reduction in the coronary artery cross-sectional area. An atherosclerotic plaque causing the occlusion may potentially lead to ACS, but it remains asymptomatic as long as it is stable.

2) Significant subcritical stenosis: Approximately 50% to 75% reduction of the coronary artery luminal diameter. Coronary blood flow may adapt to the demand to some extent, but in the case of a further increase of cardiac output (exercise or pharmacologic stress test, eg, dobutamine), the symptoms of angina will occur.

3) Critical stenosis: Approximately 75% reduction of the coronary artery luminal diameter and >90% reduction of the coronary artery cross-sectional area. Symptoms of myocardial ischemia may occur even at rest.

3. Etiology of ACS: A sudden imbalance between the myocardial oxygen demand and supply, most frequently due to sudden occlusion of a coronary artery by a thrombus formed on a ruptured atherosclerotic plaque.

1) UA most frequently results from rupture of an eccentric plaque. The resulting thrombus reduces coronary blood flow, but the occlusion is not complete.

2) NSTEMI is the result of a process similar to UA and is associated with elevation of troponin levels.

3) In STEMI, the thrombus usually causes a complete and sudden occlusion of a coronary artery. Necrosis starts to develop within 15 to 30 minutes of the cessation of blood flow and spreads from the subendocardium to the epicardium. The rate at which necrosis develops depends on the diameter of the occluded artery and the collateral circulation.

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