Ischemic Heart Disease

How to Cite This Chapter: Devereaux PJ, Jaeschke R, Budaj A, Beręsewicz A, Undas A. Ischemic Heart Disease. McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. Accessed September 30, 2020.
Last Updated: July 12, 2019
Last Reviewed: July 12, 2019
Chapter Information

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

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


1. Classification of CAD:

1) Stable CAD:

a) Stable angina pectoris.

b) Vasospastic angina (Prinzmetal variant angina).

c) Microvascular angina (syndrome X).

d) Angina associated with myocardial bridging of coronary arteries.

2) Acute coronary syndromes (ACSs).

2. ACS classification based on initial electrocardiographic (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 (acute or preexisting), pacemaker rhythm, or infarction diagnosed on the basis of clinical and biochemical criteria, with ECG 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 PathogenesisTop

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, anatomic 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 [shock]), anemia, myocardial bridging), or aortic dissection.

2. Etiology of ACS: A sudden imbalance between the myocardial oxygen demand and supply, most frequently due to a 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 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 diameter of the occluded artery and collateral circulation.

3. Myocardial injury versus MI: Myocardial injury is defined as elevation of cardiac troponin values >99th percentile. In some situations myocardial injury is associated with MI (Table 3.11-1).


Table 3.11-1. Types of MI based on the fourth universal definition of MI

Criteria for types 1 and 2 MIa

Type 1

MI caused by atherothrombotic event precipitated by plaque erosion or plaque rupture with thrombus formation

Type 2

Ischemic myocardial injury, usually in the setting of coronary atherosclerosis, from oxygen supply-demand mismatch without plaque erosion or rupture (eg, sudden anemia, prolonged tachyarrhythmia, coronary artery spasm or dissection, shock)

Criteria for type 3 MI

Sudden cardiac death with new ischemic ECG changes or ventricular fibrillation with symptoms suggestive of myocardial ischemia; death occurs before blood biomarkers can be obtained or before increases in biomarkers are identified

Criteria for types 4 and 5 MI (procedure-related MI within 48 hours after index procedure)b

Type 4a

PCI-related MI

Type 4b

In-stent thrombosis documented angiographically or by the same criteria as type 1 MI

Type 4c

In-stent restenosis or restenosis after balloon angioplasty documented angiographically or by the same criteria as type 1 MI

Type 5

CABG-related MI

a Rise and fall of cardiac troponins with ≥1 troponin value >99th percentile of URL along with either new ischemic ECG changes, development of pathologic Q waves, symptoms of acute myocardial ischemia, imaging evidence of new wall motion abnormality or loss of viable myocardium, or angiographic identification of coronary thrombus

b Further specific criteria: Coronary procedure–related MI ≤48 hours after the index procedure with an elevation in cardiac troponin values >5 × >99th percentile of URL for type 4a MI, >10 × for type 5 MI in patients with normal values at baseline. Patients with elevated but stable or declining baseline values must meet the criterion of >5-fold or >10-fold increase as well as have a change ≥20% from the baseline value. Patients must also have one of the following: new ischemic changes (type 4a MI only), new pathologic Q waves, imaging evidence of loss of viable myocardium, or angiographic findings of a procedure-related flow-limiting complication.

Adapted from Circulation. 2018;138(20):e618-e651.

CABG, coronary artery bypass graft; ECG, electrocardiography; MI, myocardial infarction; PCI, percutaneous coronary intervention; URL, upper reference limit.

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