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Coronary Artery Disease: Etiology and Pathogenesis

*Morbus ischemicus cordis*

For medical students2 min readUpdated 2026-10-10

Coronary artery disease (CAD) is a clinical syndrome characterized by myocardial ischemia due to coronary insufficiency. The underlying mechanism is an acute or chronic imbalance between coronary blood flow and the metabolic demands of the myocardium.

Core PathologyMismatch between myocardial blood supply and metabolic demand
Primary CauseArterial lumen occlusion by atherosclerotic plaques
Perfusion PhaseMyocardial blood supply occurs predominantly during diastole
Normal StateOxygen delivery fully meets metabolic demands

Causes and Clinical Presentations

The development of ischemia is directly linked to the obstruction (narrowing) of the coronary arteries. There are three main causes of impaired main vessel blood flow:

The clinical presentation and diagnosis depend on the disease course. Chronic CAD presents with recurrent episodes of substernal chest pain known as angina pectoris. Acute presentations manifest as myocardial infarction.

Coronary Anatomy and Collaterals

Understanding the pathogenesis of CAD requires a knowledge of cardiac vascular topography. The ostia of the coronary arteries arise directly from the aorta, located just superior to the aortic valve cusps.

Each artery subsequently divides into two interconnected systems of branches, classified by their depth within the myocardial wall:

  1. Subepicardial network: vessels running in the outer layers, between the epicardium and myocardium.
  2. Subendocardial network: vessels running in the deep layers, between the endocardium and myocardium.

These two systems are not isolated; they are extensively interconnected by vascular channels called anastomoses (collaterals). The physiological role of collateral circulation is local blood volume redistribution. When main vessel blood flow is impaired, these anastomoses provide partial ischemic compensation.

Phase-Dependent Coronary Blood Flow

A critical concept for understanding the mechanism of action of many antianginal drugs is the phasic nature of coronary perfusion. Myocardial blood supply occurs predominantly during the relaxation phase, diastole.

Adequate perfusion during cardiac contraction (systole) is prevented by two factors:

Oxygen Supply and Demand Balance

The physiological norm is defined as a state where oxygen ($O_2$) delivery fully covers all myocardial metabolic demands.

Myocardial oxygen demand is not static. It predictably increases during states that force the heart to work harder, such as physical exertion or psycho-emotional stress. Conversely, demand decreases at rest or in the supine position.

In a healthy organism, adequate $O_2$ delivery is maintained by a complex regulatory system. The primary mechanism is autoregulation of coronary vascular tone in response to local metabolic changes. In CAD, this balance is disrupted.

Mnemonic

To easily remember why the heart does not receive blood during systole, imagine elevator doors. When the aortic valve cusps open to eject blood, they press against the aortic walls, covering the entrances (ostia) to the coronary arteries. At the same time, the heart muscle itself contracts tightly, compressing the intramural vessels.

Frequently asked questions

Why does coronary blood flow stop during systole?

Two factors contribute to this. First, the open aortic valve cusps mechanically obstruct the coronary artery ostia. Second, the contracting myocardium compresses the vessels running within its wall.

What is the most common cause of coronary vessel obstruction?

The most frequent cause is luminal occlusion by atherosclerotic plaques. Thrombosis often develops over an existing plaque, worsening the ischemia.

What role do coronary anastomoses play?

Anastomoses connect the subepicardial and subendocardial vascular networks. They provide collateral circulation, allowing local blood redistribution and partial ischemic compensation when main blood flow is compromised.

What determines myocardial oxygen demand?

Oxygen ($O_2$) demand increases during physical exertion and psycho-emotional stress. At rest or in the supine position, myocardial oxygen demand decreases.

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