Causes of development and clinical forms
The development of ischemia is directly related to obstruction (narrowing of the lumen) of the coronary arteries. There are three main causes of impaired trunk blood flow:
- Atherosclerotic lesion: the formation of plaques inside the vessel is the most frequent cause of organic narrowing.
- Thrombosis: often occurs in the area of an existing atherosclerotic plaque, leading to a sharp occlusion of the lumen.
- Coronary spasm: a functional narrowing of vessels, which is significantly less common than organic lesions.
The clinical presentation and diagnosis depend on the course of the process. The chronic form of CAD manifests as regular episodes of retrosternal pain — angina pectoris (angina pectoris). The acute form manifests as myocardial infarction (myocardial infarction).
Anatomy of the coronary bed and collaterals
To understand the pathogenesis of CAD, it is necessary to consider the topography of the heart vessels. The ostia of the coronary arteries depart directly from the aorta, located just above the cusps of the aortic valve.
Further, each artery divides into two interconnected systems of branches, classified by their depth within the heart wall:
- Subepicardial network: vessels run in the outer layers, between the epicardium and myocardium.
- Subendocardial network: vessels run in the deep layers, between the endocardium and myocardium.
Both of these systems are not isolated from each other. They are abundantly connected by special junctions — anastomoses (collaterals). The physiological role of collateral circulation lies in the local redistribution of blood volumes. When main blood flow is impaired, it is the anastomoses that provide partial compensation for ischemia.
Phasic nature of blood flow
The most important aspect determining the action of many antianginal drugs is the phasic nature of coronary perfusion. Myocardial blood supply is carried out predominantly during the relaxation phase — diastole.
At the moment of heart contraction (systole), adequate perfusion is impossible. This is hindered by two factors:
- Mechanical: the powerful muscle layer of the contracting myocardium literally compresses the coronary vessels passing through its thickness.
- Hemodynamic: the open cusps of the aortic valve temporarily block the ostia of the coronary arteries.
Balance between oxygen delivery and demand
The criterion of physiological norm is a state in which oxygen ($O_2$) delivery fully covers all metabolic demands of the myocardium.
The heart's oxygen demand is not a static value. It predictably increases under conditions that force the heart to work harder: during physical exertion or against the background of psycho-emotional stress. Conversely, the demand decreases at rest or upon assuming a horizontal position.
In a healthy body, the adequacy of $O_2$ delivery is maintained by a complex system of interrelated regulation. The main mechanism here is the autoregulation of coronary vessel tone in response to local metabolic changes. In CAD, this balance is disrupted.
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 walls of the aorta, closing the entrances (ostia) to the coronary arteries. And the heart muscle itself at that moment is tightly squeezed, blocking the vessels inside it.
Class and exam questions
Why does coronary blood flow stop during systole?
Two factors contribute to this. First, the open cusps of the aortic valve mechanically block the ostia of the coronary arteries. Second, the contracting myocardium compresses the vessels passing through its thickness.
What is the most frequent cause of coronary vessel obstruction?
The most frequent cause is the occlusion of the vessel lumen by atherosclerotic plaques. Against the background of an existing plaque, thrombosis can also occur, worsening ischemia.
What role do anastomoses play in the heart?
Anastomoses connect the subepicardial and subendocardial vascular networks. They provide collateral circulation, which allows local redistribution of blood and partial compensation for ischemia when the main blood flow is impaired.
What does myocardial oxygen demand depend on?
Oxygen ($O_2$) demand increases during physical exertion and psycho-emotional stress. At rest or in a horizontal position, the heart muscle's oxygen demand decreases.
What else to study on this topic
- Mechanisms of autoregulation of coronary vessel tone in response to metabolic changes.
- Pathogenesis of atherosclerotic plaque formation and thrombosis.
- Differences in the pathogenesis of stable angina pectoris and myocardial infarction.
- Pharmacological targets for managing the balance of myocardial oxygen delivery and demand.
Master the entire topic in the «Pharmacology» course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Coronary Artery Disease: Etiology and Pathogenesis" and 5,304 more pages of the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 116 video lessons on the subject
Other topics in the "Antiarrhythmic Agents" section
Free video lessons: pharmacologyShort lessons with study notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.