HUMAN MEDICAL BIOLOGY, ANATOMY, PHYSIOLOGY AND PATHOLOGY - Ya.I. Fedoniuk 2010

ANATOMY, PHYSIOLOGY, PATHOLOGY

CHAPTER 5. THE PROCESS OF BLOOD AND LYMPH CIRCULATION. ITS PATHOLOGY

CARDIOVASCULAR DISEASES

CORONARY HEART DISEASE

1. ACUTE CORONARY HEART DISEASE. MYOCARDIAL INFARCTION

Myocardial infarction (MI) is an acute condition caused by The Development of one or more foci of ischemic necrosis in The Heart Muscle due to absolute or relative insufficiency of coronary Blood flow. The direct causes include prolonged spasm, thrombosis, or thromboembolism of the coronary Arteries, as well as functional overstrain in the presence of atherosclerotic occlusion of these vessels.

Myocardial infarction is classified taking into account the size and localization of necrosis.

Depending on the size of the lesion, large-focal (macrofocal) and small-focal (microfocal) myocardial infarctions are distinguished.

Taking into account the depth of myocardial involvement, the following forms of myocardial infarction are distinguished:

- transmural (the lesion extends across the entire thickness of the myocardium);

- intramural (necrosis develops within the myocardial wall, without reaching the endocardium and epicardium).

In small-focal myocardial infarctions, the following forms are distinguished:

- subepicardial (involving the myocardial layers adjacent to the epicardium);

- subendocardial (necrosis located in the myocardial layer adjacent to the endocardium).

The Pathogenesis of MI is primarily driven by the cessation of blood flow to a specific area of the heart muscle, which leads to myocardial damage, necrosis, and impaired viability of the peri-infarction zone.

Myocardial necrosis causes prolonged pain syndrome, may manifest as arrhythmias and heart blocks, while transmural necrosis can lead to cardiac rupture or acute aneurysm.

Myocardial necrosis and dysfunction of the peri-infarction zone contribute to a decrease in stroke volume and cardiac output. Clinically, this manifests as acute left ventricular failure, presenting as pulmonary edema and (or) cardiogenic Shock. The latter is accompanied by a sharp drop in Blood supply to vital Organs, leading to microcirculatory disorders, tissue Hypoxia, and the accumulation of metabolic products. The reduction in coronary blood flow further impairs the Pumping Function of the Heart and exacerbates cardiogenic shock and pulmonary edema, which are the main causes of death in myocardial infarction.

Metabolic Disorders in the myocardium cause severe heart rhythm disturbances that frequently result in ventricular fibrillation.

Morphological examination of the heart in patients who died from myocardial infarction confirms varying degrees of coronary atherosclerosis.

Three main zones of alterations can be identified in myocardial infarction: the focus of necrosis, the pre-necrotic zone, and the area of the heart muscle remote from the necrotic zone. 6–8 hours after the onset of the disease, edema of the interstitial tissue and muscle fibers appears, accompanied by capillary dilation and blood stasis within them. After 10–12 hours, these changes become more distinct, accompanied by marginal margination of leukocytes and erythrocytes in the vessels, and diapedetic hemorrhages at the periphery of the affected area.

As early as 3–5 hours after the development of myocardial infarction, severe and irreversible structural Changes in the muscle fibers occur in the heart muscle, leading to their death.

The ultimate consequence of myocardial necrosis is The formation of a Connective Tissue scar.