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

ANATOMY, PHYSIOLOGY, PATHOLOGY

CHAPTER 5. BLOOD AND LYMPH CIRCULATION PROCESSES AND THEIR PATHOLOGY

CARDIOVASCULAR DISEASES

ATHEROSCLEROSIS

Atherosclerosis is a chronic disease characterized by systemic damage to Arteries, manifested by the deposition of Lipids and calcium salts in the tunica intima, followed by hardening of the vessel walls and narrowing of their lumen.

WHO definition: "atherosclerosis encompasses various combinations of Changes in the intima of arteries, manifested by focal accumulation of lipids, complex carbohydrate compounds, Blood elements and substances circulating in the blood, formation of Connective Tissue, and calcium deposition."

Sclerotic vessels (most commonly localized in the aorta, coronary arteries, cerebral arteries, and Arteries of the lower extremities) are distinguished by increased rigidity and fragility. Due to impaired elasticity, they fail to appropriately adjust their lumen in response to the blood supply demands of Organs or Tissues.

A pronounced atherosclerotic process typically leads to the narrowing and even complete occlusion of the arterial lumen. In cases of gradual arterial sclerosis, organs with compromised blood supply undergo atrophic changes with the progressive replacement of functionally active parenchyma by connective tissue.

Rapid narrowing or complete occlusion of an arterial lumen (due to thrombosis, thromboembolism, or Hemorrhage into a plaque) results in the Necrosis of the ischemic area of the organ, i.e., an infarction. Myocardial infarction is the most frequent and severe complication of coronary atherosclerosis.

The Essence of the process lies in the appearance of a gruel-like lipid-protein detritus (athere) in the arterial intima along with focal proliferation of connective tissue (sclerosis), leading to The formation of an atherosclerotic plaque. Arteries of elastic and muscular-elastic types are most commonly affected.

The atherosclerotic process is characterized by a staged progression with changing MACROSCOPIC AND MICROSCOPIC features.

Macroscopic examination reveals the following types of atherosclerotic changes reflecting the dynamics of the process: 1) fatty streaks or bands; 2) fibrous plaques; 3) complicated lesions manifesting as fibrous plaques with ulceration, hemorrhages, and deposition of thrombotic masses; 4) calcinosis or atherocalcinosis.

Fatty streaks are yellow or yellowish-gray patches (Fig. 5.53 a) that merge to form bands. Fatty streaks and bands contain lipids, do not protrude above the intimal surface of the vessel, and primarily appear on the posterior wall of the aorta and at the sites of origin of its branches.

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Fig. 5.53. Atherosclerosis (aorta)

Fibrous plaques are firm, oval or rounded, white or yellowish-white formations (Fig. 5.53 b) that rise above the intimal surface and contain lipids. Fibrous plaques often merge with one another, causing the inner surface of the vessel to become nodular and resulting in the narrowing of its lumen (stenosing atherosclerosis).

Complicated lesions are characterized by the destruction of the plaque cap, ulceration—upon which thrombotic masses may deposit—and hemorrhages into the body of the plaque (Fig. 5.53 c, d, e). These complicated lesions are associated with: atheromatous embolization, vascular thromboembolism with potential organ infarction, aneurysm formation, and arterial hemorrhage resulting from ulcer erosion of the vessel wall.

Calcinosis, or atherocalcinosis, is the terminal stage of atherosclerosis, characterized by the deposition of calcium salts into fibrous plaques, i.e., their calcification. The plaques acquire a stony consistency, causing severe deformation of the vascular wall at the affected site.