Pathogenesis, Progression, and Complications of Atherosclerosis and Ischemic Heart Disease

Cellular and Molecular Mechanisms of Atherosclerosis

Atherosclerosis is a chronic inflammatory disease of the arterial walls caused by the accumulation of lipids and immune cells. This condition leads to the narrowing of blood vessels and, eventually, ischemic heart disease.

Pathogenesis of Atherosclerosis

1. Endothelial Dysfunction

The initial step involves damage to the endothelial lining due to factors such as hypertension, hypercholesterolemia, diabetes, and smoking.

2. Lipid Accumulation and Foam Cell Formation

Low-density lipoproteins (LDL) infiltrate the damaged endothelium and undergo oxidation, leading to immune activation and macrophage infiltration.

3. Inflammatory Response

Macrophages engulf oxidized LDL to form foam cells, resulting in plaque formation and increased local inflammation.

Progression of Atherosclerosis

1. Plaque Growth and Fibrous Cap Formation

As foam cells accumulate, a fibrous cap forms, stabilizing the plaque.

2. Plaque Rupture and Thrombosis

If the fibrous cap weakens, plaque rupture can occur, leading to clot formation and arterial blockage.

Complications of Atherosclerosis

1. Ischemic Heart Disease

The narrowing of coronary arteries results in reduced oxygen supply to the heart muscle, causing angina and myocardial infarction.

2. Stroke

Carotid artery plaques may lead to embolism and cerebral infarction.

3. Peripheral Artery Disease

Blockages in peripheral arteries reduce blood flow to extremities, causing pain and tissue damage.

Conclusion

Understanding the molecular mechanisms of atherosclerosis aids in early diagnosis and treatment. Lifestyle modifications, medications, and interventional procedures play a crucial role in managing ischemic heart disease.