Fatty lesions, beginning as cholesterol crystals, are deposited on the arteries' intimal layer. This develops and stimulates fibrous tissue and smooth muscle growth, creating additional layers where larger plaques grow. The plaques develop into obstructive lesions, forming fibroblasts, which deposit dense connective tissue, leading to sclerosis.
Patients become symptomatic when 75% of the coronary vessel is occluded, which leads to decreased coronary blood flow. Ischemia can develop and lead to angina pectoris with resulting myocardial infarction and tissue damage, even death if there is no intervention in time.
The cells become increasingly irritable and vulnerable to fibrillation, alterations in the conduction pathways, and thrombus formation.
Age, gender, genetic predisposition, obesity, hyperlipidemia, hypertension, stress, diabetes mellitus, and smoking. CAD is exacerbated by PVD, carotid disease, and compromised pulmonary system.
Extreme elevation of fatty substances in the blood, such as hypercholesterolemia and hypertriglyceridemia.
Increased risk for atherosclerosis, and thus cardiac disease and stroke.
Mostly genetically but it can be attributed to dietary intake.
High-density (healthy) cholesterol is a hyperlipidemia that protects from plaque buildup.