Coronary Atherosclerosis

CAD is thought to begin with damage or injury to the intimal layer of coronary artery, sometimes as early as childhood. The damage may be caused by various factors, including: smoking, hypertension, hypercholestromia, diabetes or insulin resistance, radiation therapy to the chest, as used for certain types of cancer, and sedentary lifestyle. Once the intimal layer of coronary artery is damaged, fatty deposits (plaques) made up of cholesterol and other cellular waste products tend to accumulate at the site of injury in a process called atherosclerosis. If the surface of these plaques breaks or ruptures, platelets will clump at the site to try to repair the artery. This clump can block the artery, leading to a heart attack. Recent research has
supported the evidence that stenosis does not contribute much to the development of acute coronary injury or MI; it is the sudden rupture of the plaque that leads to the acute events (citation). Inadequate flow of blood to the myocardial cells causes ischemia or infarction. It leads to myocardial damage, resulting myocardial death and later scarring without heart muscle regeneration. Chronic high-grade stenosis of the coronary arteries can induce transient ischemia, which leads to the induction of a ventricular arrhythmia, which may terminate into ventricular fibrillation leading to death.
Typically, CAD occurs when part of the smooth, elastic lining inside a coronary artery develops inflammation or
atherosclerosis. With atherosclerosis, the artery's lining becomes hardened, stiffened, and swollen with calcium deposits, fatty deposits, and abnormal inflammatory cells - to form a plaque.
Cardiac syndrome X is a term that describes chest pain (Angina pectoris) and chest discomfort in patients who do not show signs of blockages in the larger coronary arteries of their hearts when an angiogram (coronary angiogram) is being performed. The exact cause of cardiac syndrome X is unknown. One explanation is microvascular dysfunction. For reasons that are not well known, women are more likely than men to have it; however, hormones and other risk factors unique to women may play a role. In summary the pathophysiology of an acute coronary event includes (1) endothelial damage through plaque disruption, irregular luminal lesions, and shear injury; (2) platelet aggregation; (3) thrombus formation causing partial or total lumen occlusion; (4) coronary artery vasospasm; and (5) reperfusion injury caused by oxygen free radicals, calcium, and neutrophils. In patients with non-infarction ACS, spontaneous fibrinolysis of the thrombus occurs rapidly, minimizing ischemic insult; persistence of the occlusive thrombus, however, results in
MI.