cardiovascular disorders
Overview of Coronary Artery Disease
Pathophysiology of Coronary Artery Disease
 is often irregularly distributed in different vessels but typically occurs at points of turbulence (eg, vessel bifurcations). As the atheromatous plaque grows, the arterial lumen progressively narrows, resulting in ischemia (often causing Angina Pectoris ). The degree of stenosis required to cause ischemia varies with oxygen demand. Occasionally, an atheromatous plaque ruptures or splits. Reasons are unclear but probably relate to plaque morphology, plaque calcium content, and plaque softening due to an inflammatory process. Rupture exposes collagen and other thrombogenic material, which activate platelets and the coagulation cascade, resulting in an acute thrombus, which interrupts coronary blood flow and causes some degree of myocardial ischemia. The consequences of acute ischemia, collectively referred to as Overview of Acute Coronary Syndromes (ACS) (ACS), depend on the location and degree of obstruction and range from unstable angina, non-ST elevation myocardial infarction (NSTEMI), to ST elevation myocardial infarction (STEMI), which can result in transmural infarction, and other is a transient, focal increase in vascular tone, markedly narrowing the lumen and reducing blood flow; symptomatic ischemia ( Variant Angina ) may result. Marked narrowing can trigger thrombus formation, causing infarction or life-threatening arrhythmia. Spasm can occur in arteries with or without atheroma. In arteries without atheroma,basal coronary artery tone is probably increased, and response to vasoconstricting stimuli is probably exaggerated. The exact mechanism is unclear but may involve endothelial cell abnormalities of nitric oxide production or an imbalance between endothelium-derived contracting and relaxing factors. In arteries with atheroma,the atheroma causes endothelial dysfunction, possibly resulting in local hypercontractility. Proposed mechanisms include loss of sensitivity to intrinsic vasodilators (eg, acetylcholine) and increased production of vasoconstrictors (eg,angiotensin II, endothelin, leukotrienes, serotonin, thromboxane) in the area of the atheroma. Recurrent spasm may damage the intima, leading to atheroma formation. Use of vasoconstricting drugs (eg,cocaine,nicotine) and emotional stress also can trigger coronary spasm. Coronary artery dissectionis a rare, non-traumatic tear in the coronary intima with creation of a false lumen. Blood flowing through the false lumen expands it, which restricts blood flow through the true lumen sometimes causing coronary ischemia or infarction. Dissection may occur in atherosclerotic or non-atherosclerotic coronary arteries. Non-atherosclerotic dissection is more likely in pregnant or postpartum women and/or patients with fibromuscular dysplasia or other connective tissue disorders. 