Coronary Artery Disease-audio

Coronary artery disease (CAD) results from the narrowing of the coronary arteries over time because of atherosclerosis. The primary effect of CAD is a diminished supply of oxygen and nutrients to myocardial tissue because of decreased blood flow.
Causes
Atherosclerosis (most common)
Dissecting aneurysm
Infectious vasculitis
Syphilis
Congenital abnormalities
Pathophysiology
Fatty, fibrous plaques progressively occlude the coronary arteries, reducing the volume of blood that can flow through them and leading to myocardial ischemia.
As atherosclerosis progresses, luminal narrowing is accompanied by vascular changes that impair the ability of the diseased vessel to dilate. The consequent precarious balance between myocardial oxygen supply and demand threatens the myocardium distal to the lesion. When oxygen demand exceeds what the diseased vessel can supply, the result is localized myocardial ischemia.
Myocardial cells become ischemic within 10 seconds after coronary artery occlusion. Transient ischemia causes reversible changes at the cellular and tissue levels, depressing myocardial function. Within several minutes, oxygen deprivation forces the myocardium to shift from aerobic to anaerobic metabolism, leading to accumulation of lactic acid and reduction of cellular pH. Without intervention, this sequence of events can lead to tissue injury or necrosis.
The combination of hypoxia, reduced energy availability, and acidosis rapidly impairs left ventricular function. As the fibers become unable to shorten normally, the force of contractions and velocity of blood flow in the affected myocardial region become inadequate. Moreover, wall motion in the ischemic area becomes abnormal and each contraction ejects less blood from the heart. Restoring blood flow through the coronary arteries restores aerobic metabolism and contractility. Failure to do so results in myocardial infarction (MI).
Signs and symptoms
Angina (pain may be described as burning, squeezing, or tightness that radiates to the left arm, neck, jaw, or shoulder blade)
Nausea and vomiting
Cool extremities and pallor
Diaphoresis caused by sympathetic stimulation
Fatigue and dyspnea
Xanthelasma (fat deposits on the eyelids)
Diagnostic test results
Electrocardiography shows ischemic changes during anginal episode.
Stress testing detects ST-segment changes during exercise or pharmacologic stress.
Coronary angiography reveals the location and degree of coronary artery stenosis or obstruction, collateral circulation, and the condition of the artery beyond the narrowing.
Myocardial perfusion imaging with thallium-201 may be performed during treadmill exercise to detect ischemic areas of the myocardium.
Stress echocardiography shows abnormal wall motion in ischemic areas.
Electron-beam computed tomography identifies calcium deposits in coronary arteries.
Cardiac catheterization reveals blockage in the coronary arteries.
Lipid profile shows elevated cholesterol levels.
Treatment
Drug therapy: angiotensin-converting enzyme inhibitors, thrombolytics, diuretics, glycoprotein IIb/IIIa inhibitors, nitrates, beta-adrenergic or calcium channel blockers; antiplatelet, antilipemic, antihypertensive drugs
Coronary artery bypass graft (CABG) surgery
“Keyhole” or minimally invasive surgery, an alternative to traditional CABG
Angioplasty
Atherectomy
Stent placement to maintain patency of reopened artery
Lifestyle modifications to limit progression of CAD: stopping smoking, exercising regularly, maintaining ideal body weight, and eating a low-fat, low-sodium diet

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