Coronary Artery Disease.pptx Coronary artery disease (CAD) involves impairment of blood flow through the coronary arteries, most commonly by atheromas
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A history of previous episodes of anginal pain with recent worsening may be present. The pain of infarction is similar in character and distribution is similar to anginal pain. But it is more severe, prolonged (lasts more than 20 minutes), persisting at rest and not responding to nitrates. There may be vomiting, anxiety and a feeling of impending death One or more of the physical signs of myocardial ischemia may be present Other common physical signs include pallor, sweating, cyanosis, hypotension, arrhythmias (most commonly ventricular ectopic beats), pericardia! friction rub, signs of congestive heart failure and cardiogenic shock. ? Salient investigations include serial electrocardiograms and cardiac injury enzymes In developed countries, CAD is the leading cause of death in both sexes, accounting for about one third of all deaths. Mortality rate among white men is about 1/10,000 at ages 25 to 34 and nearly 1/100 at ages 55 to 64. Mortality rate among white men aged 35 to 44 is 6.1 times that among age-matched white women. Mortality rate among women increases after menopause and, by age 75, equals or even exceeds that of men.
Coronary Artery Disease.pptx Coronary artery disease (CAD) involves impairment of blood flow through the coronary arteries, most commonly by atheromas
- 1. CORONARY ARTERY DISEASE DR SWETHA B P ASSISTANT PROFESSOR DEPARTMENT OF PRACTICE OF MEDICINE
- 3. INTRODUCTION ? Coronary artery disease (CAD) involves impairment of blood flow through the coronary arteries, most commonly by atheromas ? Clinical presentations include silent ischemia, angina pectoris, acute coronary syndromes (unstable angina, MI), and sudden cardiac death.
- 4. EPIDEMIOLOGY ? In developed countries, CAD is the leading cause of death in both sexes, accounting for about one third of all deaths. ? Mortality rate among white men is about 1/10,000 at ages 25 to 34 and nearly 1/100 at ages 55 to 64. ? Mortality rate among white men aged 35 to 44 is 6.1 times that among age- matched white women. Mortality rate among women increases after menopause and, by age 75, equals or even exceeds that of men.
- 5. ETIOLOGY ? Usually, CAD is due to subintimal deposition of atheromas in large and medium-sized coronary arteries. ? Less often, CAD is due to coronary spasm. ? Rare causes include coronary artery embolism, dissection, aneurysm (eg, in Kawasaki disease), and vasculitis (eg, in SLE, syphilis).
- 6. PATHOPHYSIOLOGY ? Coronary atherosclerosis 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 produce ischemia varies with O2 demand.
- 8. ? Occasionally, an atheromatous plaque ruptures or splits. ? Reasons are unclear but probably relate to plaque morphology, plaque Ca content, and plaque softening due to an inflammatory process. ? Rupture exposes collagen and other thrombogenic material, which activates 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 acute coronary syndromes (ACS), depend on the location and degree of obstruction and range from unstable angina to transmural infarction.
- 10. CORONARY ARTERY SPASM ? Is a transient, focal increase in vascular tone, markedly narrowing the lumen and reducing blood flow. ? 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 abnormalities of nitric oxide production or an imbalance between endothelium-derived contracting and relaxing factors.
- 11. CORONARY ARTERY SPASM ? In arteries with atheroma, the atheroma may cause 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.
- 12. RISK FACTORS ? Risk factors for CAD are the same as those for atherosclerosis: 1. high blood levels of low-density lipoprotein (LDL) cholesterol and lipoprotein a, low blood levels of high-density lipoprotein (HDL) cholesterol, diabetes mellitus (particularly type 2), smoking, obesity, and physical inactivity. 2. Smoking maybe a stronger predictor of MI in women (especially those < 45). Genetic factors play a role, and several systemic disorders (eg, hypertension, hypothyroidism) and metabolic disorders (eg, hyperhomocysteinemia) contribute to risk.
- 13. TREATMENT ? Percutaneous coronary intervention ? For acute thrombosis, sometimes fibrinolytic drugs ? Coronary artery bypass grafting ? Treatment generally aims to reduce cardiac workload, improve coronary artery blood flow, and, over the long term, halt and reverse the atherosclerotic process. Coronary blood flow can be improved by percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). An acute coronary thrombosis may sometimes be dissolved by fibrinolytic drugs
- 14. PREVENTION ? Prevention of CAD involves modifying atherosclerosis risk factors a. smoking cessation, weight loss, a healthful diet, regular exercise, modification of serum lipid levels, and control of hypertension and diabetes. b. Modification of serum lipid levels may slow or even partially reverse the progression of CAD. LDL targets are < 100 mg/dL (< 2.59 mmol/L) for patients with known CAD or 70 to 80 mg/dL (1.81 to 2.07 mmol/L) for those with a history of an ischemic event.