ISCHEMIC HEART DISEASE Afsar fathima M.Pharm

ANGINA PECTORIS Angina pectoris is a clinical syndrome of chest discomfort caused by reversible myocardial ischemia that produces disturbances in myocardial function without causing myocardial necrosis.

Suffocating substernal pain in the chest, over the heart, on exertion which may radiate to left arm , neck of the jaw, and is relieved by rest

EPIDEMIOLOGY incidence rate - 1.5% Cardiovascular diseases (CVD) claimed 949,619 lives 1 of every 2.5 deaths, in the United States in 1998. four to five times more common in men in their mid-30s

Reasons & risk factors Coronary artery spasm Partial coronary thrombosis Abnormal endothelial functions Stress variation in blood pressure Impairment in NO production Risk factors; Anemia, hypertension, acute & chronic anxiety, thyrotoxicosis, obesity, heart failure

Classification Classical or stable angina( angina of effort or exertional angina) Atherosclerosis of larger coronary arteries Cresendo or unstable angina ( Preinfraction angina) Recurrent attacks of angina Results from combination of atherosclerotic plaques, platelet aggregation at ruptured plaque & vasospasm.

Variant or prinzmetal angina (Vasospastic angina) Pain appears even during rest or during sleep & is usually unrelated to exercis recurrent localized coronary vasospasm Silent Myocardial Ischemia With out producing anginal pain

Coronary Artery

Pathophysiology

Pathophysiology

Pathophysiology of MI

Pathophysiology of MI

Pathophysiology Angina Pectoris is mainly due to diminished coronary perfusion relative to the myocardial demand because of narrowing of the epicardial coronary arteries, intraluminal thrombosis, platelet aggregation and vasospasm

C L I N I C A L PRESENTATION OF ANGINA SYMPTOMS Sensation of pressure or burning over the sternum or near it, often but not always radiating to the left jaw, shoulder, and arm; also, chest tightness and shortness of breath. Pain usually lasting from 0.5 to 30 minutes, often with a visceral quality (deep location). Precipitating factors include exercise, cold environment, walking after a meal, emotional upset, fright, anger, and coitus. Relief occurs with rest and nitroglycerin. SIGNS Abnormal heart sounds  

LABORATORY TESTS Typically, no laboratory tests are abnormal; however, if the patient has intermediate- to high-risk features for unstable angina, electrocardiographic changes are seen, and serum troponin or creatine kinase concentrations may become abnormal   Hemoglobin should be checked to make sure that the patient is not anemic. OTHER DIAGNOSTIC TESTS A resting electrocardiogram (ECG) followed by an exercise tolerance test usually are the first tests done in stable patients. A chest x-ray should be done if the patient has heart failure symptoms.

NORMAL ECG ST segment depression & T Wave Inversion In Myocardial Ischaemia

NORMAL ECG ST segment elevation & T Wave Inversion In Myocardial Infraction

PHARMACOLOGIC THERAPY Organic Nitrite and Nitrates:- amyl nitrite, nitroglycerin, Isosorbide dinitrate Isosorbide -5- mononitrate Erythrityl tetranitrate Pentrerythrityl trinitrate β-Adrenergic Receptor Blockers:- Propranolol Metoprolol, Atenolol, Sotalol, Nodalol, Acebutolol, Pindolol. Calcium Channel Blockers: Nifedipine, Diltazem, Verapamil, Nicardipine Miscellaneous coronary vasodilators: Potassium Channel Openers - Nicorandil, Cytoprotective Drugs - Trimetazidine Antiplatelet Drugs Low dose Aspirin, Clopidogrel Statins(plaque stabilization)

Drugs used in myocardial infarction Oxygen Morphine. i.v. Aspirin low dose Nitroglycerin.SL, Streptokinase. i.v. furosemide.i.v. Propranolol. PO ACEI Heparin/or warfarin Clopidogrel

Consequences of Hypertension: Left Ventricular Hypertrophy Cerebral Infarction (Stroke) Heart Hypertensive cardiomyopathy, IHD, MI. Brain: Hemorrhages infarction

Aim of the treatment Depends on clinical type Symptomatic management of acute episode Anti-thrombotic therapy to prevent progression to MI Long term management Prevent attack & reduce the risk of other cardiovascular events

Aspirn + Clopidogrel

Anti anginal drugs- nitrates Nitrates increase 02 supply & decrease demand. reduce myocardial work- decrease pre & after load Vasodilator & venodilator. Reduce left ventricular diastolic volume & pressure. Routes: SL, PO & i.v.

Interactions with nitrates +sildenafil: contraindicated +alcohol: sustained fall of BP +propranolol: reflex tachycardia suppressed attenuation of beta blocker induced ventricular dilatation therapeutic synergy

Beta blockers in angina-rationale HR is reduced Myocardial contractility is decreased High blood pressure declines Cardiac arrhythmias control Reduce myocardial 02 requirement not for Prinzmetal’s, RSP disorders, bradyarrhythmias & CCF