Cardiovascular Disorders Lecture 3 Coronar Artery Diseases

Transcription

1 Cardiovascular Disorders Lecture 3 Coronar Artery Diseases By Prof. El Sayed Abdel Fattah Eid Lecturer of Internal Medicine Delta University

2 Coronary Heart Diseases It is the leading cause of death in most industrialized nations The clinical spectrum: - Silent (asymptomatic) ischemia. - Chronic stable angina pectoris. - Unstable angina. - Acute myocardial infarction. Pathophsiology - Atherosclerosis of the coronary artery. - Endothelial dysfunction is the earliest abnormality in atherosclerosis. - Endothelial injury > Nitric Oxide (NO), produces a local prothrombotic state and endothelial accumulation of macrophages and LDL. Risk Factors Nonmodifiable risk factors: 1) Advanced age 2) Male sex 3) Family history Modifiable risk factors: 1) Hyperlipidemia 2) Hypertension 3) Diabetes mellitus 4) Cigarette smoke What are non-atherosclerotic causes of cardiac ischemia? 1- Acute embolization. 2- Chest wall trauma. 3- Coronary artery dissection. 4- Arteritis involving the coronary arteries. 5- Hematologic disorders e.g Polycythemia and sickle cell anemia. 6- Spontaneous coronary spasm. 7- Cocaine. 8- Syndrome X: (20% of atypical angina & 3% of MI) Normal coronary arteries at arteriography. Young, commonly women Minimal cardiac risk factors Relatively good prognosis. 9- Mismatch of the myocardial oxygen supply and demand.

3 Evaluation of Angina pectoris History Angina Pectoris - Classic symptoms: Dyspnea, chest pain radiating to the left shoulder, arm and forearm. - Not all patients have classic symptoms. - Some present with dyspnea on exertion or atypical chest pain or silent ischemia. Examination: May be normal both between and during ischemic episodes. During an anginal episode: Hypertension and tachycardia. Transient S4. Transient LV systolic dysfunction. Investigation: 1-ECG: - Between episodes: normal or nonspecific ST ± T wave changes or evidence of underlying cardiac disease (left ventricular hypertrophy, old infarction). - During an anginal episode: ST segment depression ± T wave inversion. ST segment and T wave changes usually rapidly return to normal. The persistence of ECG changes predicts a poorer prognosis. 2- Stress testing: - Indicated if the diagnosis is not clear. - Determines: Exercise capacity or Effectiveness of medication. 3- Electron-beam or ultrafast computed tomogravy (CT): The presence of coronary calcification is diagnostic of coronary atherosclerosis.

4 4- Coronary Angiography. Medical Management: 1-Risk factor modification: Control of hypertension, diabetes, hyperlipidemia, cessation of smoking & lower weight in obese patients 2- Lifestyle changes: Regular tolerated exercise to maintain physical conditioning. Avoid Isometric exercises such as weight lifting & cold weather exercise 3- Control Precipitating factors (anemia, COPD, hyperthyroidism). 4-Pharmacotherapy - Aspirin: mg each day for all patients with known or suspected CAD unless contraindicated. It suppresses the platelet-dependent thrombotic response to atherosclerotic plaque rupture. -Lipid-lowering therapy. - Nitrates. - β blockers. - Calcium channel blockers. The Three are unlike aspirin and lipid-lowering therapy, as they have not decreased mortality, they are effective in controlling symptoms.

5 Unstable Angina Change in frequency, severity, or duration of the episodes or with decreasing levels of exertion. Treatment: 1- Rest for 24 to 48 hours, analgesics & oxygen therapy. 2- Beta blockers or calcium channel blockers. 3- Aspirin + Intravenous heparin or Low-molecular-weight heparins: continuing aspirin therapy after stopping heparin. 4- Glycoprotein llb/ilia receptor blockade: They block the final common pathway of platelet aggregation (cross-linking of platelets by fibrinogen). 5- Early cardiac catheterization and coronary revascularization: if failure of medical management or high-risk markers. Revascularization in patients with angina: They are indicated in patient with failure of medical therapy to control anginal symptoms or in the presence of high-risk markers: Methods: 1- Surgical revascularization (coronary artery bypass graft surgery {CABG}). 2- Percutaneous transluminal coronary angioplasty {PTCA}. 3- PTCA with coronary stents.

6 Acute Myocardial Infarction Presentation: Like Angina but more severe & more prolonged (>30 minutes) acute typical chest pain usually associated with dyspnea, nausea. Not relieved with rest or sublingual nitroglycerine. Silent infarctions in diabetics (20%) and atypical symptoms in elder. Unusually heavy physical or emotional stress or surgery precipitates AMI. Examination: Uncomfortable and distressed. Tachycardia or bradycardia. Mild hypertension. S4 is common. MR. Pulmonary congestion: LV filling pressure due to systolic dysfunction. Diagnosis: WHO criteria for the diagnosis of an AMI mandate that at least two of the following: 1- Ischemic-type chest discomfort 2- Evolution of ECG changes 3- Rise and fall in serum markers of cardio-myocyte necrosis. 1-ECG: Serial ECGs is better as 1/2 cases has normal 1st ECG.

7 * Q wave MI - Pathologic Q waves (>0.04 msec in duration and >1/3 the height of R wave) - Early hyperacute T resolves after minutes as ST segment elevation develops. * Non-Q wave MI (Subendocardial Infarction) - Intermediate syndrome - ST segment depression and/or T wave inversions & no pathologic Q waves. 2-Echocardiogram may be helpful if ECG is nondiagnostic. 3- Cardiac enzymes: Specific for Diagnosis if increased : * The CK-MB * Serum lactate dehydrogenase and aspartate aminotransferase * Troponins Treatment of AMI: The highest rate of mortality occurs in the first hours 2ry to arrhythmia. Prophylactic treatment with antiarrhythmic agents is not indicated Over 50% of all deaths from AMI occur before hospital presentation. Initial hospital care: - Diagnosis of AMI - Continuous ECG monitoring (malignant arrhythmias). - Limited physical activity during the first 12 to 24 hours. - Stool softeners.

8 Drug therapy 1) Morphine (2 to 4 mg as needed) for pain and anxiety: HR, BP, Sympathetic. 2) Oxygen 3) Nitroglycerin sublingual or intravenous but may be avoided in hypotension 4) Aspirin to chew (160 to 325 mg) reduces mortality. 5) Atropine (0.5 mg IV) for symptomatic bradycardia should be administered. 6) Beta Blockers IV: Avoided in hypotension, pulmonary congestion, or heart block. 7) Reperfusion Therapy: a- Thrombolytic therapy: Streptokinase (SK) & tissue-type plasminogen activator (tpa). Indications: ischemic-type chest pain; ECG evidence of AMI. The benefit is greater within 6 hours of symptom onset up to 12 hours Mortality by about 22%. b- Primary Percutaneous transluminal coronary angioplasty (PTCA): The best for establishing normal coronary blood flow Complications of AMI 1-Mechanical: left ventricular failure, right ventricular failure, cardiogenic shock 2-Structural: free wall rupture, ventricular septal defect or papillary muscle rupture with acute mitral regurgitation 3-Conduction abnormality: first-, second-, and third-degree heart block; or bundle branch and fascicular block.