CVS Pathology Lecture 5: Ischemic Heart Disease PDF

pathology - CVS Ischemic heart disease LECTURE (5) Ischemic heart disease Dr. M. Shalaby pathology - CVS Ischemic heart disease DEFINITION  Group of diseases due to insu...

pathology - CVS Ischemic heart disease LECTURE (5) Ischemic heart disease Dr. M. Shalaby pathology - CVS Ischemic heart disease DEFINITION  Group of diseases due to insufficient arterial blood flow to myocardium. ACUTE ISCHEMIA CHRONIC ISCHEMIA  Results in myocardial infarction.  Results in angina pectoris CLASSIFICATION ① Stable ② Unstable.  Gradual incomplete occlusion and manifested mainly as angina pectoris.  Angina pectoris:  Temporary relative acute Ischemia on top of chronic ischemia.  Manifested by attacks of severe retrosternal pain : DEFINITION PRECIPITATED BY RELIEVED BY ① Physical effort.  Rest ② Emotional excitement. ③ Heavy meals. ④ Cold. ① Atheroma & Anemia. ② Factors increasing load on heart as in hypertension, valvular disorders (aortic), CAUSES cardiomyopathy and hyperthyroidism. ③ Ventricular hypertrophy due to any cause. ④ Coronary vasospasm. ① Stable angina: evoked by exercise and relieved by rest. ② Unstable angina: severe pain precipitated by less and less effort (pre-infarction TYPES OF angina) ANGINA ③ Prinzmetal (vasospastic) angina: occurs at rest, due to coronary spasm, relieved by vasodilator (nitroglycerine) therapy. Dr. M. Shalaby pathology - CVS Ischemic heart disease  Sudden stoppage of arterial blood flow in coronary arteries or one of the major DEFINITION branches. A- Complicated atheroma of coronary vessel. ① Thrombosis. ② Rupture of the plaque or hemorrhage into the plaque. CAUSES AND B- Unusual causes: RISK FACTORS ① Embolism due to vegetations of bacterial endocarditis of aortic valve. ② Polyarteritis nodosa ③ Occlusion of coronary ostia in dissecting aneurysms and syphilis ④ Coronary spasm.  Depend on extent of arterial disease, size of obstructed vessels and collaterals.  The possibilities are:  50% sudden death from ventricular fibrillations. EFFECTS  25% develop infarct and die from it.  25% live either with myocardial infarct, or with silent occlusion (adequate collaterals). Dr. M. Shalaby pathology - CVS Ischemic heart disease  Massive area of coagulative necrosis of myocardium due to complete cut of DEFINITION arterial blood supply.  Sudden complete coronary occlusion (Thrombosis, embolism, spasm)  It may be ① Transmural: involving the whole thickness of the heart wall in certain CAUSES anatomical area supplied by certain coronary artery. ② Circumferential subendocardial: involving subendocardium of left and less commonly right ventricles.  Caused by hypo perfusion not actual coronary artery occlusion. Dr. M. Shalaby pathology - CVS Ischemic heart disease  The left ventricle is mainly affected.  In order of frequency: ① Anterior descending of left coronary (40%)  The infarct is in anterior wall of left ventricle, anterior wall of right ventricle and anterior part of interventricular septum and apex. ② Right coronary artery (40%):  Posterior wall of Left. ventricle, posterior wall of Right Ventricle and posterior part of interventricular septum. ③ Circumflex branch of left coronary: Lateral wall of Left ventricle. ④ Left coronary. Dr. M. Shalaby pathology - CVS Ischemic heart disease N/E M/E BEFORE 6 HOURS No changes.  Affected area is pale, opaque and  Coagulative necrosis (Cytoplasm 6-8 HOURS dry. becomes more acidophilic, striations lost, Nuclei disappear)  Slightly soft  Polymorphs invade the area of NEXT DAY  Color is grey then yellow. necrosis to remove the necrotic tissue.  The infarct is soft yellow center and  Polymorphs infiltrate and soften 24-72 HOURS well circumscribed. the infarct.  Fully formed recent infarct which is  Macrophages appear with swollen yellow, soft and friable polymorphs to remove the necrotic 3-10 DAYS surrounded by zone of hyperemia. tissue and granulation tissue is seen  Usually involves the whole at the periphery. thickness of myocardium.  Removal of necrotic tissue and  Granulation tissue invades the organization with scar formation. infarct and starting formation of  Complete healing takes different fibrous tissue which is usually 4-6 WEEKS times, according to the size of completed by the end of 6 weeks. infarct.  Sero-fibrinous or hemorrhagic  It may be associated with pericarditis and mural thrombus pericarditis and mural thrombus may be seen. Dr. M. Shalaby pathology - CVS Ischemic heart disease Dr. M. Shalaby pathology - CVS Ischemic heart disease Dr. M. Shalaby pathology - CVS Ischemic heart disease ① ECG and echocardiography. ② Laboratory diagnosis : CK-MB TROPONIN LDH 6-HOURS + Wk + WK - 12-16 HOURS +++ St +++St - 24 HOURS Peaks Peaks - 2 DAY Persists Persists - 3 DAY --- Persists Peaks 4-7 DAY --- Persists Persists ① ARRHYTHMIA  Most common cause of death in 1st few hours following infarction. ② MYOCARDIAL  Lead to congestive heart failure and/or cardiogenic shock. (PUMP) FAILURE  4-7 days after Infarction (due to neutrophilic liquifactive enzymes). ③ MYOCARDIAL  Can lead to cardiac temponade and compression of heart by RUPTURE hemorrhage into pericardial space.  papillary muscle → mitral incompetence. ④ RUPTURE OF  Interventricular septum → acute heart failure. ⑤ Myocardial  With thrombosis inside. aneurysm ⑥ EMBOLISM  From mural thrombi or thrombi in cardiac aneurysm. ⑦ PROLONGED BED  Weak cardiac action🡪leg thrombosis &pulmonary embolism REST ⑧ DRESSLER’S  Autoimmune disorder resulting from damage of myocardium → release SYNDROME of auto-antigens → autoimmune pericarditis and pleurisy. ⑨ ACUTE PERICARDITIS ⑩ RECURRENCE in cases of extensive atheroma. Dr. M. Shalaby pathology - CVS Ischemic heart disease Dr. M. Shalaby