MYOCARDIAL INFARCTION THEORY .pptx

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1. MYOCARDIAL INFARCTION DR MANJULA N MBBS MD (PATHOLOGY)

2. CORONARY ARTERIES 2 Branches. Supplies Left atrium, Left Ventricle and Interventricular Septum. 2 Branches. Supplies Right atrium, Right Ventricle, part of Left ventricle and electrical conduction system. 2 coronary arteries emerge from base of aorta. LEFT CORONARY ARTERY RIGHT CORONARY ARTERY

3. MI aka "heart attack" - death of cardiac muscle (coagulative necrosis) resulting from ischemia. DEFINITION Myocardial infarction is a irreversible myocardial injury and necrosis as a result of prolonged myocardial ischemia. Characterized by: Unequivocal ECG changes Chest pain Release of cardiac markers

4. Entire thickness of ventricular wall 1/3 to ½ of of ventricular wall thick

5. Morphologic Changes in Myocardial Infarction Time Gross changes Microscopic changes 0 - 4hr None None, by electron microscope you see necrosis (not seen in LM) 4 - 12hr Mottling Coagulation necrosis 12- 24hr Mottling More coagulation necrosis; neutrophils come in 2 - 7day Yellow infarct center Neutrophils die, macrophages come to eat dead cells 1 - 2week Yellow center, red borders Granulation tissue 2 - 8week Scar collagen (fibrosis)

6. Characteristic chest pain ECG changes Elevated cardiac enzymes DIAGNOSIS Angiography Radionuclide imaging Echocardiogram

7. CLINICAL FEATURES PAIN Severe crushing, sub-sternal chest pain, which may radiate to the neck, jaw, epigastrium, shoulder or left arm. Pain lasts for hours to days and is not relieved by nitroglycerin. PULSE is rapid and weak. Diaphoresis (sweating) Dyspnea.

8. CHARACTERISTIC ECG CHANGES ST segment elevation over area of damage ST depression in leads opposite infarction Pathological Q waves Reduced R waves Inverted T waves

9. LABORATORY EVALUATION 1- Troponins: Tn T , Tn I  more specific marker. After acute MI both troponins become detectable after 2 to 4 hours, peaks at 48 hours. Their levels remain elevated for 7 to 10 days. 2- CK-MB  second best marker: It begins to rise within 2 to 4 hours of MI, peaks at 24 to 48 hours and returns to normal within approximately 72 hours. So at day 3, if you find normal CK-MB; it doesn't mean that your patient doesn’t have MI. 3- Lactate dehydrogenase  LDH Rise 24 hrs, peaks 72 hrs, persists 72 hrs.

10. OUTCOMES OR COMPLICATIONS Cardiac arrhythmia Left ventricular failure Myocardial rupture: Rupture of free wall, septum, rupture of papillary muscle (leading to papillary muscle and associated valve incompetence/dysfunction) Thromboembolism Pericarditis Progressive late heart failure in the form of chronic IHD. Infarct extension and expansion. Cardiogenic shock. Ventricular aneurysm in which the ventricle is dilated and the wall is thinned out. External rupture of the infarct with associated bleeding into the pericardial space ( hemopericardium ). Post myocardial infarction syndrome / DRESSLER Syndrome – delayed pericarditis.

11. A papillary muscle may rupture as well to produce sudden valvular insufficiency. Rupture through the septum results in a left-to-right shunt and right heart failure PAPILLARY MUSCLE RUPTURE

12. Rupture (at the arrow) into the pericardial sac can produce a life-threatening cardiac tamponade, as seen here. The septum may also rupture. CARDIAC TAMPONADE

13. A complication of infarction is aneurysm formation, which is the bulge seen here in the left ventricular wall. Note the very thin white wall of the aneurysm toward the apex. ANEURYSM FORMATION

14. Mural thrombus can form in the aneurysm, and is seen here as the dark red layers extending inward from the thin aneurysmal wall. Portions of the mural thrombus could break off and embolize to the systemic circulation. MURAL THROMBI