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ACUTbbbbbhjjjE Myocardial Infarction.ppt
- 1. Myocardial Infarction Khaled Dajani,MD, MBA Division of Cardiology
- 2. Background Myocardial Infarction ifthe rapid development of myocardial necrosis by a critical imbalance between oxygen supply and demand to the myocardium
- 3. Classification Acute coronary syndromesinclude ST-elevation MI (STEMI) Non ST-elevation MI ( NSTEMI) Unstable Angina Cardiac markers in circulation indicates myocardial infarction and help categorize MI and is a useful adjunct to diagnosis
- 4. Classification Anatomic or morphologic Transmural=Full thickness Non-transmural= Partial thickness ECG Q wave MI Non Q wave MI Does not distinguish transmural from a non- transmural MI as determined by pathology
- 5. Prevalence In the US,1.3 million cases of nonfatal MI were reported in 2006 Incidence of 600 per 100,000 people Increase in the proportion of NSTEMI compared to STEMI Approximately 500,000 to 700,000 deaths are caused by heart disease annually in the United States
- 6. History The history iscritical in making the diagnosis of MI and sometimes provide only the only clues that lead to the diagnosis in the initial phase of presentation
- 7. History Chest Pain- anteriorprecordium tightness Pain may radiate to jaw, neck and epigastrium Dyspnea- angina equivalent, poor LV function Nausea/abdominal pain with posterior MI Anxiety
- 8. History Nausea with andwithout vomiting Diaphoresis or sweating Syncope or near syncope Elderly present with MS changes, fatigue, syncope or weakness As many as half of MI are clinically silent
- 9. Physical The physical examcan often be unremarkable Hypertension Hypotension Acute valvular dysfunction may be present Rales Neck vein distention
- 10. Physical Third heart soundmay be present A fourth heart sound poor LV compliance Dysrhythmias Low grade fever
- 11. Causes Most frequent causeis rupture of an atherosclerotic lesion within coronary wall with subsequent spasm and thrombus formation Coronary artery vasospasm Ventricular hypertrophy Hypoxia Coronary artery emboli
- 12. Causes Cocaine Arteries Coronary anomalies Aortic dissection PediatricsKawasaki disease, Takayasu arteritis Increased afterload which increases myocardial demand
- 13. Risk factors foratherosclerosis Age Male gender Smoking Hypercholesterolemia and triglyceridemia Diabetes Mellitus Poorly controlled hypertension Type A personality
- 14. Risk factors foratherosclerosis Family History Sedentary lifestyle
- 15. Differentials Acute coronary syndrome Anxiety Aorticstenosis Asthma Cholecystitis and biliary colic Cholethiasis COPD
- 16.
- 17. Mechanisms of Myocardialdamage The severity of an MI is dependent of three factors The level of the occlusion in the coronary The length of time of the occlusion The presence or absence of collateral circulation
- 18. Cardiac Biomarkers Cardiac biomarkersare protein molecules released into the blood stream from damaged heart muscle Since ECG can be inconclusive , biomarkers are frequently used to evaluate for myocardial injury These biomarkers have a characteristic rise and fall pattern
- 19. Troponin T andI These isoforms are very specific for cardiac injury Preferred markers for detecting myocardial cell injury Rise 2-6 hours after injury Peak in 12-16 hours Stay elevated for 5-14 days
- 20. Creatinine Kinase (CK-MB) Creatinine Kinase is found in heart muscle (MB), skeletal muscle (MM), and brain (BB) Increased in over 90% of myocardial infraction However, it can be increased in muscle trauma, physical exertion, post-op, convulsions, and other conditions
- 21. Creatine Kinase (MB) Timesequence after myocardial infarction Begins to rise 4-6 hours Peaks 24 hours returns to normal in 2 days MB2 released from heart muscle and converted to MB1. A level of MB2 > or = 1 and a ratio of MB2/MB1 > 1.5 indicates myocardial injury
- 22. Myoglobin Damage to skeletalor cardiac muscle release myoglobin into circulation Time sequence after infarction Rises fast 2hours Peaks at 6-8 hours Returns to normal in 20-36 hours Have false positives with skeletal muscle injury and renal failure
- 23. Renal Failure andRenal Transplantation Diagnostic accuracy of serum markers of cardiac injury are altered in patients with renal failure Cardiac troponins decreased diagnostic sensitivity and specificity in patients receiving renal replacement therapy Current data show levels of troponin I are unaltered while levels of troponin T may be elevated
- 24. CBC CBC is indicatedif anemia is suspected as precipitant Leukocytosis may be observed within several hours after myocardial injury and returns returns to levels within the reference range within one week
- 25. Chemistry Profile Potassium andmagnesium levels should be monitored and corrected Creatinine levels must be considered before using contrast dye for coronary angiography and percutanous revascularization
- 26. C-reactive Protein (CRP) C-reactive protein is a marker of acute inflammation Patients without evidence of myocardial necrosis but with elevated CRP are at increased risk of an event
- 27. Chest X-Ray Chest radiographymay provide clues to an alternative diagnosis ( aortic dissection or pneumothorax) Chest radiography also reveals complications of myocardial infarction such as heart failure
- 28. Echocardiography Use 2-dimentional andM mode echocardiography when evaluating overall ventricular function and wall motion abnormalities Echocardiography can also identify complications of MI ( eg. Valvular or pericardial effusion, VSD)
- 29. Electrocardiogram A normal ECGdoes not exclude ACS High probability include ST segment elevation in two contiguous leads or presence of q waves Intermediate probability ST depression T wave inversions are less specific
- 30. Localization of MI STelevation only Inferior wall- II, III, aVF Lateral wall_ I, aVL, V4-V6 Anteroseptal- V1-V3 Anterolateral- V1-V6 Right ventricular- RV4, RV5 Posterior- R/S ratio >1 in V1 and T wave inversion
- 31. Therapy The goals oftherapy in AMI are the expedient restoration of normal coronary flow and the maximum salvage of functional myocardium
- 32. Antiplatelet Agents Aspirin atlease 160mg immediately Interferes with function of cyclooxygenase and inhibits the formation of thromboxane ASA alone has one of the greatest impact on the reduction of MI mortality. Clopidogrel, ticlopidine, have not been shown in any large scal trail to be superior to Aspirin in acute MI
- 33. Supplemental Oxygen Because MIimpairs the circulatory function of the heart, oxygen extraction by the heart and other tissues may be diminished Supplemental oxygen should be administered to patient with symptoms and or signs of pulmonary edema or pulse oximetry readings less than 90%.
- 34. Nitrates IV nitrates toall patients with MI and congestive heart failure, persistent ischemia, hypertension, or large anterior wall MI Primary benefit vasodilator effect Metabolized to nitric oxide in the vascular endothelium, relaxes endothelium Vasodilatation reduces myocardial oxygen demand and preload and afterload
- 35. Beta-blockers Recommended within 12hours of MI symptoms and continued indefinitely Reduces Myocardial mortality by decreasing arrythmogenic death Decrease the rate and force of myocardial contraction and decreases overall oxygen demand
- 36. Unfractionated heparin Forms achemical complex with antithrombin III inactivates both free thrombin and factor Xa Recommended in patients with MI who undergo PTCA or fibrinolytic therapy with alteplase
- 37. Low-molecular weight heparin Directactivity against factors Xa and IIa Proven to be effective in treating ACS that are characterized by unstable angina or non ST- elevation MI Their fixed doses are easy to administer and laboratory testing to measure their therapeutic effect is not necessary makes them attractive alternative of un- fractionated heparin
- 38. Thrombolytics Indicated with MIand ST segment elevation greater than 0.1mV in 2 contiguous ECG leads, or new onset LBBB, who present less than 12 hours but not more than 24 hours after symptom onset The most critical variable in achieving successful fibrinolysis is time form symptom onset to drug administration
- 39. Thrombolytics As a classthe plasminogen activators have been shown to restore coronary blood flow in 50-80% of patients Contraindication active intracranial bleeding, CVA 2months, CNS neoplasm, HTN, coagulopathy Retaplase slightly higher angiographic patency but did not translate into survival benefit Intracranial bleed risk major drawback
- 40. Glycoprotein IIb/IIIa Antagonists Potentinhibitors of platelet aggregation Use during PCI and in patients with high risk features ACS have been shown to reduce the composite end points of death, reinfraction and the need for target lesion
- 41. Percutanous Coronary Intervention Alternativeif performed by skilled operator in an experienced center Standard is a “ door to balloon” time of 90 minutes PCI can successfully restore coronary blood flow in 90 to 95% of MI patients PCI definitive survival advantage over fibrinolytics for MI patients who are in cardiogenic shock
- 42. Surgical Revascularization Emergent orsurgical revascularization in setting of failed PTCA in patients with hemodynamic instability and coronary anatomy amendable to surgical grafting Also indicated of mechanical complications of MI including VSD, free wall rupture, or acute MR Carries a higher risk of perioperative mortality than elective CABG
- 43. Lipid Management All postMI patients should be on AMA step II diet ( < 7% of calories from saturated fats) Post MI patients with LDL > 100 mg/dl are recommended to be on drug therapy to try to lower levels to <100 mg/dl Recent data indicate that all MI patients should be on statin therapy, regardless of lipid levels or diet
- 44. Long term Medications Mostoral medications instituted in the hospital at the time of MI are continued long term Aspirin, beta blockers and statin are continued indefinitely ACEI indefinitely in patients with CHF, ejection fraction <.40, hypertension, or diabetes
- 45.