Snapshot A 65-year-old male has been in the CCU for the last three days following an anteroseptal myocardial infarction. On day #4 of this admission, his chest pain returns. On exam, he is found to have a third heart sound (S3) and bibasilar rales. Labs demonstrate an elevated CK-MB and a LDH1/LDH2 flip. Introduction An occlusion or spasm causing myocardial ischemia and subsequent myocardial tissue death. Most commonly caused by acute thrombus formation on a ruptured atherosclerotic plaque. Risk factors are the same as in ischemic heart disease. Presentation Symptoms acute-onset chest pain that may radiate to the left arm, jaw, neck, and shoulder diaphoresis shortness of breath nausea/vomiting lightheadedness/dizziness be aware of silent MIs biggest concern in the elderly, post-menopausal women, and diabetics Physical exam tachycardia new mitral regurgitation via ruptured papillary muscle S4 hypotension secondary to cardiogenic shock from decreased cardiac output crackles from pulmonary edema caused by backflow secondary to decreased cardiac output Evaluation Diagnosis made by demonstrating at least 2 out of 3 of the following signs, symptoms, and risk factors ST-elevation or ST-depression reflects transmural ischemia or subendothelial ischemia, respectively occurs within minutes and resolves after 24-48 hours T-wave inversion reflects transmural infarction occurs within hours, returns to upright after weeks Q-waves reflect transmural infarction occur within hours can be a sign of an old infarction new-onset left bundle branch block positive cardiac enzymes troponin is standard in first 8 hours CK-MB standard in the first 24 hours LDH1 is best for 2-7 days after symptoms diagnosis of re-infarction made if CK-MB rises four days after the initial presentation Differential Angina, PE, aortic disection, pneumothorax, pericarditis, PUD, GERD, cholecystitis, esophageal spasm, aortic dissection Treatment All patients with suspected MI are to be: hospitalized in CCU or cardiac step-down unit and not to be discharged home until ruling out-MI 24-hr cardiac enzymes and serial EKGs Acute management morphine oxygen nitroglycerin contraindicated in right inferior wall infarction ACEI aspirin beta-blockers (if no hypotension, bradycardia, or pulmonary edema) heparin Percutaneous coronary intervention (PCI) should be performed within 90 minutes from first medical contact (e.g. arrive at ED) if patient is at a PCI-capable center If PCI is not available on site, recommend rapid transfer to a PCI center if available, so PCI can be performed within 120 minutes from first medical contact In the first 6-hours can use thrombolytics (TPA) heparin (give 48 hrs post-infarct if TPA has been used to lyse the clot) streptokinase Five days following episode if stress test is positive, then order cardiac catherization Long term therapy (post-MI) aspirin beta-blockers lipid-lowering drugs HMG-CoA reductase inhibitors decrease mortality post-MI ACEIs reduction of social habit risk factors smoking cessation potentially schedule for CABG or stenting procedures if needed dual anti-platelet therapy needed s/p stent placement Prognosis, Prevention, and Comlications Time to restoration of coronary blood flow is the strongest predictor of long-term prognosis Cardiac arrhythmias (90%) are the most common cause of death LV failure and pulmonary edema (60%) Thromboembolism Cardiogenic shock via decreased cardiac output Ventricular wall rupture leading to cardiac tamponade if pericardium intact or massive intrathoracic blood loss and death Papillary muscle rupture with mitral regurgitation Fibrinous pericarditis results in friction rub 3-5 days post MI Dressler's Syndrome autoimmune disease leads to fibrinous pericarditis several weeks post-MI