Snapshot A 55-year-old man presents to the emergency department due to substernal chest pain. His symptoms began a few hours ago. He describes the pain as "crushing" and it radiates down the left arm. Medical history is significant for type 2 diabetes and hypertension. On physical exam the patient is diaphoretic. An electrocardiogram demonstrates ST-segment elevations and cardiac troponins are significantly elevated. Introduction Clinical definition death of myocardial tissue secondary to prolonged and severe ischemia also known as a "heart attack" Types ST-segment elevation myocardial infarction (STEMI) an acute coronary syndrome (ACS) with ST-segment elevations found on electrocardiogram (ECG) biomarkers of myocardial necrosis are present Non-STEMI (NSTEMI) an ACS without ST-segment elevations found on ECG biomarkers of myocardial necrosis are present unstable angina an ACS without ST-segment elevations found on ECG and no elevation biomarkers of myocardial necrosis Epidemiology incidence increases with age risk factors hypertension cigarette smoking hyperlipidemia hypercholesterolemia male postmenopause genetic and behavioral predispositions to arteriosclerosis e.g., high-fat diet Etiology occlusion of a coronary artery can be caused by atheromatous plaque rupture with subsequent thrombi expansion vasospasm emboli, which can be secondary to atrial fibrillation, sending an embolus from the left atrium to the coronary arteries vegetations from infective endocarditis material from an intracardiac prosthetic paradoxical emboli Pathophysiology occlusion of a coronary artery disrupts the blood supply to a region in the myocardium ischemia ensues, the myocytes become rapidly dysfunctional when ischemia persists, this can result in myocyte death after 30 minutes of severe ischemia, the damage becomes irreversible infarction patterns subendocardial myocyte necrosis involving the inner cardiac wall this is normally the least perfused portion of the myocardium may be referred to as an NSTEMI transmural myocyte necrosis involving the full thickness of the cardiac wall may be referred to as a STEMI ECG Changes and STEMI ECG Changes and STEMI Infarction Location Involved ECG Leads Involved Coronary Artery Inferior wall II, III, and aVF RCA Antero-apical V3 and V4 LAD (distal) Antero-septal V1 and V2 LAD Antero-lateral V5 and V6 LAD or LCX Lateral I and aVL LCX Posterior ST depression and tall R waves in V1-3 V7-V9 Posterior descending artery Evolution of MI Morphological Myocardial Changes in an MI Time Gross Features Light Microscopy Complications 0-24 hours Initially no gross findings; however, over the course of the first 24 hours, dark mottling ensues Early coagulation necrosis Wavy fibers Elongated myocytes Neutrophil infiltration Arrhythmia Heart failure 1-3 days Mottling with a yellowish infarct center Extensive coagulation necrosis Brisk neutrophil infiltration Fibrinous pericarditis 3-14 days 3-7 days hyperemic with central yellowing 7-10 days yellow-tan with reddish tan margins 10-14 days reddish gray infarct borders Macrophage infiltration and tissue granulation Myocardial wall rupture may lead to cardiac tamponade Papillary muscle rupture mitral regurgitation posterolateral muscle rupture is more likely than anteromedial muscle rupture Pseudoaneurysm of a ventricular wall may rupture 2 weeks - several months 2-8 weeks gray-white scar > 2 months complete scar Collagenous scar Dressler syndrome Heart failure True ventricular aneurysm a thrombus may form Presentation Symptoms chest pain features squeezing crushing substernal radiation jaw neck left shoulder or down the arm nausea and vomiting dyspnea asymptomatic typically seen in patients with diabetic neuropathy nerve fibers are damaged and impair their ability to sense pain Physical exam diaphoresis variable findings e.g., S3 or S4, signs of heart failure, bradycardia (in cases of an inferior wall MI) Imaging Coronary angiography indication diagnostic study to assess coronary anatomy and to determine where the occlusion is Studies 12-lead ECG perform as soon as possible findings STEMI hyperacute or peaked T-waves earliest finding ST elevation Q waves a late finding (~2 weeks post-MI) new left bundle branch block (LBBB) considered to be an equivalent to a STEMI NSTEMI ST depression T wave inversion Late pathologic Q waves Q wave in leads V2–V3 lasting longer than 0.02 seconds Q wave anywhere lasting longer than 0.03 seconds with an amplitude greater than 0.1 mV Biomarkers Troponin preferred marker as it has a high sensitivity and specificity for myocardial necrosis troponin I increases after 4 hours and peaks around 24 hours remains elevated for 7-10 days CK-MB a sensitive but not specific biomarker since skeletal muscle can also release it useful for assessing reinfarction Differential Unstable angina differentiating factor no elevation in cardiac biomarkers Costochondritis differentiating factor chest pain that is reproducible with palpation Treatment Conservative lifestyle modification e.g., smoking cessation Medical initial medical treatments include aspirin oxygen nitroglycerin hypotension in an inferior wall infarction secondary to reduced preload morphine only give if there is unacceptable pain appears to be associated with a mortality increase P2Y12 (ADP) receptors blockers indication given in addition to aspirin heparin indication given in addition to antiplatelet therapy β-blockers indication given to all patients if there are no contraindications statin indication given to all patients angiotensin-converting enzyme (ACE) inhibitor indication given to patients with a myocardial infarction recommended when there is anterior infarction heart failure left ventricular ejection fraction < 40% reduces mortality contraindication shock bilateral renal artery stenosis allergy Reperfusion therapy percutaneous coronary intervention (PCI) indications if STEMI symptoms developed in < 12 hours and the procedure can be performed within 90-120 minutes if fibrinolytic therapy is contraindicated coronary artery bypass graft (CABG) indication when coronary anatomy does not allow for PCI 3 vessel occlusion or 2 vessel occlusion in a patient with diabetes significant stenosis of the left main coronary artery fibrinolytic therapy indication for patients who cannot receive PCI within 120 minutes Complications Heart failure Sudden cardiac death Arrhythmia Myocardial stunning