Snapshot A 60-year-old man presents to the emergency department due to substernal chest pain. He describes the pain as "crushing" and it radiates down the left arm. Medical history is significant for hypertension and hypercholesterolemia. On physical exam the patient is diaphoretic. An electrocardiogram demonstrates ST-segment elevations and cardiac troponins are significantly elevated. After appropriate acute therapy, the coronary catheterization lab is activated and cardiology is consulted. 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 cocaine use male postmenopause genetic and behavioral predispositions to arteriosclerosis e.g., high-fat diet coronary heart disease risk equivalents diabetes mellitus chronic kidney disease noncoronary atherosclerotic disease carotid artery disease abdominal aortic aneurysm peripheral artery disease 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 STEMIInfarction LocationInvolved ECG LeadsInvolved Coronary ArteryInferior wallII, III, and aVFRCAAntero-apicalV3 and V4LAD (distal)Antero-septalV1 and V2LADAntero-lateralV5 and V6LAD or LCXLateralI and aVLLCXPosteriorST depression and tall R waves that can be seen anywhere in V2-5 (not all leads mandatory)ST elevations in V7-V9Posterior descending artery Evolution of MI Morphological Myocardial Changes in an MI Time Gross Feature 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 Neutrophil infiltration Arrhythmia Heart failure 1-3 days Mottling with a yellowish infarct center Extensive coagulation necrosisBrisk neutrophil infiltration Fibrinous pericarditis 3-14 days 3-7 dayshyperemic with central yellowing7-10 daysyellow-tan with reddish tan margins10-14 daysreddish gray infarct borders Macrophage infiltration and tissue granulation Myocardial wall rupture - sudden hypotension, tachycardia, and pulseless electrical activity - may lead to cardiac tamponade Papillary muscle rupture -mitral regurgitation Pseudoaneurysm of a ventricular wall - may rupture 2 weeks - several months 2-8 weeksgray-white scar> 2 monthscomplete scar Collagenous scar Dressler syndrome Heart failure True ventricular - aneurysma thrombus may form - evaluate with echocardiograph - ECG with persistent ST elevation in original MI leads with a deep QS wave 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, and 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 ST depression may present initially followed by pseudonormalization of the ST segment followed by ST elevation Q-waves a late finding (~2 weeks post-MI) or indicative or previous infarction new left bundle branch block (LBBB) in isolation does not denote a STEMI ECG findings prolonged QRS duration dominant S wave in V1 broad monophasic or M-shaped R wave in the lateral leads (I, aVL, and V5-V6) prolonged R wave peak time in the left precordial leads (V5-6) can complicate diagnosis of MI - use Sgarbossa criteria (3 points or more concerning for MI) ST elevation 1 mm or greater in a lead with an upward QRS (5 points) ST depression 1 mm or greater in V1, V2, or V3 (3 points) ST elevation or depression 5 mm or greater in a lead with a downward QRS complex (2 points) heart block can include first-, second-, and third-degree heart block more common in inferior infarctions the right coronary artery most commonly serves the AV node fasicular blocks left anterior and posterior fascicular blocks may occur from other stressors or secondary to ischemia NSTEMI ST depression T-wave inversion 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 can be elevated in other conditions including states of physiologic stress such as hypotension or sepsis 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 Hibernating myocardium decreased contractility of the myocardium secondary to ischemia without necrosis reversible when stenting restores bloodflow Brugada syndrome sodium channelopathy coved ST elevation risk for sudden cardiac death Wellens syndrome deeply inverted or biphasic T waves indicative of critical left anterior descending artery stenosis De Winter T waves ST depression and peaked T waves in precordial leads anterior STEMI equivalent requires cardiac catheterization Cerebral T waves inverted and wide T waves prolonged QT associated with head trauma and intracranial pathology (such as a subarachnoid hemorrhage) Arrhythmogenic right ventricular dysplasia common cause of syncope and sudden death epsilon wave on ECG Precordial catch syndrome sudden, sharp, and severe paroxsyms of chest pain no ECG or troponin abnormalities Spontaneous coronary artery dissection (SCAD) more common in women, postpartum period, and connective tissue disorders may cause unstable angina, NSTEMI, or STEMI Treatment Conservative lifestyle modification e.g., smoking cessation Medical initial medical treatments include aspirin first priority even before diagnostic work-up confers significant benefit to mortality when given early oxygen nitroglycerin Reduces chest pain by lowering preload and thus myocardial oxygen demand contraindicated in a right inferior wall infarction (give fluids to maintain blood pressure) reduces preload leading to cardiovascular collapse morphine only give if there is unacceptable pain appears to be associated with a mortality increase benzodiazepines in cocaine-induced myocardial ischemia typically given with nitrogylcerin 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 contraindication acute decompensated heart failure bradycardia 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 cardiac catheterization and percutaneous coronary intervention (PCI) indications if STEMI symptoms developed in < 12 hours and the procedure can be performed within 90 minutes highest mortality lowering intervention complications cholesterol embolism retroperitoneal hematoma 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 90 minutes Complications Heart failure Sudden cardiac death Arrhythmia Myocardial stunning