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myocardial infarction (MI); heart attack

Also see STEMI, NSTEMI & acute coronary syndrome. Classification: Killip classification 1) class 1: no pulmonary congestion 2) class 2: mild pulmonary congestion or isolated S3 3) class 3: pulmonary edema 4) class 4: hypotension & evidence of shock clinical classification 1) type 1: coronary thrombosis 2) type 2: myocardial ischemia due to increased oxygen demand or decreased oxygen supply - older, more often female, more comorbidities & lower LVEF than type 1 - higher mortality than type 1 (49% vs 26%) [53] 3) type 3: suspected MI-related death - cardiac death in a setting suggestive of myocardial ischemia without definitive biomarker evidence 4) type 4A: PCI-related MI type 4B: cardiac stent thrombosis 5) type 5: CABG-related MI Etiology: 1) occlusion of one or more of the coronary arteries a) if not reversed within 30 minutes, myocardial ischemia generally results in myocardial infarction b) without collaterals 90% of the supplied myocardium is infarcted within 3 hours of occlusion 2) thrombus overlying or adjacent to ruptured atherosclerotic plaque 3) advanced lesions > 85% stenosis are unlikely to be sites of occlusion giving rise to MI because of collateral circulation which develops in slowly progressive lesions 4) lesions with about 50% stenosis are most likely sites for occlusive thrombi* because of: a) significant risk for plaque rupture b) lack of significant collateral circulation 5) increased sympathetic tone increases risk a) circadian pattern b) early morning & early evening peaks c) emotional stress stimulates sympathetic activity & increases risk of MI [71] (RR=2.44) - emotional stress in combination with intense exercise further increases risk of MI [71] (RR=3.05) - bereavement increases risk of MI [37] - divorce in women increases risk of MI [65] - holidays (Christmas & New Year) increase risk - highest risk (RR=1.4) on Christmas eve [87] d) sympathomimetics including cocaine use stimulate sympathetic activity & increase risk of MI 6) acute respiratory tract infections transiently increase risk [23,81,88] - pneumonia, acute bronchitis, influenza, respiratory syncytial virus confer 3-6 fold increased risk [88] 7) in young patients, consider Kawasaki disease 8) weather conditions associated with small increased risk - temperature below freezing strongest weather risk [86] - low atmospheric air pressure, high wind speed, shorter daylight - coronary vasoconstriction is the most probable mechanism [86] 9) also see etiology of MI without coronary artery disease 10) also see cardiac risk factors * the majority of MIs occur in patients with non-obstructive coronary artery disease [56] Pathology: 1) mortality from MI is greatest within the 1st 2 hours 2) earliest histologic evidence of myocardial infarction occurs after 8-12 hours 3) after myocardial infarction, the epicardium stops producing FSTL1 [66] Genetics: - ALOX5AP haplotypes hapA & hapB are associated with susceptibility to myocardial infarction - other implicated genes: PALLD Clinical manifestations: 1) chest pain, resembling angina pectoris* a) more severe & longer in duration than angina 1] typically > 20 minutes to several hours in duration 2] angina is typically < 10 minutes in duration 3] a dull pain may persist for days after severe pain subsides b) association with exertion c) radiation to one or both arms* d) not relieved by rest or nitroglycerin e) chest pain may be absent: 1] post-operative 2] elderly 3] diabetes 4] hypertension 2) dyspnea 3) nausea/vomiting 4) diaphoresis 5) palpitations 6) exacerbation of CHF/cardiogenic pulmonary edema 7) confusion 8) hypotension* may indicate cardiogenic shock - cardiogenic shock with JVD, but without pulmonary congestion suggests RCA occlusion (inferior wall & right heart) 9) jugular venous distension (JVD) indicates right ventricular failure; clear lungs, bradycardia, hypotension suggests right ventricular infarction 10) S3* suggests heart failure 11) S4 indicates decreased left ventricular compliance 12) new systolic murmur a) mitral regurgitation b) ventricular septal defect 13) pericardial friction rub in 15% of cases 14) signs/symptoms may be different in women * chest pain with radiation to both arms, S3 & hypotension are the most predictive features of myocardial infarction # association of chest pain with exertion is a stronger indicator of AMI than association with dyspnea, pressure, or stress [57] Diagnosis: - serum tropinin I or serum troponin T > 99% of a normal reference population, plus one or more of [43] - symptoms of ischemia - new significant ST sement or T wave changes or left bundle branch block - pathologic Q waves on ECG - new loss of viable myocardium or regional wall motion abnormality, as observed on imaging - intracoronary thrombus diagnosed by angiography or autopsy Laboratory: 1) markers of myocardial infarction a) creatine kinase MB fraction - serum CK-MB increases 4-6 hours after MI - peak levels 12-20 hours - returns to baseline in 36-48 hours - serum CK MB index > 5% indicates MI (max value is 20%) b) serum troponin - serum troponin-I - upon presentation & 1 hour later [61] - within 6 hours (performance measure) [80] - high-sensitivity serum cardiac troponin T - a single high-sensitivity serum cardiac troponin T + ECG can rule out MI [74] c) serum lactate dehydrogenase (LDH) isozymes - elevations in serum LDH become detectable in 12 hours - peak levels in 24-48 hours - remain elevated for 10-14 days - LDH1/LDH2 ratio > 1.0 indicates myocardial infarction - most useful in patients presenting 24 hours after onset of symptoms d) serum aspartate transaminase (serum AST, SGOT) e) serum myoglobin - non-specific marker - elevation in serum within 1-3 hours of MI 2) routine labs a) complete blood count - leukocytosis may accompany myocardial necrosis - hemoglobin <10 g/dL may be indication for transfusion b) serum electrolytes c) serum glucose d) serum creatinine Special laboratory: - electrocardiogram: a) the majority of patients with MI have ECG changes b) ST segment elevation, > 1 mm in 2 contiguous leads 1] convex 2] peaked or inverted T waves c) prolongation of QTc preceeds ST segment elevation [29] d) ST segment depression 1] reciprocal depression 2] non Q wave MI e) new Q waves > 40 msec may occur with: 1] MI 2] prolonged ischemia 3] myocarditis f) new or presumed new left bundle branch block g) accelerated idioventricular rhythm common within 1st 24 hours [6] - coronary angiography with revascularization - revascularization of all significantly blocked arteries not just culprit arteries involved in MI [55] Radiology: - chest X-ray to assess for congestive heart failure, pneumothorax Differential diagnosis: (see chest pain) Complications: see complications of myocardial infarction 1) mortality from MI is greatest within the 1st 2 hours 2) myocardial pump failure a) occurs 2-7 days after MI b) congestive heart failure c) cardiogenic shock d) pulmonary edema e) hepatic congestion from right heart failure f) myocardial rupture - generally occurs after 3-7 days, but may occur later - interventricular septum - ventricular septal defect (10%) - loud holosystolic murmur, thrill, pulmonary edema [6] - left ventricular free wall (85%) - sudden death, pulseless electrical activity g) left ventricular aneurysm h) rupture of papillary muscle (5%) - mitral regurgitation - loud holosystolic murmur, thrill - pulmonary edema i) evaluate with emergent echocardiography 3) cardiac arrhythmias a) ventricular arrhythmias most lethal - sustained ventricular arrhythmias early post-infarction are predictive of recurrent arrhythmias & 1-year mortality [107] - premature ventricular depolarizations - ventricular tachycardia (VT) - ventricular fibrillation (VF) - accelerated idioventricular rhythm (AIVR) common within 1st 24 hours (no treatment generally needed) [6] b) supraventricular arrhythmias - sinus tachycardia - paroxysmal supraventricular tachycardia (PSVT) - atrial fibrillation (AF) - excess risk of death is highest for AF developing > 30 days after MI [36] - atrial flutter c) bradyarrhythmias - sinus bradycardia - AV block due to right coronary artery occlusion (90%) - temporary cardiac pacing if indicated - delay insertion of a permanent pacemaker for several days to determine if heart block is transient or permanent [6] - coronary reperfusion therapy (PCI) [6] 4) pericarditis - acute pericarditis - results from transmural infarction & irritation of the pericardium - nay occur within a few days of myocardial infarction (2 days [102]) - Dressler's syndrome - non-acetylated salicylate is treatment of choice; avoid NSAIDs (with anti-platelet activity) 5) thromboembolism - intracardiac thrombus occurs in 40% of patients with anterior wall MI - systemic thromboembolism occurs in 50% of patients with anterior wall MI 6) right ventricular infarction - occurs in 40% of patients with inferior wall MI - jugular venous distension - clear lung fields 7) recurrent myocardial infarction [6] - risk about 10% in the 1st year - peak incidence within 1st 6 weeks - 4-6 weeks necessary for myocardium & ruptured coronary plaque to heal - life time risk of 2nd MI is 50% [11] 8) renal disease associated higher risk of death after MI [12] - small increase in serum creatinine during hospitalization for MI associated with increased risk of ESRD & death [31,38] 9) depression increases risk of adverse outcomes [28] 10) women treated with fibrinolytic therapy, antiplatelet agents, or anticoagulation have a higher risk of bleeding complications than men [6] 11) 30 day rehospitalization 19%; 43% of these related to incident MI [42 12) myocardial infarction is associated with faster declines in memory, executive function, & global cognition [98] 13) falls in the elderly are common after myocardial infarction Management: 1) goals of management - relieve pain - recognize & treat complications of MI - minimize the size of the infarction 2) serial ECGs, upon presentation & QD during hospitalization 3) initial medical therapy - clopidogrel plus aspirin 81 mg, avoid NSAIDs [35] - oxygen - beta blocker - analgesia: nitrates vs IV fluids (see below), morphine - target mean arterial blood pressure = 60-100 mm Hg [6] - beta blockers & nitrates 1st line - avoid hydralazine [6] - heparin for 48 hours - glycoprotein IIb/IIIa inhibitor (NSTEMI) [6] 4) aspirin 160-325 mg PO immediately (chewed, not EC) & QD - clopidrogrel may be of benefit (see COMMIT trial) - aspirin + prasugrel or ticagrelor for 1 year (STEMI) [84] 5) oxygen: - 2-4 liters/min by nasal cannula - do not continue for more than 3 hours unless hypoxia is present [7] - similar 1-year mortality & rehospitalization rate vs ambient air unless oxygen saturation < 90% [79,84] 6) IV fluids - right ventricular MI (avoid nitrates) - posterior wall MI with hypotension 7) analgesia a) nitrates - nitroglycerin - relieves angina, lowers blood pressure - may reduce infarct size - decrease in wall tension - affects remodelling - may diminish susceptibility to ventricular fibrillation - contraindications to IV nitroglycerin - hypotension - right ventricular infarction - may reduce mortality in patients with large anterior wall myocardial infarction & congestive heart failure - nitrates reduce mortality (4-8 deaths/1000) at 2 days when administered within 24 hours of an MI [62] - no mortality benefit when continued beyond 48 hours - isosorbide 10-30 mg TID - do not give every 8 hours - need relatively drug free period each day with TID schedule (8 AM, 12 noon, 5 PM) - reduces need for SL NTG b) morphine for anxiety & discomfort 8) beta-blockers a) decrease myocardial oxygen consumption - decreased heart rate - decreased LV contractility - decreased BP b) of no benefit during acute MI - delayed treatment may be modestly beneficial [62] c) IV beta blockers - decrease infarct size & mortality - decrease incidence of ventricular fibrillation - indicated in patients who present within 4-6 hours after onset of symptoms d) chronic oral cardioselective beta blockers - atenolol, metoprolol - used within 3-21 days [6] - used within 48 hours reduces mortality [70] - continued use 1 year after MI may not reduce mortality [70] - progressively decreasing benefit of beta-blocker over time [70] - may not improve 1 year survival in patients without heart failure or LV systolic dysfunction [76] - beta-blocker may not benefit revascularized patients without LV systolic dysfunction after MI [104] e) contraindications - heart rate < 55/min - systolic blood pressure < 95 torr - AV block - obstructive lung disease - history - wheezing on examination - evidence of significant heart failure - inferior wall MI with high vagal tone f) use diltiazem or verapamil if beta-blocker contraindicated g) specific beta-blockers - metoprolol (cardioselective) - up to 15 mg IV, given in 5 mg doses 5 min to 2 hours apart - 50 mg PO every 12 hours - atenolol (cardioselective) - 5-10 mg IV - 100 mg PO QD - labetalol - 20-80 mg IV every 10 minutes, up to 300 mg - useful in patients in state of adrenergic excess, circumvents unopposed alpha activity with beta adrenergic antagonists - cocaine - alcoholism - hyperthyroidism - pheochromocytoma - timolol - 1 mg IV repeated after 10 minutes, 0.6 mg/kg infusion for 24 hours, followed by - 10 mg PO every 12 hours - esmolol drip - 250-500 ug/kg bolus - infusion of 50 ug/kg/min - useful for patients at risk for complications from beta blockers because of short 1/2 life h) functional decline occurs in 2% of impaired elderly prescribed beta-blockers after MI [72] 9) ACE inhibitor or angiotensin receptor antagonist (ARB) [17] a) early treatment is beneficial - initiate therapy when hemodynamically safe (2-3 days post MI; within 24 hours [6]) & continue for at least 6 weeks - increased long term (42 month) survival - prevents remodeling of infarcted myocardium - ramipril, perindopril may be better than lisinopril, enalapril, fosinopril, captopril, or quinapril [20,21] - sacubitril/valsartan no better than ramapril for MI complicated by left ventricular dysfunction or pulmonary congestion [95] b) long term management of LV dysfunction following MI 10) calcium channel blockers - diltiazem or verapamil if beta-blocker contraindicated [3] - others without benefit & potential for harm 11) use of diuretics after acute MI may be associated with increased mortality - use of chlorthalidone vs HCTZ associated with lower cardiovascular morbidity & mortality [105] 12) amiodarone is agent of choice for arrhythmias not controlled by beta blockers 13) anticoagulation a) heparin - appears to reduce mortality in patients with MI - risk of bleeding complications probably outweighs benefit in patients at low risk for complications - no benefit of heparin [64] b) warfarin: documented thrombus c) enoxaparin (Levonox, low molecular weight heparin) - avoid in obesity, renal failure [6] 14) PCI (PTCA) more effective than thrombolytic therapy [15,27] - thrombolytic therapy generally indicated only for STEMI when PCI is not available - multivessel or distal disease may favor thrombolytic therapy vs PCI - perform within 90 minutes of 1st medical contact [6] - survival benefit for up to 12 hours after symptom onset (see PCI) - PCI improves outcomes with cardiogenic shock [26] (see SHOCK trial) - transfer to PCI-capable hospital should routinely follow thrombolysis [32] - atrial natriuretic peptide (ANP) 0.025 ug/kg/min for 3 days post reperfusion may improve outcomes [30] - thrombolysis prior to PCI may worsen outcomes [22] - complete revascularization may improve outcomes relative to infarct-related artery only revascularization [54] - complete multivessel revascularization at the time of PCI in patients with acute myocardial infarction who present with cardiogenic shock [94] - fewer early complications & lower mortality with culprit vessel only revascularization [94] - early PCI associated with reduced mortality but higher costs, balanced by lower 180-day expenditures [82] - also see PCI & STEMI 15) intra-aortic balloon pump: [3] - superior to LV assist device for post MI cardiogenic shock [82] - acute mitral regurgitation or ventricular septal defect - intractable ventricular tachycardia - refractory angina 16) temporary cardiac pacemaker - symptomatic bradycardia, including complete heart block - alternating LBBB & RBBB - new or indeterminant age bifascicular blodk with 1st degree AV block [6] 17) blood transfusion may increase mortality [45] 18) in hospital strategies that reduce mortality - monthly meetings to review myocardial infarction cases with hospital clinicians & staff who transport patients to the hospital - having an on-site cardiologist at all times - cultivating an environment in which clinicians are encouraged to solve problems creatively - avoiding cross-training of intensive care unit nurses for cardiac catheterization laboratories - having at least one quality-improvement champion who is a physician rather than a nurse 19) recovery (also see follow-up below) a) HMG CoA reductase inhibitor in hospital [24] - see PROVE-IT & REVERSAL studies - continue or begin within 24-96 hours [6] - high-dose atorvastatin more effective than low-dose (see statin clinical trial) - associated with lower mortality in patients < 80 years but not in those >= 80 years, as a group [51,69] - no benefit to starting statin within 14 days of MI [61] - target serum LDL cholesterol < 70 mg/dL - add ezetimibe 10 mg to high-dose atorvastatin as needed to achieve LDL cholesterol goal [100] b) aldosterone antagonist at discharge for eligible STEMI & NSTEMI patients (quality measure) [80] c) prevention of coronary thrombosis - low-dose aspirin (81 mg) long term - dual antiplatelet therapy for one year - clopidogrel (Plavix) or ticagrelor plus aspirin 81 mg [11] appears to be treatment of choice [6] - esomeprazole more effective than famotidine in preventing GI bleed [40] - dual antiplatelet therapy for 1-3 years improves cardiovascular outcomes [59,68] - warfarin - superior to aspirin in reducing subsequent cardiac events & death [10] - target INR of 2.5-3.5 [11] (without aspirin) - combination of warfarin + 81 mg aspirin (INR 2.0-3.0) better than aspirin or warfarin alone [11,13,19] - direct-acting oral anticoagulant as add-on to antiplatelet therapy - favorable benefit/risk for STEMI; not so for NSTEMI [83] - avoid NSAIDs other than low-dose aspirin - NSAIDS increase risk of cardiovascular events [60] - concurrent administration of proton pump inhibitor with NSAID &/or antithrombotic agent lowers risk of bleeding [67] - polypill containing aspirin, statin, & ACE inhibitor improved outcomes in older patients with recent myocardial infarction [97] d) eplerenone (Inspra) for LV dysfunction [6] e) prolonged bedrest not recommended f) treat depression (see depression & heart disease) g) cardiac stem cell infusion h) implantable cardioverter-defibrillators (ICDs) - > 40 days since MI - LVEF <36% & NYHA class 2 or 3 heart failure - LVEF <31% & NYHA class 1 heart failure [6] - confers no survival advantage in high-risk patients early after myocardial infarction - recurrent MI & cardiac rupture (non-arrhythmic) account for 50% of mortality after MI [33] i) chelation therapy with EDTA (40 infusions) reduces post-MI mortality in patients with diabetes mellitus [47] - no benefit in patients without diabetes mellitus - authors stop short of recommending chelation therapy for any group of patients [47] j) omega-3 fatty acid 1 g/day reduces mortality 45% [16] - may be reasonable [73] k) colchicine 0.5 mg/day within 30 days may reduce risk of adverse cardiovascular events after myocardial infarction (RR=0.77) [90]; (RR=0.65) [103] type-2 diabetes - greatest risk reduction for stroke (RR-0.26) [90] - may do so at the cost of increased all-cause mortality [93] l) dietary fibers, especially from grains & cereals, reduces mortality in patients after myocardial infarction [50] m) noninvasive stress testing before discharge in medically- treated patients (performance measure) [80] 20) follow-up a) screen for depression: associated with increased morbidity & mortality [6] b) physical therapy & occupational therapy c) cardiac rehabilitation - rehabilitation treadmill testing 8-10 days post MI - only 1/3 of survivors undergo cardiac rehabilitation [78] d) echocardiogram - if LVEF < 40% (new onset LV dysfunction), perform coronary angiography [ref 48 cites ref 4] - if LVEF < 30%, place AICD - wait >= 40 days before placing AICD e) coronary angiography - if indicated by rehabilitation treadmill testing or echocardiogram - post infarction angina - unable to exercise - within 48 hours (TACTICS-TIMI trial) [9] f) PneumoVax, PCV13 & annual influenza virus vaccine [8] g) patients may resume sexual activity >= 1 week after uncomplicated acute MI if asymptomatic during mild or moderate physical activity [58] h) electronic reminders, financial incentives, & social support without effect on clinical outcomes or medication adherence [77] i) continue beta-blocker used for secondary prevention [106] 21) post-MI non-cardiac surgery: delay (if possible) 4-6 weeks (uncomplicated MI) [49,52] - 4-6 weeks for recipients of bare-metal stents - 6-12 months for recipients of drug-eluting stents 22) prognosis a) renal insufficiency portends poor prognosis [18] - 3.7 fold increase in mortality with serum creatinine > 2.0 mg/dL b) hypokalemia or hyperkalemia associated with increased risk of ventricular fibrillation & mortality - serum potassium < 3.0 meq/L or > 5.0 meq/L - mortality unaffected by potassium supplementation [39] c) diabetes mellitus associated with poorer prognosis (see VALIANT study) d) impairment in timed get-up & go test predicts functional decline [89] e) presentation at off hours worsens prognosis [48] f) financial strain (subjective assessment of inability to make ends meet) associated with increased 6 month mortality [96] g) risk calculator to predict 6-month prognosis in elderly [91] Comparative biology: - FSTL1 patches on the epicardial surface over an infarcted area of myocardium in mice or pigs resulted in regeneration of cardiomyocytes, increased vascularization, diminished scarring, improved contractility, & lengthened lifespan [66] - in mice, monocytes producing tumor necrosis factor enter the brain after a myocardial infarction & induce slow wave sleep resulting in a reduction of cardiac inflammation [108] Notes: - gene therapy with microRNAs resulted in cardiac muscle regeneration after myocardial infarction in mice [44]

Interactions

disease interactions

Related

acute coronary syndrome; unstable angina (ACS) angina pectoris clinical trials for myocardial infarction complications of myocardial infarction coronary artery disease; coronary atherosclerosis (CAD) etiology of myocardial infarction (MI) without coronary atherosclerosis markers of myocardial injury/infarction myocardial ischemia

Useful

coronary angiography Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock (SHOCK) trial thrombolysis for acute myocardial infarction

Specific

anterior wall myocardial infarction (MI) inferior wall myocardial infarction (MI) Myocardial Infarction No Obstructive Coronary Artery disease (MINOCA) non ST segment elevated myocardial infarction (nonSTEMI, NSTEMI) non-Q-wave myocardial infarction posterior wall myocardial infarction (MI) reperfusion-eligible acute myocardial infarction right ventricular myocardial infarction (MI) silent myocardial infarction (silent MI) ST segment elevated myocardial infarction (STEMI)

General

infarction myocardial injury

References

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OMIM 608557 Figures/diagrams/slides/tables related to myocardial infarction