infarction

Acute Myocardial Infarction : 

Acute Myocardial Infarction David Putnam, MD Albany Medical College

Acute MI : 

Acute MI Any degree of myocardial necrosis caused by myocardial ischemia and detected using a sensitive and specific preferred biomarker, such as cardiac troponin.

Acute Myocardial Infarction : 

Acute Myocardial Infarction Annual incidence in US: 900,000 Mortality: 225,000 Pre-admission mortality: 125,000

Slide 4: 

Acute Coronary Syndromes (ACS) Van de Werf F. Throm Haemost. 1997; 78(1):210-213.

Acute MI: Pathophysiology : 

Acute MI: Pathophysiology Acute plaque fissuring and rupture Superimposed thrombus Transient or permanent occlusion

Slide 6: 

Clinical manifestations of arterial thrombosis UA/NQMI:Partially-occlusive thrombus (primarily platelets) Intra-plaque thrombus (platelet dominated) Plaque core ST  MI:occlusive thrombus (platelets, red blood cells, and fibrin) Intra-plaque thrombus (platelet dominated) Plaque core SUDDEN DEATH Adapted from Davies MJ. Circulation. 1990; 82 (supl II): 30-46.

Slide 7: 

Pathophysiology of UA/NQMI White HD. Am J Cardiol. 1997; 80 (4A): 2B-10B.

Acute Myocardial Infarction : 

Acute Myocardial Infarction Lipid-rich soft plaques surrounded by a thin fibrous cap are more dangerous in terms of thrombus than collagen-rich and hard plaques.

Slide 9: 

Large lipid core with thin fibrous cap, macrophages interacting with thrombus Reduced lipid core with thick fibrous cap reinforced with increased smooth muscle cells Thrombus Lumen Endothelium ThickFibrous cap Smooth Muscle cells Lipid rich core Macrophage Platelets Thin fibrous cap Stable and Vulnerable Plaques

Small, vulnerable plaques are responsible for causing MI : 

Small, vulnerable plaques are responsible for causing MI MI Patients (%) Falk et al: Circulation 1995;92:657–671

Acute MIInitial Recognition and Management : 

Acute MIInitial Recognition and Management Time is of the essence Initial evaluation ideally should be accomplished within 10 minutes Goal: treatment within 1 hour after symptom onset

Acute MI: Diagnostic Criteria : 

Acute MI: Diagnostic Criteria Clinical history of ischemic-type chest discomfort Changes on serially obtained ECG tracings Rise and fall in serum cardiac markers

Acute MI: ECG Changes : 

Acute MI: ECG Changes

Correlation of ECG Changes and Areas of Damage : 

Correlation of ECG Changes and Areas of Damage

Acute Anterior MI : 

Acute Anterior MI

Acute Anterior Wall MI : 

Acute Anterior Wall MI

Acute Anterior Wall MI : 

Acute Anterior Wall MI

Acute Inferior MI : 

Acute Inferior MI

Acute Inferior Wall MI : 

Acute Inferior Wall MI

Acute Posterior MI : 

Acute Posterior MI

Acute Inferior Wall MI with Posterior Extension : 

Acute Inferior Wall MI with Posterior Extension

Right Ventricular Infarction : 

Right Ventricular Infarction ST segment elevation V4R highly predictive of RV infarct Higher in-hospital mortality Higher incidence of in-hospital complications NEJM 1993(APR);328:981-8.

Acute Right Ventricular Wall MIRight Sided Leads : 

Acute Right Ventricular Wall MIRight Sided Leads

Chest Pain Patients in the Emergency Room : 

Chest Pain Patients in the Emergency Room 10% have ST-segment elevation 10% have non-diagnostic ECG changes 30% have cardiac ischemia without infarction 50% have symptoms of non-cardiac origin ARCH INT MED 1987;147:843.

Acute MI: Initial ECGNon-diagnostic ECG’s : 

Acute MI: Initial ECGNon-diagnostic ECG’s Normal Subtle ST-T changes Isolated T-wave changes Negative U-waves Normalization of previous abnormal ST-segment and T-waves Conduction defects “Silent” areas: right, posterior

Acute MI: Serum Markers : 

Acute MI: Serum Markers

Acute MI: Serum Markers : 

Acute MI: Serum Markers

Acute MI: Serum Markers : 

Acute MI: Serum Markers

Acute MI: Serum Markers : 

Acute MI: Serum Markers

Acute MI: Troponin LevelsGUSTO-IIa Trial : 

Acute MI: Troponin LevelsGUSTO-IIa Trial Troponin T levels above 0.1 ng/ml were predictive of early MI/death even in patients with no ST-segment elevation or CPK elevation. NEJM 1996;335:1333-41.

Acute MI TreatmentCurrent Standard of Care : 

Acute MI TreatmentCurrent Standard of Care Early sustained reperfusion of jeopardized myocardium using thrombolytic agents or primary angioplasty in appropriate patients Other measures to reduce myocardial damage

Acute MI: Outcome : 

Acute MI: Outcome Outcome after acute myocardial infarction is a function of vessel patency rate and time from occlusion to reperfusion

Benefits of Rapid Reperfusion : 

Benefits of Rapid Reperfusion Decreased mortality Decreased morbidity Increased myocardial salvage Increased left ventricular function

Patients with Suspected MIEarly Treatment : 

Patients with Suspected MIEarly Treatment Oxygen by nasal prongs Sublingual nitroglycerin Adequate analgesia (morphine or meperidine) Aspirin, 160 to 325 mg 12-Lead electrocardiogram

Thrombolytic Therapy Effect on Mortality : 

Thrombolytic Therapy Effect on Mortality Lancet Ltd 1994;343:311-322

Acute MI: Thrombolysis : 

Acute MI: Thrombolysis Benefit greatest if therapy initiated early Highly significant reduction in mortality Benefits patients irrespective of age, gender, and comorbid conditions Slightly increased risk of intracerebral hemorrhage

ThrombolysisCandidates : 

ThrombolysisCandidates Time to therapy 12 hours or less Acute ST-segment elevation Symptoms consistent with acute MI and presence of Left Bundle Branch Block Patients without ST-segment elevation should not receive thrombolytic therapy

Thrombolytic TherapyContraindications : 

Thrombolytic TherapyContraindications Active bleeding Recent major surgery Stroke within 2 months Markedly elevated blood pressure Significant bleeding diathesis

Thrombolytic Agents : 

Thrombolytic Agents Nonspecific agents deplete coagulation factors A. Streptokinase B. Anistreplase C. Urokinase Specific agents do not deplete coagulation factors A. Alteplase (tPA) B. Reteplase

Primary PTCA : 

Primary PTCA Alternative to thrombolytic therapy if performed in a timely fashion by skilled individuals in high-volume centers Reperfusion strategy in patients with risk of bleeding contraindications to thrombolytic therapy

Acute MI : 

Acute MI Adjunctive Drug Therapy

AspirinPotential Benefits : 

AspirinPotential Benefits Inhibition of tromboxane A2 formation Blockage of platelet aggregation and thrombus propagation Prevention of coronary reocclusion after successful thrombolysis

AspirinISIS-2 Trial : 

AspirinISIS-2 Trial Mortality decreased 23% Non-fatal MI decreased 44% Non-fatal stroke decreased 46% 42% reduction in mortality when added to Streptokinase

AspirinGuidelines : 

AspirinGuidelines Chewable Aspirin is preferred Dose of 160 to 325 mg should be given as soon as possibel Contraindicated in patients with known hypersensitivity (may substitute Ticlopidine or Clopidagrel Caution in patients with active or recent hemorrhaging, including stroke or peptic ulcer disease

HeparinPotential Benefits : 

HeparinPotential Benefits Prevention of venous thrombosis Decrease left ventricular mural thrombus Decrease arterial embolization Decrease re-infarction or extension of infarct

Heparin : 

Heparin Post thrombolytic therapy, heparin administration based more on current practice than on evidence

Heparin : 

Heparin Should be used in large AWMI or in patients with LV mural thrombus to reduce risk of stroke For patients with smaller MI and without thrombus, little data on benefit of heparin

High Risk for Systemic Embolization : 

High Risk for Systemic Embolization Large or anterior MI Atrial fibrillation Previous embolus Known LV thrombus

HeparinGuidelines : 

HeparinGuidelines Intravenously in patients receiving alteplase/retaplase Subcutaneously in all patients not treated with thrombolytic therapy Intravenous form preferred in patients at high risk of embolic event

Beta Blockers : 

Beta Blockers Patients without contraindications should receive intravenous beta blockers when acute infarction is suspected, followed by oral agents when they are hemodynamically stable

Beta BlockersPotential Benefits : 

Beta BlockersPotential Benefits 13% reduction in mortality in the pre-thrombolytic trials Reduce chest pain Reduce myocardial-wall stress Reduce infarct size

Beta BlockersContraindications : 

Beta BlockersContraindications Bradycardia Second- or third-degree AV block Hypotension Clinical evidence of congestive heart failure Cardiogenic shock Active bronchospasm

Beta BlockersGuidelines : 

Beta BlockersGuidelines All patients within 12 hours of myocardial infarction Continuing or recurrent ischemic pain Tachyarrhythmias

NitratesPotential Benefits : 

NitratesPotential Benefits Primary action is vasodilation May increase myocardial perfusion May increase peri-infarct ischemia Systemic arterial vasodilation decreases blood pressure and decreases myocardial oxygen demand Increased venous capacitance decreases preload

Nitrates : 

Nitrates GISSI-3 yielded an insignificant mortality reduction in patients treated with IV nitroglycerin ISIS-4 yielded an insignificant mortality reduction in patients treated with oral isorbide mononitrate Pooled date demonstrates a 5.5% reduction in mortality

NitratesGuidelines : 

NitratesGuidelines Intravenously for first 24 to 48 hours A. Acute MI and CHF B. Large anterior infarction C. Persistent ischemia D. Hypertension Beyond 48 hours in patients with recurrent angina or persistent pulmonary congestion

ACE InhibitorsPotential Benefits : 

ACE InhibitorsPotential Benefits Mortality benefit when administered within 24 hours of MI Systemic and coronary vasodilation may: A. Reduce peri-infarct ischemia B. Limit infarct expansion C. Prevent early remodeling May have some antithrombotic properties

ACE Inhibitors : 

ACE Inhibitors ISIS-4 demonstrated 7% reduction in mortality with oral captopril GISSI-3 demonstrated 11% reduction in mortality with oral lisinopril No benefit has been shown with intravenous ACE inhibitors

Early ACE Inhibitors : 

Early ACE Inhibitors Meta-analysis of 845 patients ACE inhibitors administered within 6 to 9 hours of MI No effect on attenuation of LV dilation in patients receiving thrombolysis JACC 2000(DEC);36:2047-2053

ACE InhibitorsGuidelines : 

ACE InhibitorsGuidelines Within first 24 hours in patients with congestive heart failure and without hypotension Patients with LV ejection fraction less than 40% after acute MI Option in all patients with acute MI

Calcium Channel BlockersPotential Benefits : 

Calcium Channel BlockersPotential Benefits Reduce angina Reduce blood pressure Reduce coronary spasm No reduction in mortality Short-acting nifedipine may increase mortality (TRENT, SPRINT II)

Acute MI: Diltiazem : 

Acute MI: Diltiazem Nonsignificant 2% increase in overall mortality 41% increase in cardiovascular events (cardiac death/non-fatal MI) in patients with CHF 23% decrease in cardiac events in patients without CHF MDPTT Trial

Acute MI: Verapamil : 

Acute MI: Verapamil No reduction or increase in mortality 20% reduction in first major events due to cardiovascular causes (death or reinfarction) 19% reduction in reinfarction DAVIT I, DAVIT II, CRIS Trials

Calcium Channel BlockersGuidelines : 

Calcium Channel BlockersGuidelines Not recommended as standard first-line therapy May be used for significant hypertension or refractory ischemia

MorphinePotential Benefits : 

MorphinePotential Benefits Pain/anxiety relief Blocks sympathetic efferent discharge Peripheral venous/arterial dilation Reduction in preload/afterload Decrease in myocardial oxygen demand Decrease in circulating catecholamines Possible arrhythmia reduction

MorphineGuidelines : 

MorphineGuidelines Recurrent, small, intravenous doses for: A. Chest pain B. Agitation C. Congestive heart failure D. Hypertension

Hospital ManagementEarly, General Measures : 

Hospital ManagementEarly, General Measures Electrocardiographic monitoring (telemetry) Bed rest with bedside commode privileges for initial 12 hours in stable patients Avoidance of valsalva Careful attention to maximum pain relief

Early Coronary Angioraphy : 

Early Coronary Angioraphy Recurrent/continued ischemia Shock Pulmonary congestion LV dysfunction

Rhythm DisturbancesAtrial Fibrillation : 

Rhythm DisturbancesAtrial Fibrillation Electrical cardioversion for unstable patients (ischemic chest pain, hypotension, congestive heart failure) Slow the ventricular response: A. IV Digitalis B. IV Beta Blockers C. IV Diltiazem or Verapamil

Rhythm DisturbancesVentricular Tachycardia/Fibrillation : 

Rhythm DisturbancesVentricular Tachycardia/Fibrillation V-fib: unsynchronized electric shock Sustained v-tach without palpable pulse: unsynchronized electric shock Unstable (angina, pulmonary edema, hypotension) sustained v-tach: synchronized electric shock Stable, sustained v-tach: medical treatment

Ventricular Fibrillation : 

Ventricular Fibrillation

Acute Ischemic SyndromesAntiarrhythmic Agents : 

Acute Ischemic SyndromesAntiarrhythmic Agents

Bradyarrthymias/Heart BlockAtropine : 

Bradyarrthymias/Heart BlockAtropine Symptomatic sinus bradycardia Ventricular asystole Symptomatic AV block occurring at the AV nodal level

Temporary PacingTrancutaneous Patches : 

Temporary PacingTrancutaneous Patches Symptomatic sinus bradycardia unresponsive to Atropine Mobitz type II second-degree AV block Third-degree heart block Bilateral BBB New or indeterminate age bifascicular block

Temporary PacingTransvenous Pacing : 

Temporary PacingTransvenous Pacing Asystole Symptomatic bradycardia unresponsive to Atropine Bilateral BBB New or indeterminate age bifascicular block

Acute MI: Acute Complications : 

Acute MI: Acute Complications Papillary muscle rupture Postinfarction VSD Free wall rupture Postinfarction ventricular aneurysm associated with ventricular tachyarrhythmias/CHF

Post MI Prognosis : 

Post MI Prognosis Left ventricular ejection fraction Number of diseased coronary arteries Presence of spontaneous/inducible ischemia Presence and extent of ventricular ectopy

Non-Invasive Evaluation/Low Risk PatientsExercise Stress Testing : 

Non-Invasive Evaluation/Low Risk PatientsExercise Stress Testing Prognostic assessment/functional capacity A. Before discharge B. Early after discharge (14 to 21 days) C. Late after discharge (3 to 6 weeks) if early stress was submaximal D. Nuclear stress or echo stress in patients with abnormal ECG

Exercise Testing Post MI : 

Exercise Testing Post MI

Treatment of Acute MISummary : 

Treatment of Acute MISummary