Acute Myocardial Infarction


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Thanks a lot!!!
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its realy good.very helpful in understanding better management.
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1 : Acute Myocardial Infarction David Putnam, MD Albany Medical College
2 : Acute MI Any degree of myocardial necrosis caused by myocardial ischemia and detected using a sensitive and specific preferred biomarker, such as cardiac troponin.
3 : Acute Myocardial Infarction Annual incidence in US: 900,000 Mortality: 225,000 Pre-admission mortality: 125,000
4 : Acute Coronary Syndromes (ACS) Van de Werf F. Throm Haemost. 1997; 78(1):210-213.
5 : Acute MI: Pathophysiology Acute plaque fissuring and rupture Superimposed thrombus Transient or permanent occlusion
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.
7 : Pathophysiology of UA/NQMI White HD. Am J Cardiol. 1997; 80 (4A): 2B-10B.
8 : 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.
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 Thick Fibrous cap Smooth Muscle cells Lipid rich core Macrophage Platelets Thin fibrous cap Stable and Vulnerable Plaques
10 : Small, vulnerable plaques are responsible for causing MI MI Patients (%) Falk et al: Circulation 1995;92:657–671
11 : Acute MI Initial 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
12 : Acute MI: Diagnostic Criteria Clinical history of ischemic-type chest discomfort Changes on serially obtained ECG tracings Rise and fall in serum cardiac markers
13 : Acute MI: ECG Changes
14 : Correlation of ECG Changes and Areas of Damage
15 : Acute Anterior MI
16 : Acute Anterior Wall MI
17 : Acute Anterior Wall MI
18 : Acute Inferior MI
19 : Acute Inferior Wall MI
20 : Acute Posterior MI
21 : Acute Inferior Wall MI with Posterior Extension
22 : 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.
23 : Acute Right Ventricular Wall MI Right Sided Leads
24 : 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.
25 : Acute MI: Initial ECG Non-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
26 : Acute MI: Serum Markers
27 : Acute MI: Serum Markers
28 : Acute MI: Serum Markers
29 : Acute MI: Serum Markers
30 : Acute MI: Troponin Levels GUSTO-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.
31 : Acute MI Treatment Current Standard of Care Early sustained reperfusion of jeopardized myocardium using thrombolytic agents or primary angioplasty in appropriate patients Other measures to reduce myocardial damage
32 : Acute MI: Outcome Outcome after acute myocardial infarction is a function of vessel patency rate and time from occlusion to reperfusion
33 : Benefits of Rapid Reperfusion Decreased mortality Decreased morbidity Increased myocardial salvage Increased left ventricular function
34 : Patients with Suspected MI Early Treatment Oxygen by nasal prongs Sublingual nitroglycerin Adequate analgesia (morphine or meperidine) Aspirin, 160 to 325 mg 12-Lead electrocardiogram
35 :
36 : Thrombolytic Therapy Effect on Mortality Lancet Ltd 1994;343:311-322
37 : 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
38 : Thrombolysis Candidates 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
39 : Thrombolytic Therapy Contraindications Active bleeding Recent major surgery Stroke within 2 months Markedly elevated blood pressure Significant bleeding diathesis
40 : 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
41 : 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
42 : Acute MI Adjunctive Drug Therapy
43 : Aspirin Potential Benefits Inhibition of tromboxane A2 formation Blockage of platelet aggregation and thrombus propagation Prevention of coronary reocclusion after successful thrombolysis
44 : Aspirin ISIS-2 Trial Mortality decreased 23% Non-fatal MI decreased 44% Non-fatal stroke decreased 46% 42% reduction in mortality when added to Streptokinase
45 : Aspirin Guidelines 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
46 : Heparin Potential Benefits Prevention of venous thrombosis Decrease left ventricular mural thrombus Decrease arterial embolization Decrease re-infarction or extension of infarct
47 : Heparin Post thrombolytic therapy, heparin administration based more on current practice than on evidence
48 : 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
49 : High Risk for Systemic Embolization Large or anterior MI Atrial fibrillation Previous embolus Known LV thrombus
50 : Heparin Guidelines 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
51 : Beta Blockers Patients without contraindications should receive intravenous beta blockers when acute infarction is suspected, followed by oral agents when they are hemodynamically stable
52 : Beta Blockers Potential Benefits 13% reduction in mortality in the pre-thrombolytic trials Reduce chest pain Reduce myocardial-wall stress Reduce infarct size
53 : Beta Blockers Contraindications Bradycardia Second- or third-degree AV block Hypotension Clinical evidence of congestive heart failure Cardiogenic shock Active bronchospasm
54 : Beta Blockers Guidelines All patients within 12 hours of myocardial infarction Continuing or recurrent ischemic pain Tachyarrhythmias
55 : Nitrates Potential 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
56 : 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
57 : Nitrates Guidelines 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
58 : ACE Inhibitors Potential 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
59 : 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
60 : 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
61 : ACE Inhibitors Guidelines 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
62 : Calcium Channel Blockers Potential Benefits Reduce angina Reduce blood pressure Reduce coronary spasm No reduction in mortality Short-acting nifedipine may increase mortality (TRENT, SPRINT II)
63 : 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
64 : 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
65 : Calcium Channel Blockers Guidelines Not recommended as standard first-line therapy May be used for significant hypertension or refractory ischemia
66 : Morphine Potential 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
67 : Morphine Guidelines Recurrent, small, intravenous doses for: A. Chest pain B. Agitation C. Congestive heart failure D. Hypertension
68 : Hospital Management Early, 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
69 : Early Coronary Angioraphy Recurrent/continued ischemia Shock Pulmonary congestion LV dysfunction
70 : Rhythm Disturbances Atrial 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
71 : Rhythm Disturbances Ventricular 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
72 : Ventricular Fibrillation
73 : Acute Ischemic Syndromes Antiarrhythmic Agents
74 : Bradyarrthymias/Heart Block Atropine Symptomatic sinus bradycardia Ventricular asystole Symptomatic AV block occurring at the AV nodal level
75 : Temporary Pacing Trancutaneous 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
76 : Temporary Pacing Transvenous Pacing Asystole Symptomatic bradycardia unresponsive to Atropine Bilateral BBB New or indeterminate age bifascicular block
77 : Acute MI: Acute Complications Papillary muscle rupture Postinfarction VSD Free wall rupture Postinfarction ventricular aneurysm associated with ventricular tachyarrhythmias/CHF
78 : Post MI Prognosis Left ventricular ejection fraction Number of diseased coronary arteries Presence of spontaneous/inducible ischemia Presence and extent of ventricular ectopy
79 : Non-Invasive Evaluation/Low Risk Patients Exercise 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
80 : Exercise Testing Post MI
81 : Treatment of Acute MI Summary

 

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