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ACUTE STEMI

Assessment guidelines
H+P: check risk factors, symptoms (less likely to be MI if: pain above nose, below umbilicus, brief episodes, well localized), signs (diaphoresis, elevated JVP, critical AS, transient S3), DOCUMENT time of initiation of symptoms (crucial for determination of management) ECG: always check right sided leads in cases of inferior MIs to assess for right ventricular involvement (1 mm ST elevation in RV4 is highly specific for right ventricular infarct; ST elevation in lead III > lead II is highly sensitive for RV infarct) CK-MB increases initially at 3-12 hs, peaks at 12-48 hs and normalizes 24-48 hs later cTnI and cTnT: more sensitive markers of myocardial damage; elevated troponins and negative CPKs seen in following cases: 1) recent MI 2-10ds prior 2) Microinfarct and 3) ESRD: slightly elevated troponin levels in ESRD patients may not indicate acute coronary syndrome but does portend increased likelihood of major adverse cardiac events

Treatment
Aspirin ASA 160 mg qd 325 mg qd studied (ISIS-2 study demonstrated 23% relative risk reduction in death in the ASA arm of study Beta-blockers Metoprolol 5 mg IV q5 mins as needed to goal HR 55-60; initiate oral therapy at the same time to allow for longer effects (BHAT showed 26% reduction in mortality with propanolol, ISIS-1 revealed 11% reduction in mortality with IV atenolol) ACE inhibitors Consider captopril 6.25 mg po tid within 24-48 hours of presentation with attention paid to renal function and hypotension Definite but modest benefit for ACE-inhibitors shown in various trials in the acute setting of STEMI depending on subgroup analyzed Meta-analysis of CONSENSUS-II, GISSI-3, ISIS-4, CCS-1 revealed that the following groups had an increased benefit from ACE-inhibitors: o Anterior MI o High risk patients (Killip class 2-3) o Tachycardia with HR > 100 HOPE trial can be used to extend the use of ACE-inhibitors to a larger population (those with preserved EF) based on the presence of existing CAD, PVD, CVA, or DM + 1 or more cardiac risk factors Heparin Heparin can be initiated with goal PTT 50-70 (70U/kg bolus 14U/kg drip) Adjunctive use of heparin with tPA lysis was supported by early angiographic and pilot studies There is conflicting data regarding the use of heparin outside of the context of thrombolysis although it is used widely ( LATE (positive) vs. ISIS-2 (negative)) There is some data to support use of heparin in cases of large anterior MI to prevent occurrence of left ventricular mural thrombi Lipid lowering drugs Statins can be considered for plaque stabilization therapy in the acute setting Some support for the use of lipitor 80 mg was shown by the MIRACL trial but almost all of the benefit was derived from the endpoint of recurrent symptomatic ischemia and NOT death and nonfatal MI with marginal p value (p = 0.048) Thrombolysis RARELY (if ever) used at Cornell given 24 hour cath lab availability tPA (alteplase): 100 mg total over 90 mins (15 mg bolus 50 mg over 30 mins 35 mg over 60 mins) rPA (reteplase): 10 U bolus at time 0 10U bolus at time 30 mins

Cornell Cardiology Curriculum 2003-2004

TNK (tenecteplase): 0.5mg/kg single bolus (max 50 mg) EKG indications for lysis: 1) ST elevations 1mm in 2 contiguous leads 2) New LBBB 3) ST depression 2 mm in leads V2-3 if felt to be posterior MI within >30 mins but <12 hours of onset of anginal symptoms Contraindications to thrombolysis Absolute Major surgery, trauma or organ bx past 6 wks History of hemorrhagic or undefined stroke History of brain tumor, neurosurgery, or head trauma Melena or marked hematuria History of bleeding diathesis Relative > 10 mins of chest compressions Age > 75 SBP > 180; DBP > 110, cardiogenic shock, remote stroke or recent TIA Occult fecal blood Concurrent warfarin

Assessing success of restoring flow with thrombolysis: 1) resolution of chest pain AND 2) resolution of ST elevations (70% resolution of ST elevation at 90 minutes correlates with angiographically confirmed TIMI 3 flow from TIMI 14 study dataDeLemo et al., 2000) The decision to use lytics over PTCA is dependent on clinical circumstance and the availability and proximity of cardiac catheterization facilities Benefit for lytics strongest with patients with highest absolute mortality (e.g. large anterior MI) Risk/benefit ratio for patients with complicated inferior MI (e.g. RVI, conduction disease) favors use of lytics but isolated, stable inferior MIs are subject to controversy No benefit has been shown for the use of half-dose lytics + glycoprotein IIbIIIa inhibitors regimens to date (GUSTO V, ASSENT-3); in fact, significantly higher rates of intracranial hemorrhage were seen in patients > 75 years of age

Coronary angioplasty PTCA is clearly preferable to lysis in certain subgroups such as anterior MI and cardiogenic shock This is the treatment of choice at Cornell for ST elevation MI PAMI study comparing tPA versus PTCA revealed PTCA arm with decreased death/MI during hospitalization and at 6 months (8.5% v. 16.8%); overall in-hospital mortality was no different between 2 arms but in higher risk subgroup (age > 65, anterior MI, tachycardia on presentation) there was decreased mortality in PTCA arm (2% v. 10%) Zijlstra study compared SK versus PTCA which showed that all cause mortality was lower in PTCA (13% v. 24%) Extent of mortality benefit is also dependent on the amount of volume in the institution where the PTCA is performed (Magid et al., 2000) There is no study clearly delineating a role for routine PTCA post thrombolysis: o Immediate routine PTCA (first few hours after onset of symptoms) may INCREASE incidence of bleeding, recurrent ischemia and need for urgent revascularization o Early routine PTCA (hours to days after onset of symptoms): NO significant benefit seen with PTCA (SWIFT, TIMI IIB studies) o Late routine PTCA (> 4 days): NO significant benefit seen with PTCA (Barbash et al., 1992) o Nonetheless, recurrent infarction in the first few days after thrombolytic therapy for acute myocardial infarction is clearly high risk (24% hospital morality if no revascularization) (Gibson et al., 2003); some believe that many of the above studies were performed in the earlier days of balloon angioplasty and therefore may not be applicable to current practice Rescue angioplasty is often done as it is the only method of obtaining TIMI 3 flow through the infarct related artery after failed thrombolysis; initial trials revealed an increased incidence of in-hospital complications in such cases which was initially thought to be secondary to the procedure itself; more recent studies show that PTCA after failed lysis is generally safe (Polonski et al, 2003)

Cornell Cardiology Curriculum 2003-2004

Major mechanical complications of acute STEMI


If cardiogenic shock in the first few days post MI, check the following STAT: Physical exam to assess for new holosytolic murmur Check TTE If RHC in place, perform O2 sat run (check RA, PA sats) and assess PCWP tracings Possible therapy: vasodilators v. pressors as indicated, emergent PCI or IABP, surgery Free wall rupture Signs: hemodynamic collapse Studies: Urgent TTE with tamponade, RHC with equalization of diastolic pressures Accounts for 10% of post-MI death, associated with large anterior/lateral infarcts (terminal portion of LAD), increased risk post-thrombolysis; 90% medical mortality 50% surgical mortality Ventricular septal defect Signs: new holosytolic murmur (90%) Studies: Urgent TTE, RHC sat run with step up of > 5% between RA and PA Accounts for 5% post-MI deaths, if anterior MI, defect is in apical septum, if inferior MI, defect is in basal inferior septum (difficult to localize and repair) Papillary muscle rupture Signs: new holosystolic murmur (50%) Studies: Urgent TTE, RHC with new giant v waves Accounts for 5% post-MI deaths, generally associated with inferior MIs with posteromedial papillary muscle rupture (more common than rupture of AL rupture from anterior MI)

REFERENCES
Antman, E and Braunwald, E. Acute myocardial infarction. In: Braunwald, ed. Heart disease: a textbook th of cardiovascular medicine, 5 ed. Philadelphia: W.B. Saunders Co., 1997: 1184. Barbash et al. Randomized controlled trial of late in-hospital angiogrpahy and angioplasty versus conservative management after treat,ent with recombinant tissue-type plasminogen activator in acute myocardial infarction. Am J Cardiol 1990; 66: 538. BHAT Trial research group. A randomized trial of propanolol in patients with acute myocardial infarction: I. Mortality results. JAMA 1982; 247: 1707 De Lemos et al. ST-segment resolution and infarct-related artery patency and flow after thrombolytic therapy. Am J Cardiol 2000; 85: 299-304. Gibson et al. Early and long-term clinical outcomes associated with reinfarction following fibrinolytic adminsitration in thrombolysis in myocardial infarction trials. JACC 2003; 42: 7. GUSTO V Reperfusion therapy for acute myocardial infarction with fibrinolytic therapy or combination reduced fibrinolytic therapy and platelet glycoprotein IIb/IIIa inhibition: the GUSTO V randomised trial. Lancet 2001; 357: 1905 GUSTO-1 An international randomized trial comparing four thrombolytic strategies for acute mycoardial infarction. NEJM 1993; 329: 673 HOPE Effects of an angiotensin-converting enzyme, ramipril, on cardiovascular events in high risk patients. NEJM 342:145-53 2000 ISIS-2 Collaborative group. Randomized trial of intravenous streptokinase, oral aspirin, both or neither among 17,187 cases of suspected acute myocardial infarction. Lancet 1988; 349. ISIS-4 ISIS-4: A randomized factorial trial assessing early captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected myocardial infarction. Lancet 1995; 345: 669 Magid et al. Relation Between Hospital Primary Angioplasty Volume and Mortality for Patients With Acute MI Treated With Primary Angioplasty vs Thrombolytic Therapy JAMA 2000; 284: 3131 MIRACL Effects of Atorvastatin on Early Recurrent Ischemic Events in Acute Coronary Syndromes: The MIRACL Study: A Randomized Controlled Trial. JAMA 2001; 285: 1711 PAMI Grines et al. A comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction. NEJM 1993; 328: 673

Cornell Cardiology Curriculum 2003-2004

Polonski et al. Outcomes of primary coronary angioplasty and angioplasty after initial thrombolysis in the treatment of 374 consecutive patients with acute myocardial infarction. Am Heart J 2003; 145: 855. SWIFT SWIFT Trial of delayed elective intervention v. conservative treatment after thrombolysis with anistreplase in acute myocardial infarction. BMJ 1991; 302: 555. Ziljstra et al. Long-term benefit of primary angioplasty as compared with thrombolytic therapy for acute myocardial infarction. NEJM 1999;341:1413

Cornell Cardiology Curriculum 2003-2004