ACUTE STEMI

							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



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•   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                                             Relative
    Major surgery, trauma or organ bx past 6 wks          > 10 mins of chest compressions
    History of hemorrhagic or undefined stroke            Age > 75
    History of brain tumor, neurosurgery, or head         SBP > 180; DBP > 110, cardiogenic shock,
    trauma                                                remote stroke or recent TIA
    Melena or marked hematuria                            Occult fecal blood
    History of bleeding diathesis                         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 data—DeLemo 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)




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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



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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




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