Myocardial Injury/Infarction

Early Management of Acute Myocardial Injury

Early Management of Acute Myocardial Injury (MONA? ONA may be better) Chest pain can sometimes be relieved by nitroglycerin (0.4 mg SL q5m x 3), but often cannot (esp. if patient was already taking nitrates). Also, never give nitro in patients with right heart infarction or who have taken PDE inhibitors within 24 hours. Morphine used to be the analgesic of choice [ACC/AHA guidelines, JACC 16: 249, 1990], ex. 4 mg slow IV push repeated q5m as necessary. Beware, however, as The CRUSADE Initiative (a nonrandomized, retrospective, observational registry of patients with NSTEMI) showed a higher adjusted risk of death (odds ratio [OR] 1.48, 95% CI 1.33-1.64) for patients treated with morphine. Relative to those receiving nitroglycerin, patients treated with morphine also had a higher adjusted likelihood of death (OR 1.50, 95% CI 1.26-1.78) [Am Heart J. 149: 1043, 2005]. Always watch for hypotension and give volume if SBP < 100 mm Hg. If hypotension persists, move to atropine but do not give pressors to patients with MI. Aspirin (non-coated) should be given ASAP if the patient didn’t take it at home. For aspirin-allergic patients, consider clopidogrel as an alternative. Several studies have even showed that combined therapy reduced mortality [NEJM 345: 494, 2001, Lancet 366(9497): 1607, 2005]. β-blockers are recommended as early treatment in any patient without a contraindication (HR < 40, 2nd or 3rd degree block, decompensated systolic heart failure, hypotension, reactive airways, or cocaine). ACE inhibitors are definitely indicated in any patient with anterior MI, heart failure, LVEF < 40%, or tachycardia, and should probably be given to all patients (0.5% mortality reduction in all comers) but only as PO therapy

Always search for evidence of other life-threatening illnesses, such as aortic dissection (look for “ripping” quality of pain, aortic insufficiency, get MRI or TEE if suspected and treat with labetalol to drop BP without increasing CO), pulmonary embolus, pericarditis, and/or esophageal rupture. Also look for complications of MI including heart failure or cardiogenic shock. Thrombolysis has no documented benefit in the setting of acute heart failure or cardiogenic shock [JACC 18: 1077, 1991]

Stratify patients by rapid data acquisition: get troponin, EKG, and TIMI score

Treatment of Unstable Angina/NSTEMI

Anti-ischemic treatment of UA/NSTEMI

Anti-ischemic treatment in this group should include:

  • Oxygen (SaO2 > 90%)
    • Data?
  • Nitrates
    • No decrease in mortality
  • Morphine (4 mg IV slow)
    • If persistent symptoms of CHF
  • B-blockers (metoprolol 5 mg IV q3 then 25 PO q6h, titrate to HR 55-60)
    • 13% decrease in progression to MI [JAMA 260: 2259, 1988]
    • Contraindicate if HR < 60, SBP < 100, mod/severe CHF, 2/3 AVB, severe bronchospasm
  • CCB
    • Only in patients who cannot tolerate metoprolol secondary to bronchospasm

Anti-thrombotic treatment of UA/NSTEMI

Anti-thrombotic treatment in this group should include (note that these patients do NOT get thrombolytics):

  • ASA 325 mg PO crushed then chewed, then 81 mg qday
    • 50-70% decrease in D/MI [NEJM 319: 1105, 1988; Lancet 336: 827, 1990]
  • LMWH (enoxaparin) 1 mg/kg SC bid +/- initial 30 mg IVPB or dalteparin 120 IU/kg SC bid
    • Consider instead of UFH. Enoxaparin preferred to UFH. 20% decrease in D/MI/UR [ESSENCE, NEJM 337: 447, 1997; TIMI 11-B, Circ 100:1593, 1999]
  • UFH 60-75 U/kg IVB (max 5000U) or 12-15 U/kg/hr (max 1000 U/hr), titrate to PTT 50-70s
    • Only give if LMWH not available and if history c/w ACS, EKG changes, or + cardiac enzymes. 24% decrease in D/MI [JAMA 276: 811, 1996]
  • Clopidogrel 300 mg PO x 1 then 75 mg qd
    • If conservative therapy or PCI planned (ie no surgery). 20% decrease in D/MI/stroke [CURE, NEJM 345: 494, 2001]. Defer if starting IIB/IIIA?

If patients are high risk (TRS > 2, + troponin, or ST depression > 0.5 mm) or if they will get PCI, they benefit from GP IIa/IIIb inhibitors. If they are high risk and/or have a decreased EF, recent PCI, or prior CABG, they benefit from early angiography [JACC 41: 89S, 2003] in addition to above treatment regimen.

  • Abciximab 0.25 mg/kg IVB -> 0.125 uk/kg/min x 18-24 hours
    • In patients in whom PCI is planned. 50% decrease in D/MI [CAPTURE, Lancet 349: 1429, 1997; ESPRIT, Lancet 356: 2037, 2000]

Angiography within 24 – 48 hours results in a 25% decrease in D/MI and is indicated in high risk patients (recurrent ischemia, + enzymes, ST changes, TIMI > 2, CHF, decreased EF, recent PCI, CABG [NEJM 344: 1879, 2001; RITA-3, Lancet 360: 743, 2002]). Angiography within 6 hours is superior to “cooling off” for 3 – 5 days [JAMA 290: 1593, 2003]. If patients are low risk and are followed conservatively (no GP IIa/IIIb or PCI), they should receive a stress test once stabilized and prior to discharge

Treatment of STEMI

There is no benefit to thrombolytic therapy if given after the 12 hour window [GISSI trial, Lancet 1: 397, 1986]. Lytic therapy causes ICH in 0.5 – 1% of cases [Emerg Med Clin 13: 735, 1995]

Anti-ischemic treatment of STEMI

Anti-ischemic treatment in this group should include (morphine ↑ mortality?):

  • Oxygen (SaO2 > 90%)
    • Data?
  • Nitrates
    • Questionable 5% decrease in mortality [GISSI-3, Lancet 343: 115, 1994], contraindicated in hypovolemia, RV infarct, sildenafil, or w/lytics
  • Morphine (4 mg IV slow)
    • If persistent symptoms of CHF. Reduces preload
  • B-blockers (metoprolol 5 mg IV q3 then 25 PO q6h, titrate to HR 55-60)
    • 15% decrease in mortality [ISIS-1, Lancet 2: 57, 1986]
    • Contraindicated if HR < 60, SBP < 100, mod/severe CHF, 2/3 AVB, severe bronchospasm
  • Captopril 6.25 mg TID or lisinopril 5 mg qd, then titrate up as tolerated
    • 10% decrease in mortality at 4-6 weeks [GISSI-3, Lancet 343: 115, 1994], greatest benefit in anterior MI, EF < 40%, or prior MI
    • Contraindicated in severe hypotension or renal failure
  • ARB
    • Appear equal to ACE-I [VALIANT, NEJM 349: 20, 2003]
  • Insulin
    • DIGAMI trial (DIGAMI-2 was a poor study)

Anti-thrombotic treatment of STEMI

Anti-thrombotic treatment in this group should include:

  • ASA 325 mg PO crushed then chewed, then 81 mg qday
    • 23-49% decrease in death [ISIS-2, Lancet 349: 1988]
  • LMWH (enoxaparin) 1 mg/kg SC bid + initial 30 mg IVPB. Consider instead of UFH in lysis, age < 75, or Cr < 2.0
    • 25% decrease in D/MI/recurrence [ASSENT-3, Lancet 358: 605, 2001]
  • UFH 60 U/kg IVB (max 4000U) or 12 U/kg/hr (max 1000 U/hr), titrate to PTT 50-70s
    • No decrease in mortality. Increased patency with fibrin-specific lytics
  • Abciximab 0.25 mg/kg IVB -> 0.125 uk/kg/min x 18-24 hours
    • As soon as possible if PCI is planned. 60% decrease in D/MI/urg [ADMIRAL, NEJM 344: 1895, 2001]. Not indicated if thrombolysis is to take place.

PCI should be performed within 90 minutes, and is worth waiting for if the patient travels up to 2 (some say 3) hours. It is superior to lysis, especially in cardiogenic shock, CHF, anterior MI, or Sx > 3 hours. UFH is recommended over LMWH in STEMI patients undergoing reperfusion with lytics or stents [Circulation 110: 588, 2004]

A recent randomized, controlled trial of 2g MgSO4 in STEMI patients showed no change in 30 day mortality [Lancet 360: 1189, 2002]. Insulin administration is also contested, with DIGAMI showing a benefit but DIGAMI-2 failing to (notably, DIGAMI-2 also failed to show an increase in glucose control in the treatment arm).

Early complications of myocardial injury include arrhythmia and pump failure (increases the benefit of angioplasty). If the patient falls into a low cardiac output state, vasodilators are effective at decreasing myocardial VO2. If the patient goes into cardiogenic shock, IABP is the best method for decreasing myocardial VO2.