Non-ST-elevation myocardial infarction

Background

1. 33% w/ confirmed MI have no CP on presentation (esp older, female, DM, CHF)
2. 5% of NSTEMI will develop cardiogenic shock (60% mortality)
3. Age >65 w/ MI and anemia had 33% reduction in 30 day mort if transfused to keep HCT >30
4. Association between quantity of troponin and risk of death

Diagnosis

1. ACS = STEMI, NSTEMI, UA
2. Angina is considered unstable with 1 or more:
   1. Occurs for 1st time
   2. Occurs at rest
   3. Accelerating frequency or severity
3. ECG is normal in 8% of all confirmed MI's
4. Intensity of Rx should be based on likelihood that sx are due to acute coronary thombosis

TIMI RISK STRATIFICATION SCORE

1. 1 point for each
   1. Age ≥65 years
   2. Presence of at least three risk factors for CHD
   3. Prior coronary stenosis of ≥50 percent
   4. Presence of ST segment deviation on admission ECG
   5. At least two anginal episodes in prior 24 hours
   6. Elevated serum cardiac biomarkers
   7. Use of aspirin in prior seven days
2. Likelihood of mortality, new or recurrent MI, or require revascularization at 14 days
   1. Score of 0/1 - 4.7 percent
   2. Score of 2 - 8.3 percent
   3. Score of 3 - 13.2 percent
   4. Score of 4 - 19.9 percent
   5. Score of 5 - 26.2 percent
   6. Score of 6/7 - 40.9 percent

Treatment

1. Anti-ischemia
   1. Oxygen
      1. ACC recs O2 for sats <90% (evidence indeterminant)
   2. Nitrates
      1. no mortality benifit
      2. dilates coronary arts, decr preload, slight decr afterload. theoretically leads to decr O2 demand of heart.
      3. use of viagra within 24 hr can lead to profound and prolonged vasodilation and death!
      4. B-block to avoid reflex tachy.
   3. B-Blockers
      1. Goal HR is 50-60.
      2. Contraindicated if HR<50 or SBP<90, acute CHF or pr >240ms
      3. (Decr progression from UA to MI by 13%(jama 10/88))
      4. decr inotropic and chronotropic response to catechols, thus decr O2 consumption.
      5. Decr progression from UA to MI by 13%(jama 10/88)
      6. Contraindicated if HR<50 or SBP<90, acute CHF or pr>240ms.
      7. use dilt or verap if cant use b-block (nifedipine clearly harmful)
      8. no IV BB in ED, PO within 24 H
   4. ACE Inhibitor
      1. start short-acting (captopril) within 24 hours of admission
      2. reduces RR of 30 day mort by 7% (circulation 6/98)
      3. those w/ recent MI (esp ant) and LVdysf(x) benefit most.
   5. Transfusion
      1. transfuse to keep Hb >10 (NEJM 10/01; 33% reduction in 30 day mort)
   6. MSO4
      1. may use if pain after 3 doses of NTG.
      2. reduces pain and theoretically can decr HR and SBP and O2 demand
      3. use associated with higher mortality in MI pts (and cause of higher mortality in CHF exacerbation pts)
2. Antiplatelet
   1. (plaque rupture=exposed endothelium=platelets=thrombus)
   2. ASA
      1. rec dose is 160-325mg chewed.
      2. reduces death from MI from 12.5-6.4% (circualtion 10/02)
      3. inhibits COX-1, reducing thromboxane A2
      4. should be used in all ACS unless contraindicated (far better than any new drugs we have)!! (circualtion 10/02).
   3. Clopidogrel (plavix, 300mg po then 75qd)
      1. in addition to ASA
      2. used over ticlopidine b/c faster onset & less s/e (ttp,aplastic anemia etc).
      3. mortality benifit with NSTEMI
      4. ADP antagonist, noncompet inhibits platelet adp receptor.
      5. main risk and contraind is bleeding (stop 7days before cabg)
      6. CURE trial showed decr in CV death, MI or stroke from 11.5% to 9.3% w/ this drug.
   4. GPIIb/IIIa(-) = Integrillin (eptifibatide)
      1. blocks this receptor on platelet.
      2. oral forms incr mort!!!
      3. high-risk pts benefit most.
      4. Integrillin (eptifibatide) studied in PURSUIT trial, found 30 day death or MI decr from 15.7% to 14.2%.
      5. incr ICH not seen w/ use.
      6. benefit if early pci is planned, and ? to no benefit if PCI not planned
      7. reserved (if no pci) for positive tpi or isch/ecg changes despite asa, lovenox, b-block etc.
3. Antithombotics
   1. (in 2002 ACC/AHA mgt of UA/NSTEMI includes class1A evidence to anticoagulate w/ heparin or lovenox along w/ asa +/- plavix)
   2. Heparin vs. Lovenox
      1. class1A evidence to anticoagulate w/ heparin or lovenox along w/ asa
      2. +/- plavix in NSTEMI
      3. Unfractionated Heparin
         1. Bolus 60-70u/kg (max 5000), followed by infusion of 12-15u/kg/hr (max 1000/hr), w/ goal ptt 45-75s
            1. activates antithrombin which prevents thrombus propagation but does NOT cause lysis
            2. Hirudin is approved only for pts w/ HIT.
      4. LMWH: enoxaparin (lovenox)
         1. 1mg/kg sc BID
         2. safer (20% decr in death,MI or urgent revasc w/ LMWH vs UFH)
         3. AHA recomends for mod & high risk UA/NSTEMI unless CABG w/in 24hrs
         4. adjust for CrCl<30ml and extremes of weight
         5. No needd to monitor labs!
         6. ESSENCE showed 20% decr in death, MI or urgent revasc w/ LMWH vs UFH.
4. Thrombolytics
   1. in the case of UA/NSTEMI have been shown to increase the risk of MI, with no benefit, and all the risks of TNK!
5. Angiography, if
   1. Hemodynamic instability or cardiogenic shock
   2. Severe left ventricular dysfunction or heart failure
   3. Recurrent or persistent rest angina despite intensive medical therapy
   4. New or worsening mitral regurgitation or new ventricular septal defect
   5. Sustained ventricular arrhythmias
6. Early (within 24hr) referral for angiography
   1. TIMI risk score greater than 2
   2. New or presumably new ST segment depression
   3. Elevated cardiac enzymes
   4. Prior PCI within six months or prior CABG
   5. Recurrent angina or ischemia at rest or with low level activity despite intensive antiischemic therapy
   6. LVEF <40 percent

See Also

Cards: Cocaine CP

Source

EM Practice

UpToDate