I. Definitions & Pathophysiology

  1. "Acute Coronary Syndrome" encompasses unstable angina, non-ST-elevation-MI, and ST-elevation-MI-Sometimes difficult to distinguish at initial presentation
  2. Unstable angina
    1. Defined as: Evolving pattern of angina pectoris, diff. from usual angina for the pt (change in freq, severity, dur., ex. tol., effect of NTG)
    2. No clear distinction from non-Q-wave MI, b/c can get some cardiac enzyme elevation with unstable angina
    3. Like AMI, us. precipitated by formation of thrombus on atherosclerotic placque; however, the type of thrombus may be different from that in Q-wave MI
    4. 3 mo. incidence of MI = 15-20%
    5. Clinical course less predictable than in stable angina, where isch. is reliably evoked only by increased myocard. O2 demand
    6. Predictors of risk for MI
    1. Recurrent pain on meds in-hosp is most sig.
    2. Pain at rest
    3. Prior h/o angina
    4. Episodes > 15 min
    5. No relief w/NTG
    6. Early recurrence after NTG
    7. EKG changes w/pain
    1. "Braunwald" classification of unstable angina (Circ. 80:410, 1989). Further subdivisions are based on intensity of concurrent medical therapy and presence or absence of ST-T wave changes with pain. Significantly predicts in-hospital cardiac complications in pts with unstable angina (JAMA 273:136, 1995)
      Extracardiac condition that might intensify and MI No such extracardiac condition < 2wks post-MI
    Accelerated or severe new-onset angina but no rest pain IA IB IC
    Angina at rest within past mo but not within last 48h IIA IIB IIC
    Angina at reset within last 48h IIIA IIIB IIIC
  1. Non-ST-Elevation MI (aka :subendocardial" MI)
    1. MI (confirmed by cardiac enzymes) but without development of ST elevation on ECG
    2. Presumably, zone of infarction doesn't extend though entire myocardial wall at any point, and the likelihood of substantial ischemic-but-salvageable myocardium is greater than in ST-elevation MI
    3. Better in-hosp. prognosis than STEMI
  1. ST-elevation MI (aka "transmural" MI)
    1. MI with ST elevation on ECG
    2. Usually results in eventual development of Q waves on ECG

II. Clinical presentation

  1. Symptoms of myocardial ischemia (chest pain, dyspnea, nausea, vomiting, diaphoresis, etc.)
    1. In a retrospective study in 2,525 pts with no prior h/o MI or coronary revascularization evaluated in an ED for suspected acute coronary syndrome, "typical" angina (substernal chest pain/discomfort provoked by exertion or emotional stress, relieved by rest and/or nitroglycerin), all of whom underwent provocative stress testing, incidence of eventual finding of inducible myocardial ischemia was not sig. diff. between pts with typical angina, "atypical" chest pain, and no chest pain at presentation (Am. J. Cardiol. 105:1561, 2010-JW)
  2. Decline in systolic BP (10-15mm) is common with transmural infarct
  3. Low-grade fever: common during 1st week in MI
  4. Response of sx to Organic Nitrates does not accurately predict whether the source of sx is myocardial ischemia--Click HERE for details
  5. Diagnostic studies
  1. CPK-MB elevations: us. reliable by 10-12h after onset of sx; levels return to normal 48-72h post-infarct unless huge
    1. CK-MB Subforms
      1. In a prospective trial of 955 pts with chest pain (119 had acute MI), CK-MB subform assay had highest accuracy (91.5% sens. and 89% spec.) when done 6h since onset of sx. Troponin I and T were less sensitive but more specific. After 6h, total CK-MB had highest reliability in predicting acute MI (c/w CK-MB subforms, myoglobin, and troponin I and T) (Circ. 99:1671, 1999--JW)
  2. Troponin T & Troponin I
  1. More specific than CK-MB
  2. Highly sensitive: 99% of pts with eventual dx of acute MI in one series of 976 pts had median maximal troponin T levels of at least 0.1ug/l (Circulation 93: 1651; 1996-JW)
  3. 773 pts with acute chest pain but no ST elevation on EKG and no obvious noncardiac cause had troponin T & I done on arrival & 4h later. Of the 47 who ended up ruling in for MI by CK-MB, 51% had "positive" troponin T on arrival in ER and 94% had "positive' troponin T 4h later. 66% had positive troponin I on arrival and 100% had positive troponin I 4h later. Of 34 who died or had an MI in the next mo., 79% had pos. toponin T and 94% had pos. troponin I. Summaries didn't mention data on specificity (NEJM 337:1648, 1997--JW; AFP)
  4. Can get false-positives in pts on kidney dialysis (JACC 34:448, 1999--JW) or in pts with severe heart failure
  1. Highly-sensitive Troponin assays
    1. May offer earlier confirmation of MI than traditional troponin assays
    2. Not yet widely available as of 2009
  1. ECG signs of ischemia (TWI, ST depression) and injury (ST elevation, Q waves)
    1. Serial ECG has sensitivity 68% and specificity 97% for ischemic changes
    2. Presence vs. absence of symptoms when ECG is done may not affect diagnostic usefulness of ECG
      1. In a study in 2,007 pts > 24yo presenting with symptoms suggestive of acute coronary syndrome who had initial normal or nonspecific ECG, 30d incidence of (acute coronary syndrome or death) was not sig. diff. between pts who did or did not have sx when the initial ECG was obtained (Acad. Emerg. Med. 13:1034, 2006-JW)
      2. In a prospective study in 387 pts admitted with chest pain who had initial normal ECGs, likelihood of eventual diagnosis of acute coronary syndrome did not differ significantly between pts who did or did not have chest pain when the normal ECG was obtained (Acad. Emerg. Med. 16:495, 2009-JW)
  2. Elevated ESR
  3. Elevated C-Reactive Protein
    1. Significant predictor of mortality in Q-wave MI (J. Am. Coll. Cardiol. 31:1460, 1998--JW)
    2. Elevated CRP at discharge sig. ass'd RR > 4 for admission for angina or MI in 53pts with unstable angina (Circ. 99:855, 1999--JW)
  4. PMN leukocytosis for 3-7d (12-15k/mm3)
  5. LDH elevation: goes up 24-48h post-infarct, stays up 7-14d
  6. Serum lactate > 13.5 mg/dl (1.5 mmol/l) done on presentation to ER in 129 pts with possible MI was found to be 96% sensitive but only 55% specific(Ann. Emerg. Med. 30:571, 1997--AFP)
  7. Myeloperoxidase
    1. A marker of "activated" leukocytes; found in high concentrations in ruptured atherosclerotic placques
    2. In a prospective study of 604 pts presenting to an ED with chest pain, blood myeloperoxidase levels, after adjustment for other risk factors, were sig. associated with both 30d and 6mo risk of adverse coronary outcomes (MI, revascularization, or death), more so than CRP or Troponin T (NEJM 349:1595, 2003--JW)
  8. Rest MPI can be useful in evaluating patients suspected of having acute coronary syndrome (sensitivity similar to serial troponin testing and takes less time)-Sometimes called a "hot mibi scan"
  9. Exercise stress testing for pts with acute chest pain thought to be noncardiac
    1. 212 pts with chest pain and normal (or almost normal) EKG, 6% with prior h/o coronary disease, got an ETT (modified Bruce) immediately after initial evaluation. Among the 59% who had normal ETT, 1mo f/u showed no sig. morbidity or mortality; no adverse events during ETT (Ann. Emerg. Med. 32:1, 1998--JW)

III. Distinguishing Anterior from Inferior MI:

Symtpom/sign Anterior Wall Inferior. (or post.or lat.) Wall
Nausea/vomiting Less More
Acute hypotension Less More
Infarct-related artery LAD RCA (90%), LCx (10%)
Pump Failure (CHF + hypotension) More (30%) Less (5-10%)
LV aneurysm More Less
Mortality More (15%) Less (5%)
Mortality if > 75yo More (25%) Less (10-15%)
New murmur Less (ant-lat. pap) More (post. pap; MR)
Sudden death Equal Equal
VSD resulting More Less
Late CHF (post-CCU) More Less
Late arrhythmias More Less
Association with RVMI Less More
Site of conduction problems BB & fascicles AV node
Escape rhythm (if complete block) Ventricular Junctional or ventricular

IV. Sequelae of MI:

  1. Arrhythmias (VFib, if it occurs, us. presents in 1st 24h; may be proceeded by VPCs or VT)
  2. Pump Failure (low CO + CHF)--biggest cause of in-hosp death from AMI; can be prevented by limiting infarct size
  1. "Kippil classification" of pump failure

I--no pulm/venous congestion
II--rales @ bases, tachypnea, R heart signs
III--severe CHF with APE
IV--systolic BP <90, periph. vasoconstriction, diaph, cyanosis, confusion, oliguria

  1. Mitral regurgitation due to papillary mm. rupture-Immediate Tx: NITROPRUSSIDE or NTG IV; INTRA-AORTIC BALOON counterpulsation; surgery may be necessary
  2. Septal perforation--easy to confuse with MR (same murmur, same clinical signs of decreased CO)--differentiate with S-G
  3. Ventricular aneurysm
  4. Cardiac rupture (more likely with older pts and q-wave, i.e. transmural, infarctions)
  5. Progressive left ventricular dilatation ("remodeling") occurs in months following MI
  1. Activation of renin-angiotensin II thought to be involved
  2. A poor prognostic marker
(Sources include Core Content Review of Family Medicine, 2012)