What do you think?
Computer read: “Non-specific ST abnormality, consider anterior subendocardial ischemia”
There are also very poor R-waves in V1-V4, suggesting old anterior MI
Ischemic ST depression can be of two sorts:
1) subendocardial ischemia
2) reciprocal to ST elevation in an opposite wall
This is what you get:
Acute posterior wall myocardial infarction. J Emerg Med 2001; 20:391-401.
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A large substudy of the TRITON-TIMI 38 trial (ref. 2.5), which included 3534 true STEMI, showed that 1/3 of the acute MI that had presented with “isolated precordial ST depression” (no STE elsewhere) in leads V1-V4 who had a non-urgent angiogram (mean time, 29 hours) turned out to have acute coronary occlusion (n = 314). These patients had worse outcomes than patients with ST depression without occlusion; half of these were circumflex. As approximately 25% of occluded arteries will autolyse within 24 hours, many of those with open arteries would have been occluded at the time of ECG recording, so it is estimated that half of patients with STD in V1-V4 have acute occlusion. Only a handful of these 314 patients got the benefit of emergent reperfusion therapy.
If maximal in V1-V4, then it is due to occlusion affecting the posterior (now often called lateral, or inferobasal) wall.(3) Another slightly smaller study of NSTEMIs had nearly identical results.(4)
Acute Posterior STEMI: Upright or inverted T-waves? It is a misconception that acute posterior MI presenting with precordial STD must have upright T-waves; in reality, they may be either inverted or upright. The classic criteria for a posterior MI, with ST depression, a prominent R wave, and an upright T wave in the right precordial leads likely represents a subacute, evolved MI.(5) Emphasis on these criteria could potentially delay recognition of truly acute posterior pattern: ST depression in the right-precordial leads, without significant R waves, and often with a fully inverted T wave (6).
Mechanism of T-wave orientation: Anterior leads represent summation of electrical activity from both the closer anterior wall, and the more distant posterior wall. In acute posterior MI, the posterior wall has hyperacute T-waves with a posterior vector (negative in anterior leads). The summation of the positive vector from anterior leads and negative vector from posterior leads may result in either a positive or negative T-wave in anterior leads.
With evolution, or especially after reperfusion, T-waves in posterior STEMI are always upright in precordial leads, and enlarge: the posterior wall T-wave vector turns anterior, and combined with positive anterior wall T-waves consistently results in an upright T-wave in anterior leads. Thus, reperfusion especially produces tall, peaked, anterior T waves, which we call “posterior reperfusion T-waves” or Wellens’ syndrome of the posterior wall.(7) Authors in the past have confused acutely occluded posterior MI (which may have either upright or inverted T-waves) with, on the other hand, prolonged or reperfused posterior MI (both of which do indeed have upright T-waves).
Posterior leads: Posterior leads V7-V9 are valuable for diagnosing posterior MI. About half of patients receiving elective balloon angioplasty of the circumflex will show posterior STE ≥ 1mm.(8-12) Because of low voltages in posterior leads, the STE threshold for diagnosis is only ≥ 0.5 mm in ≥ 1 posterior lead and has few false positives.(6) Use of posterior leads in ED patients without a high suspicion of ischemia does not show advantages beyond a standard 12-lead, but it does improve sensitivity in patients with high suspicion of ACS. (13, 14). When the standard 12-lead is diagnostic of posterior MI, posterior leads may be falsely negative! This is especially true if the posterior ECG is done much later than the initial ECG; by this time, the artery may have spontaneously reperfused, and the right precordial ST depression may have also resolved. In any case, ST depression in V2 should always show up as ST elevation in lead V8: they are opposite! The magnitude may be different, but the direction should be opposite. If it is not, then the state of the artery may have changed.
2.5 Pride YB, Tung P, Mohanavelu S, et al. Angiographic and Clinical Outcomes Among Patients With Acute Coronary Syndromes Presenting With Isolated Anterior ST-Segment Depression: A TRITON–TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel–Thrombolysis In Myocardial Infarction 38) Substudy Journal of the American College of Cardiology: Cardiovascular Interventions 2010;3:806-11.
13. Langer A, Goodman SG, Topol EJ, et al. Late assessment of thrombolytic efficacy (LATE) study: prognosis in patients with non-Q wave myocardial infarction. J Am Coll Cardiol 1996;27:1327-32.
Annotated Bibliography of Langer et al.:
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