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ST depression V2-V4: Posterior leads, resolution of pain, and absence of posterior wall motion abnormality ruled out posterior S

Posted Dec 06 2010 12:59pm
I saw this 59 year old male 3 weeks ago. He had no previous history of CAD, and presented with very typical waxing and waning chest pain, much worse with exertion but also present at rest and on presentation, though his pain was minimal at the time of the ECG. Blood pressure was 150/80.

There is sinus rhythm with a normal QRS, except for some increase in R-wave amplitude in V2 and V3, with ST depression in V2-V4. This is all suggestive of posterior STEMI, but not definitely diagnostic.
A posterior ECG was done and showed no ST elevation, not even 0.5 mm (0.5 mm in only one posterior lead is highly sensitive and specific for posterior STEMI). Aspirin, nitroglycerine sublingual were given and the next ECG showed no change.
I performed a bedside cardiac ultrasound and the posterior wall appeared to be contracting and shortening normally. IV nitroglycerine was started and titrated up to 60 mcg/min until the pain resolved and a repeat ECG showed near complete resolution of ST depression.
Heparin and eptifibatide were started for probable NSTEMI, though spontaneous reperfusion (of either the infarct-related artery, or through collateral circulation) of posterior STEMI was not entirely ruled out.
The ECG normalized overnight. Maximum troponin was 2.1 ng/ml. The patient was taken for angiography which showed severe proximal and mid LAD disease as the culprit. Two stents were placed. The RCA was also severely diseased. There was a new anterior, septal, and apical wall motion abnormality.
ST depression in V1-V4, isolated, may be either posterior STEMI or NSTEMI. When there is ST depression in precordial leads associated with LAD NSTEMI, it usually stretches out to V5 and V6 (it usually is not maximal in right precordial leads).
Absence of posterior ST elevation was critical in my decisions on this, as were resolution of symptoms and of ST depression with maximal medical therapy, along with ultrasound showing absence of posterior wall motion abnormality.
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