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.
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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.
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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.
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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.
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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.
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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).
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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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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.
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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).
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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.
Well, In India, our patients come very late to the hospital. The reason, they die of heart diseases which are killing many unrecognised MI's.
ReplyDeleteSorry to hear that. Need a public health campaign maybe?
ReplyDeleteIs it possible that lead misplacement (theoretically, putting them too lateral) could cause some cases of LAD NSTEMI to look like posterior STEMI?
ReplyDeleteIf you misplace them terribly badly. If you put V3 where V8 is supposed to be, then ischemic ST depression will look like posterior ST elevation. More likely is that V6 gets placed too posterior and will detect a posterior MI with posterior STE, that it might not otherwise have detected.
DeleteHello Dr Smith, thanks for this excellent case once again !
ReplyDeleteQuick question, since this post is almost 7 years old and your thinking seems to have changed by the time. In your most recent cases about posterior MI, you often say : if you have quite typical chest pain and STD in anterior precordial leads (mainly V2-V4), it IS diagnosis of posterior MI, and you don't even look at posterior leads since they can show false negative and make you not activate the cath lab.
What about this one ? Would you activate it earlier now ? Would you still do the same (that is : posterior leads, ultrasound, troponin ...) ?
Thanks a lot !
Great question. It always remains a possibility that right precordial ST depression is due to LAD NSTEMI. There is no proof that absence of STE in posterior leads helps to differentiate. A patient with right precordial ST depression due to anterior NSTEMI is probably just as likely to have, or not have, posterior ST elevation. So, yes, I would say my opinion on this has changed. Had the pain and ECG findings not resolved, the patient would need emergent angiography no matter what artery was involved, so that is the most important point.
DeleteSteve Smith
Thank you !
DeleteCan it be thrombolysed?
ReplyDeleteMarked ST depression in leads V1-V4 in the setting of ACS is usually posterior STEMI and, yes, thrombolysis is indicated. U.S. guidelines (ACC/AHA) started recommending it in 2004 (Antman et al.)
DeleteI think here its subtle and not marked ST depressions in anterior leads. So do we need more proof with serial ecgs /troponins(if no echo available) for thrombolysis? or can go ahead with thrombolysis?
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