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Pure (Isolated) Posterior STEMI -- not so rare, but often ignored!

Posted Aug 14 2009 6:48pm
Case 1.

This is a 44 yo male with h/o HTN, CABG at age 34, and 2 drug eluting stents to the first diagonal graft 3 months prior. He presented at 1810 with chest pain 5 days after stopping clopidogrel (on the instructions of another physician). The following ECG (#1) was recorded, with ECG #2 as his baseline.

#1, presenting ECG
#2, baseline from 3 months prior
#1 shows new marked ST depression in V2 and V3.

The differential diagnosis is subendocardial ischemia with probably NSTEMI vs. posterior STEMI. By ECG alone, posterior MI is more likely because of maximal ST depression in right, as opposed to left, precordial leads. However, given the history of severe 3 vessel coronary disease it is prudent to start with medical management, then observe for resolution of pain, but to also obtain an immediate echocardiogram to ascertain which wall is involved. If pain or ECG findings do not resolve, or if there is posterior wall motion abnormality, then immediate angiography with PCI is indicated.

In this case, maximal medical therapy was undertaken with Aspirin, clopidogrel, heparin, eptifibatide, metoprolol, and IV nitroglycerin and the patient was admitted to the CCU with cardiology consulted immediately. Chest pain resolved and angiogram was not done until the next day. It showed a 100% re-occluded SVG stent to D1; thrombus was suctioned out. Echo confirmed posterior wall motion abnormality. Max troponin was 47.

Case 2.

54 yo female with h/o smoking, DM, HTN, c/o chest pain for 3 hours, substernal radiating to both shoulders. She has an initial ECG which shows diffuse ST depression and she was treated for NSTEMI. She developed some pulmonary edema after metoprolol. ECG #2 was recorded:

ST depression is maximal from V2 to V4. This is due to posterior STEMI until proven otherwise. Unfortunately, it was treated as an NSTEMI for 2.5 hours until an echocardiogram showed a posterior wall motion abnormality. Cath revealed a 100% occluded circumflex. This was opened and stented, with the convalescent ECG below, which shows large upright posterior reperfusion T waves with a long QT.

How can such delay be avoided? By recording posterior leads V7-V9, at the level of the tip of the scapula and at the posterior axillary line (V7), a position midway between this and the spine (V8), and a paraspinal lead (V9). Also, obtaining a stat echo. Most of all, recognize this ECG pattern as being by far more likely to be posterior STEMI than due to subendocardial ischemia, which has maximum ST depression in leads V4-V6.

Case 3.

Here is a case of a 66 yo male with a history of CAD who presents with 1.5 hours of chest pain and is stable.

There is ST depression maximal in, again, V2-V4. The vast majority of posterior STEMI is not isolated, but rather concurrent with inferior and/or lateral involvement. In this case there is subtle ST elevtion in the inferior leads, not noticed by the treating physicians. Compare these ST segments with those of the post reperfusion ECG below:

The patient had rapid PCI of a 100% acutely thrombotically occluded mid circumflex which was opened and stented. There was 3 vessel disease.

The T-wave in posterior STEMI

Notice also that in the first (pre-reperfusion) ECG of case 3, the T wave is not upright as in previous cases. Some authors claim that the T wave must be upright for posterior STEMI. Evidence for this is lacking. In fact, an upright T wave probably indicates reperfusion of the posterior STEMI, whereas an inverted T wave is the analog of a hyperacute T wave (still occluded) but recorded from the opposite side. Either can be present in posterior STEMI, depending on the state of microvascular perfusion due to recanalization or to collateral circulation.
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