Sunday, March 16, 2014

STEMI versus NSTEMI: misunderstood, misapplied

The terminology and classification of myocardial infarction has gone through several twists and turns through the years. As far back as I can remember my folks talking about it (my father was a physician) they called it acute coronary thrombosis. The years that followed saw changes in terminology which relied on either mistaken assumptions or poor electrocardiographic surrogates. One by one they've been proven wrong. When I started my training MIs were classified as transmural or subendocardial. That later gave way to transmural versus nontransmural. These terms were based on questionable assumptions about cardiac pathology and later transitioned to descriptive electrocardiographic terminology so that in the 1980s we had Q wave versus non Q wave infarction. In recent years of course this has been replaced by the present day designation of STEMI versus NSTEMI.

Branden Phibbs, MD, professor of cardiology at the University of Arizona, began challenging these distinctions in the early 1980s with this paper in which he made the case that the electrocardiographic distinction between transmural and subendocardial MI was a myth, useless clinically and prognostically. His arguments won the day and the designation was abandoned in favor of the more descriptive terms “Q wave” and “non Q wave” infarction. But in 1999 Phibbs and several other notables in the field struck again with the publication of this paper asserting that the distinction between Q wave and non Q wave infarction was clinically meaningless. Following that publication Phibbs continued relentlessly to hammer away, appealing to the evidence and ultimately won out, putting to rest once and for all the notion of Q wave infarction.

And so arose the categories of STEMI and NSTEMI. This designation was appealing in its descriptive simplicity. But in 2010 Phibbs weighed in again with the publication of another paper, a review of the pathologic changes and outcomes associated with the designations of STEMI and NSTEMI and concluded, just as was the case with Q wave versus non Q wave or with transmural versus subendocardial infarctions, that the STEMI/NSTEMI classification was useless. I blogged the paper a short time later and noted:

So here's what he's saying: In his review of the world's literature, clinical and pathological correlations do not support a meaningful electrocardiographic distinction between STEMI and NSTEMI. At first that seems counterintuitive but as I think about it I can think of several explanations for why the distinction would be artificial. He's not arguing that there's no such thing as a STEMI or a NSTEMI (after all, some MI patients have ST elevations and some don't), but that the distinction is not clinically or pathologically meaningful. There might be a number of reasons.

I went on to say that I was convinced from the paper that the distinctions were of questionable value but added that if the patient presented with obvious ischemic ST segment elevations it made the diagnosis of acute MI easier.

The paper was important because it questioned the validity of STEMI as a surrogate for acute coronary occlusion. But by that time STEMI had become embedded in performance measures for early reperfusion of patients presenting with MI.

Since 2010 much has been written demonstrating that ST segment elevation is a poor surrogate for acute coronary occlusion, further explaining the findings in the 2010 paper by Phibbs.

That brings me to this recent post at Dr. Smith's ECG blog which demonstrates the point nicely in a case of acute inferior infarction. Note that in his discussion Dr. Smith uses the term “STEMI” even though the patient doesn't meet the traditional ST segment criteria to denote that the patient has acute coronary occlusion. The patient in question, despite having been found in the catheterization laboratory to have acute occlusion of the right coronary artery, had only trace inferior ST elevations, certainly well below the threshold for any traditional or performance driven criteria. Yet, as Dr. Smith points out, this pattern is pathognomonic of acute coronary occlusion and inferior infarction. The telltale signs are: high amplitude (relative to the magnitude of the QRS complex) and broad based inferior T waves and reciprocal change in AVL. For inferior infarction due to acute coronary occlusion the reciprocal change in AVL is much more reliable than the “indicative” inferior ST elevations according to Dr. Smith, whose research findings on this topic are the basis for a manuscript in preparation.

The ECG remains a valuable tool for the diagnosis of acute ischemic syndromes. But for the diagnosis of acute coronary occlusion the electrocardiographic findings go beyond the ST segment. I agree with Dr. Phibbs that we need to replace STEMI with a better designation for acute coronary occlusion.


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