LETTER TO THE EDITOR
Perpetuation of the myth of the Q-wave versus the non–Q-wave myocardial infarction
Brendan P. Phibbs, MDa and
Frank I. Marcus, MD
a Chief of Cardiology, Kino Community Hospital, 2800 East Ajo Way, Tucson, Arizona 85713, USA
In a recently published study, Furman et al. (1) perpetuate the myth that the non–Q-wave myocardial infarction (MI) is a "distinctive pathophysiological entity from non–Q-wave MI (NQWMI)." The results and conclusions of that study deserve careful scrutiny.
The classification of Q-wave versus NQWMI was based on the presence or absence of Q waves 24 h after hospital admission. It has been documented that at least 10% of patients will develop Q waves between 3 to 11 days after MI (2). This error could well affect the results and conclusion. Even though the same definition was used throughout the study, it is not clear whether the potential error was unchanged throughout the study.
In addition, limiting the electrocardiogram (ECG) definition of Q-wave MI (QWMI) to a Q-wave of  0.04 s and an amplitude 25% of the R-wave in that lead (in addition to evolutionary ST- and T-wave changes) is a perpetuation of an older and now discarded definition of the pathologic Q-wave. In a recent consensus document (3) the ECG criteria for establishing an MI are "any Q-wave in leads V1 through V3, Q-wave 30 msec in leads II, III, aVL, V4, V5 or V6 (the Q-wave changes must be present in any two continuous leads), and be 1 mm in depth." In addition, it was noted that criteria for Q-wave depth requires more research. Inevitably, many infarcts presenting with significant wide but shallow pathologic Q waves would be erroneously lumped by Furman et al. (1) in the NQWMI category. Thus, the criteria selected in the Furman et al. (1) study would tend to overestimate the number of patients with NQWMI. These problems in classification illustrate one of the difficulties in attempting to classify patients as Q-wave versus NQWMI.
Furman et al. (1) quote the criteria for an adequate study as outlined in our report (4) in this Journal in 1997 and they claim they corrected for the variables we listed. However, they failed to correct for one of the most important variables, and this omission can alter the results and conclusions. They recognized only the negative deflection in the first 40-ms vectors, or classic Q-wave, completely overlooking other depolarization abnormalities or "Q-wave equivalents" that have been well documented to correlate with MI. For example, ECGs that present the onset of tall R waves in leads V1 and V2 representing the "Q-wave" of posterior infarction would be classified as an NQWMI by Furman et al. (1). This error has plagued most studies in this field and is worth emphasizing. We quote from our previous publication in the Journal: "The process of infarction alters depolarization by a number of mechanisms, e.g., dispersion, slow conduction and localized block. These forces change the surface QRS in a number of ways: to suppose that they only cause negative deflections, or Q waves, is electrocardiographically naive. It is equally naive to confine attention to the initial 40 msec vectors since at least 8% to 10% of all infarcts involve the basal myocardium, which is depolarized during the middle or terminal vectors of the QRS. A tall R in the right precordium and localized R-wave diminution in the mid precordium are two obvious and accepted ‘Q-wave equivalents’ but there are others. QRS alterations correlated with infarction in a number of studies include R/S changes, acute frontal-plane right axis deviation, new left axis deviation, low voltage and QRS notching, precordial QRS notching, initial and terminal QRS notching, high-frequency notching in orthogonal leads and abnormally narrow precordial R waves. ... Summing up findings of the studies listed above in quantitative terms, it is conservative to estimate that approximately half of all infarcts without Q waves will manifest Q-wave–equivalent distortions of depolarization. ... The only scientifically valid basis for comparison would be ‘depolarization abnormality’ versus ‘repolarization abnormality only.’ Thus, even if only a third of the NQWMI in fact belong in the QWMI category—a modest assumption—the differences alleged in this study could be markedly altered" (4).
Every pathologic study in the last 20 or more years has demonstrated that the pathology of the two types of infarct is identical (5,6). Most recently Wu et al. (7) published a study correlating ECG with pathology; like all others, the researchers found that nontransmural infarcts generated Q waves 50% of the time. It is difficult to imagine the NQWMI to be a "distinct pathophysiologic entity" when the cellular pathology is exactly the same as the QWMI.
The investigators (1) erroneously reported that Edlavitch et al. (8) provided data that support the conclusion of the present study that an increase in the incidence of NQWMI and QWMI occurred over a period of time. In that study, which preceded the thrombolytic area and extended from 1970 to 1980, the attack rate for QWMI did not change significantly between 1970 and 1980, but the attack rate for NQWMI decreased significantly during this same period.
Finally, the preoccupation with Q-wave versus NQWMI should be abandoned in favor of truly significant observations that have a well-documented bearing on acute as well as long-term prognosis, such as evaluation of infarct size, left ventricular ejection fraction, New York Heart Association functional class, coronary anatomy and symptoms. These observations will be able to guide the cardiologist in the choice of therapy and prognosis. The Q versus non-Q distinction contributes nothing of pragmatic therapeutic significance, as is demonstrated by the fact that patients with NQWMI randomly assigned to an invasive or noninvasive or conservative management resulted in similar outcome (9).
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References
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1. Furman MI, Dauerman DL, Goldberg RJ, Yazbeski J, Lessard D, Gore JM. Twenty-two-year (1975–1997) trends in the incidence, in-hospital and case fatality rates from initial Q wave and non-Q wave myocardial infarction: A multi-hospital community-wide perspective. J Am Coll Cardiol. 2001;37:1571–1580[Abstract/Free Full Text]
2. Diltiazem Reinfarction Study GroupKleiger RE, Boden WE, Schechtman KB, et al. Frequency and significance of late evolution of Q waves in patients with initial non-Q wave myocardial infarction. Am J Cardiol. 1990;65:23–27[Medline]
3. The Joint European Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction. A consensus document. J Am Coll Cardiol. 2000;36:959–967[Free Full Text]
4. Phibbs B, Marcus FL, Marriott HJC, Moss A, Spodick D. Q-wave versus non-Q wave myocardial infarction: a meaningless distinction. J Am Coll Cardiol. 1999;33:576–582[Free Full Text]
5. Phibbs B. "Transmural" versus "subendocardial" myocardial infarction: an electrocardiographic myth. J Am Coll Cardial. 1983;1:561–564[Medline]
6. Spodick D. Q-wave infarction versus S-T infarction: nonspecificity of electrocardiographic criteria for differentiating transmural and non-transmural lesions. Am J Cardiol. 1983;51:914–917
7. Wu E, Judd RM, Vargas JD, Klocke FJ, Bonow RO, Kim RJ. Visualization of presence, location and transmural extent of healed Q and non-Q myocardial infarcts. Lancet. 2001;357:21–28[CrossRef][Medline]
8. Edlavitch SA, Crow R, Burke GL, Baxter J. Secular trends in Q wave and non-Q wave acute myocardial infarction: The Minnesota Heart Survey. Circulation. 1991;83:492–503[Abstract/Free Full Text]
9. Veterans Affairs non-Q-Wave Infarction Strategies in Hospital (VANQWISH) trial investigatorsBoden WE, O’Rourke RA, Crawford MH, et al. Outcomes in patients with acute non-Q wave myocardial infarction randomly assigned to an invasive as compared with a non-invasive strategy. N Engl J Med. 1998;338:1785–1792[CrossRef][Medline]
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