A significant portion of patients with previous anterior wall myocardial infarctions (AMIs) will masquerade merely having as poor R-wave progression (PRWP) on surface electrocardiography. Zema and Kligfield showed years ago that PRWP may be caused by AMI, left ventricular hypertrophy, type C right ventricular hypertrophy or may occur in otherwise normal subjects. Although it has been suggested by some that electrocardiographic algorithms to better discriminate AMI from other causes of PRWP are worthless, these studies are open to a number of criticisms. For instance, in the study by Gami et al, although the positive predictive value of our criteria for AMI in patients with PRWP was low (about 16%), the numbers were extremely small (1 of 6). In addition, with >1/2 the patients being women who underwent nuclear myocardial perfusion imaging, the presence of 5 false-positive results (electrocardiography PRWP positive for AMI with negative scan) might easily be attributed to the previously reported lack of specificity of this technique in female subjects. Including anterior ischemia, moreover, as the investigators did in a further analysis, while attempting to improve sensitivity for coronary artery disease, might further reduce specificity, because a not insignificant portion of patients with nontransmural myocardial infarctions will fail to demonstrate residual myocardial ischemia after myocardial infarction. Furthermore, our reported results using our algorithmic approach to patients with PRWP were associated with a high negative predictive value as opposed to positive predictive value, to more effectively exclude AMI in patients with PRWP. The work of Gami et al provides no information in this regard.

It is encouraging to learn that certain investigators continue to find value in attempting a proper differential diagnosis of electrocardiographic PRWP. The recently reported results by Prajapat et al, describing the possible utility of frontal plane QRS axis in further differentiating PRWP secondary to AMI compared with other patient groups, thereby increasing the specificity and positive predictive value of previously reported diagnostic criteria, are entirely consistent with our understanding of the pathogenesis of PRWP as we have previously defined it. Specifically, our normal variant group was characterized by a statistically significant leftward shift of the QRS frontal plane axis relative to previously reported normal control subjects. Likewise, the late rightward and posterior QRS forces in the horizontal plane associated with type C right ventricular hypertrophy lead to a decrease in the magnitude of the R/S voltage ratio in lead 1, shifting the QRS axis somewhat rightward. Also, since our publication, I have observed rare patients with isolated left posterior fascicular block and hence right-axis deviation, in the absence of coronary artery disease, who also manifested PRWP in the anterior precordial leads, further supporting the work of Prajapat et al.

The multivariate stepwise discriminant analysis proposed by DePace et al has been shown to improve the overall predictive accuracy of PRWP for the diagnosis of AMI. This is not surprising. The values for variable b in that equation are represented qualitatively in our previously described algorithm as ischemic repolarization abnormalities. Likewise, the values for variables d and e relate to the presence of left ventricular hypertrophy, also as previously described by us. On the basis of the preliminary work of Prajapat et al, incorporating an additional variable, f, to adjust for QRS axis in the frontal plane might further enhance the accuracy of DePace et al’s criteria and should further be investigated.