Plymen et al reported in the January 15, 2011, issue of The American Journal of Cardiology on electrical remodeling (changes on the electrocardiogram) after percutaneous pulmonary valve implantation (PPVI) in 99 patients with congenital heart disease and increased right ventricular end-diastolic volumes (RVEDVs) due to pulmonary stenosis, pulmonary regurgitation, and mixed lesions. The investigators found a mean approximate 7-mm decrease in QRS duration (QRSd) after PPVI in patients with predominantly pulmonary regurgitation; no change in QRSd in the total cohort; decreases in QRS, JT, and corrected QT dispersions; a fair correlation of RVEDV with QRSd before PPVI; and no such correlation after PPVI.

I will appreciate the kind response of Plymen et al regarding the following points: (1) Were the percentage changes in RVEDV and QRSd after PPVI correlated? (2) Considering that all contemporary electrocardiographic machines provide automated measurements, why were such measurements not used? It will be useful to evaluate whether such measurements corroborated the investigators’ findings, considering that there is less error, or reproducible error, in automated than in manual measurements, and the inevitable biases with the latter are eliminated. Besides, it is unrealistic for the investigators to use the means of measurements of all 12 electrocardiographic leads for their study variables, whereas practicing physicians in the “real world” use the automated output of their machines. Undoubtedly the generalizability of the investigators’ findings would be enhanced by the provision of an analysis based on automated measurements. (3) The readers of AJC will benefit from details on these electrocardiographic studies before and after PPVI; thus, the characterization, or its change thereof, regarding types of bundle branch blocks, right ventricular hypertrophy, frontal QRS axis, and P-pulmonale may be important. Because the investigators used magnification, it will be easy to provide P-wave measurements before and after PPVI. (4) Patients with increased RVEDVs and right ventricular decompensation often have peripheral edema; the alleviation of peripheral edema leads to augmentation of the amplitudes of the QRS complexes, with resultant increases in QRSd and corrected QT interval. This implies that there is a possibility that the degree of the real physiologic change in the electrocardiographic variables caused by PPVI was larger than that reported by the investigators, the latter being partially counterbalanced by the QRS amplitude changes. Were there increases in the QRS complexes noted after PPVI? (5) In reference to the changes in the dispersions in the variables, I have some doubts, albeit biased, about their significance. Assume that a 40-ms QRSd dispersion is calculated before PPVI, with the maximum QRSd being 140 ms and the minimum QRSd being 100 ms; after PPVI, a 20% reduction in QRSd is imparted in all 12 electrocardiographic leads, leading to a maximum QRSd of 128 ms, a minimum QRSd of 80 ms, and a resultant QRSd dispersion of 32 ms. Does this really mean that the decrease of QRSd dispersion from 40 to 32 ms reflects a homogenization of repolarization, or is it merely the result of a proportional QRSd shortening in all 12 leads? Is there such a phenomenon as “dispersion,” and is it of physiologic significance?