Abstract

Regarding the article “Electrocardiographic Time to Intrinsicoid Deflection and Heart Failure: the Multi-Ethnic Study of Atherosclerosis,”1 the intrinsicoid deflection is one of the 6 electrocardiographic (ECG) components that comprise the Romhilt-Estes score, proposed in 1968 for the ECG detection of left ventricular hypertrophy.2 This criterion achieved its place in this group because of its performance in a study of the correlation between various ECG components and heart weight, and left and right ventricular (RV) thickness, all controlled for body weight.3 In this study, it was found that the intrinsicoid deflection time (which was called ventricular activation time in this study) had a higher correlation with total heart weight than the total QRS duration. Intrinsicoid deflection time had a higher correlation with RV thickness than left ventricular thickness, and it was more often found in those patients with symptoms suggesting heart failure (HF). The possibility that increased RV thickness (and increased intrinsicoid deflection time) were related to previous episodes of HF was considered but could not be established by this study. Much more recently, we have studied the ability of the same 6 ECG components, including the intrinsicoid deflection time, to predict all-cause mortality and new cardiovascular disease.4, 5 The overall Romhilt-Estes score is highly predictive of both mortality and new cardiovascular disease, but the surprising finding was that each of the 6 ECG components was independently predictive of these outcomes, and each was unique in its ability to predict specific cardiovascular outcomes. The intrinsicoid deflection time was among the most powerful predictors of incident HF, supporting the observations reported by O'Neal et al. These previous observations suggest that prolongation of the intrinsicoid deflection time in the ECG may be more than a predictor of congestive HF; it may indicate the prior occurrence of episodes of stress-related HF, producing periods of increased pulmonary artery pressure leading to an increased RV thickness. Neither our work nor that of O'Neil is structured to prove this hypothesis, but it raises the level of clinical importance of this ECG measurement and challenges investigators to test this hypothesis in further appropriately designed studies.

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