Less Heart Is More

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Abstract
He study by St John Sutton et al1 in this issue of Circulation provides additional information on the importance of the myocardial substrate for the genesis of cardiac arrhythmias, in this instance, ventricular arrhyth- mias in the postinfarction remodeled human left ventricle (LV). The authors demonstrate significant relationships be- tween ventricular arrhythmias and LV size, mass, and func- tion at baseline, and at 1 and 2 years after infarction in a subset of 263 patients who received both echocardiographic and Holter evaluations in the Survival And Ventricular Enlargement (SAVE) trial. They found a greater preponder- ance of ventricular arrhythmias in those individuals with the largest LV mass, leading the authors to conclude that postin- farction remodeling is an important substrate for triggering ventricular arrhythmias. See p 2577 What does this important study teach us? Basically, we learn that the bigger the heart and the poorer its function, the more likely it is to manifest ventricular arrhythmias and, by inference, cause sudden cardiac death (SCD). The latter must be inferred because the endpoints used by the authors, premature ventricular complexes (PVCs) singly or 3 in a row (the definition they used for ventricular tachycardia (VT)), generally do not cause SCD in and of themselves. In fact, one can argue against accepting these endpoints, no doubt chosen as surrogates for the really important outcome, SCD. We know from the Cardiac Arrhythmia Suppression Trial (CAST)2 that abolition of asymptomatic ventricular arrhyth- mias in some circumstances can be deceiving, as such suppression by encainide, flecainide, and moricizine occurred in CAST, but so did an increase in mortality. Also, elevating 3 PVCs in a row to the status of VT, though almost universally used, is based on an arbitrary classification made many years ago. It is time to replace such a definition with clear, concise descriptions of the actual ventricular arrhyth- mias observed. Nevertheless, despite these limitations and the fact that only a single 24-hour ECG was obtained at each evaluation, the endpoints chosen correlated with LV size and function.