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Circulation. 2003;107:2531-2532
doi: 10.1161/01.CIR.0000068687.46373.04
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(Circulation. 2003;107:2531.)
© 2003 American Heart Association, Inc.


Editorial

Less Heart Is More

Douglas P. Zipes, MD

From the Division of Cardiology and the Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis.

Correspondence to Douglas P. Zipes, MD, Director, Division of Cardiology and the Krannert Institute of Cardiology, Indiana University School of Medicine, 1800 N Capitol, Suite E475, Indianapolis, IN 46202. E-mail dzipes@iupui.edu


Key Words: Editorials • death, sudden • defibrillation • myocardial infarction • remodeling


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

The 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 arrhythmias in the postinfarction remodeled human left ventricle (LV). The authors demonstrate significant relationships between ventricular arrhythmias and LV size, mass, and function 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 preponderance of ventricular arrhythmias in those individuals with the largest LV mass, leading the authors to conclude that postinfarction 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 arrhythmias in some circumstances can be deceiving, as such suppression by encainide, flecainide, and moricizine occurred in CAST, . . . [Full Text of this Article]


Related Article:

Left Ventricular Remodeling and Ventricular Arrhythmias After Myocardial Infarction
Martin St John Sutton, Douglas Lee, Jean Lucien Rouleau, Steven Goldman, Ted Plappert, Eugene Braunwald, and Marc A. Pfeffer
Circulation 2003 107: 2577-2582. [Abstract] [Full Text]



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