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(Circulation. 1999;100:1011-1015.)
© 1999 American Heart Association, Inc.

Correspondence

Atrophy of Myocardium and Its Myocytes by Left Ventricular Assist Device

Louis A. Soloff, MD¹

Emeritus Chief Cardiology Section, Temple University School of Medicine, Philadelphia, Pa,
¹ Dr Soloff died November 24, 1998.

	Introduction

 
To the Editor:

Dipla and coworkers¹ believe that their data support the notion that a temporary left ventricular assist device (LVAD) obviates the need of cardiac transplantation of the failing heart. Barry² supports this notion.

The LVAD is a double-edged sword. The beneficial effects of this device are well known. Its action ensures sufficient nutrition to the peripheral tissues so that they can recover from starvation and also eliminates or decreases the harmful effects of the increased catabolic products produced by the starved tissues. Harmful effects of the LVAD are due to the rapid, profound decrease of cardiac work (contraction) that leads to atrophy of the myocardium and its myocytes.

An excellent description of the morphological changes that occur in myocardial atrophy is present in Bargmann and Doerr's textbook.³ Modern textbooks of medicine and cardiology ignore this subject, with the exception of Braunwald's,⁴ which devotes a single sentence published in fine print to it. This is as it should be. To quote Friedberg,⁵ "myocardial atrophy is a pathological entity and not a clinical disease."

However, atrophy of the myocardium and its myocytes produced by LVAD tells a different story. It is sudden in onset and affects all the myocytes.

A photograph of the myocytes (not present in the text) taken from hearts that were on LVADs shows that these myocytes are smaller than normal, misshapen, occasionally broken, and separated from each other by wide open spaces. This is the picture of severe atrophy of the myocytes. The legend under Figure . . . [Full Text of this Article]

Kenneth B. Margulies, MD

Department of Internal Medicine

Konstantina Dipla, PhD; Julian A. Mattiello, BA; Steve R. Houser, PhD

Department of Physiology

Valluvan Jeevanandam, MD

Department of Surgery Temple University School of Medicine, Philadelphia, Pa