Ann Thorac Surg 1995;59:613
© 1995 The Society of Thoracic Surgeons
Invited Commentary
Invited Commentary
Howard R. Levin, MD
Division of Circulatory Physiology, Columbia-Presbyterian Medical Center, 177 Fort Washington Ave, MHB 5-435, New York, NY 10032
See also page 609.
Left ventricular assist devices (LVADs) have shown increasing promise in the treatment of end-stage heart disease. However, most studies have focused on their use as a bridge to transplantation. In contrast, this article by McCarthy and associates raises a timely and important question about the utility of these devices in engendering return of native heart function rather than supporting the patient until the heart is replaced. Unfortunately, they conclude that although there is a marked decrease in ventricular size immediately after LVAD implantation, there is little change in ventricular structure during the period of LVAD support and, therefore, little evidence for ``recovery'' of the heart.
Although potentially correct, their data may not fully support this conclusion. Ventricular size is not synonymous with ventricular structure. Increases in left ventricular size, or dilation, are consequent to biochemical changes and realignment of muscle fibers, or structural changes, leading to the clinically observed alterations in the shape of the chamber. Assessment of the structural and functional properties of the ventricle cannot be made by a single measurement of the size of the heart but requires measurement of the ventricular pressure–volume relationship. Thus, because ventricular dimensions during LVAD support were measured only in one volume state of maximal volume unloading, the reduced chamber size could simply be due to the active unloading of the ventricle by the device without any change in the intrinsic ventricular properties. In contrast, my colleagues and I recently have shown that the left ventricular end-diastolic pressure–volume relationship normalizes during prolonged LVAD support. Although these data suggest that there is a normalization of diastolic size and function, they do not provide any information about the effect of LVAD support on systolic function. However, we have had 1 patient with an idiopathic dilated cardiomyopathy with sufficient return of systolic function to have the LVAD removed and be discharged from the hospital although the improvement in systolic function was only maintained for 3 months. Thus, it is possible that prolonged LVAD support may have beneficial effects on systolic and diastolic function.
Despite such promising findings, the vast majority of our current clinical data support the contention of McCarthy and associates that sufficient recovery of native heart function to allow removal of the LVAD without transplantation is rare. However, because the number of donor hearts is not expected to increase significantly, the LVAD will be used for much longer durations of support or as a permanent alternative to transplantation. As McCarthy and associates point out, although we may still occasionally see evidence of functional recovery in our current patient population, it is perhaps in these new groups that we will find the full potential for recovery of native heart function.
Related Article
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Structural and Left Ventricular Histologic Changes After Implantable LVAD Insertion
- Patrick M. McCarthy, Satoshi Nakatani, Rita Vargo, Kandice Kottke-Marchant, Hiroaki Harasaki, Karen B. James, Robert M. Savage, and James D. Thomas
Ann. Thorac. Surg. 1995 59: 609-613.
[Abstract]
[Full Text]
