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Ann Thorac Surg 1996;61:645
© 1996 The Society of Thoracic Surgeons
Division of Cardiothoracic Surgery Case Western Reserve University School of Medicine, B-27 10900 Euclid Ave Cleveland, OH 44106-4929
Kinoshita and colleagues present a case for atrophy of residual intact myocardium due to long-term unloading with a left ventricular assist device (LVAD). This group has accomplished some difficult studies in the past using coronary artery ligation to induce profound heart failure [1]. Unfortunately, their clinical correlation is limited in the present study because they studied normal hearts. Kinoshita and colleagues recognize this limitation, pointing out that ``myocardial atrophy in the intact ventricle after long-standing unloading ... may not directly indicate that atrophy also occurs in remaining viable myocardium in a clinical setting ...''.
This study underscores the disparate findings of experimental and clinical studies concerning myocardial atrophy after long-term unloading of the left ventricle. It is intuitive that chronic unloading could cause myocardial atrophy just as increased afterload causes myocardial hypertrophy. Intuition aside, observations of myocardial atrophy due to LVAD unloading seem to be limited to experimental studies. The use of a normal heart in this work does not clarify this discrepancy and even further confounds matters because there is no intact residual myocardium and no failed myocardium—one part or region of the heart is not attempting to do the work of the entire heart. Earlier work from this group suggests that (within certain limits) the residual intact myocardium can take on a workload approximately equal to that of the entire normal heart [1]. In hearts with 50% infarction, the regional work of the residual intact myocardium increased to approximately double its normal level. Most interestingly, regional myocardial work in the uninjured region was normal before LVAD weaning and only after weaning was regional work increased. This earlier work more strongly suggests that the LVAD was preventing the compensatory hypertrophy of the residual intact myocardium and, therefore, that the work done by the residual myocardium is likely an important determinant of its response to chronic unloading.
This leads us to the fundamental question of whether myocardial atrophy occurs when the work done by the left ventricular assist device exceeds the (maximum) capacity of the residual intact myocardium. In the case of a normal heart, any assistance would be expected to lead to atrophy and the amount of atrophy would correlate with the amount of unloading. In the case of an injured heart, one would need to quantify the amount of viable myocardium to suggest what level of assistance is best.
Clinically, the success of weaning from LVAD in the non–bridge-to-transplantation patients has been disappointing. Whether myocardial atrophy secondary to LVAD unloading plays a role is dubious because of the greater importance of other variables. Early use of the LVAD is a critical determinant of success, and patients whose condition is poorest before LVAD placement having the poorest outcome. Insofar as rapid deployment ultimately determines the health of the residual or ``stunned'' myocardium and avoids multiorgan failure secondary to low cardiac output syndrome, the advantage of decisiveness in applying the LVAD is well recognized. Because the total artificial heart and a permanent LVAD are not yet available, making death the only alternative for these patients, it is still valuable to understand the effects of chronic unloading followed by reloading. We know little about the optimum time course for reducing assistance during the weaning process.
In the future, the use of a permanent LVAD and total artificial heart will be accepted practice. The issue of chronic unloading effects then will be less significant. Even with these advances, however, we will wish to continue to identify patients who are good candidates for weaning from LVAD—to give them freedom from the mechanical device. Studies like the one reported here by Kinoshita and colleagues need to be done in heart failure models. We need to know how best to wean LVAD patients with the goal of recovering myocardial function maximally and rapidly. Perhaps we can learn best from those few patients who are successfully weaned. In the meantime, the potential for chronic unloading exists when we apply the LVAD in patients in postcardiotomy or acute myocardial infarction cardiogenic shock who are not transplant candidates. For them, we need to mind the myocardium before, during, and after use of the LVAD, lest we burn their bridge.
Reference
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