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Ann Thorac Surg 2001;71:1755
© 2001 The Society of Thoracic Surgeons

Correspondence

Different technical approaches on cardiac binding procedures: Reply

Mario Chiavarelli, MDa, Mikhail Vaynblat, MDa

a State University of New York Health Science Center at Brooklyn, and Maimonides Medical Center, 450 Clarkson Ave, Box 40, Brooklyn, NY 11203, USA

To the Editor

We appreciate the comments raised concerning our article [1] by Dr Ünal and coworkers. They addressed several points regarding our cardiomyopathy model and our cardiac binding concept, which was first described in 1995 [2]. We agree that the cardiac binding principle has to be tested in established heart failure, and we stated it in our discussion. Experiments are in progress to study its efficacy in preventing further dilatation in a model of developed heart failure. The set of experiments in our study [1] was designed to avoid the severe cardiac constrictive effect of a fixed cardiac binding, since the interposed pericardial flap may allow for a controlled degree of dilatation.

Dr Ünal and colleagues describe a model of cardiac binding that is limited to the ventricles. Protection of the atria from compression does not prevent cardiac tamponade which is a compromise of ventricular filling due to ventricular diastolic constriction. We believe that both wrapping modalities limit ventricular dilatation and can potentially cause tamponade.

The surgical membrane is not sutured to the posterior pericardium in our experiments, and the heart is only lifted for the few seconds necessary to pass the membrane around it. As stated in our article, we did not try to achieve any degree of mechanical compression of the heart during the binding procedure. The membrane size was designed to follow the contour of the heart without hemodynamic effects. It is not clear whether Dr Ünal and colleagues compress the heart to achieve a filling pressure of 10 mmHg or to increase pressure by 10 mmHg. In our cardiomyopathy model [3], left ventricular end-diastolic pressure is an average of 15 mmHg at 12 weeks of established heart failure, and a 10 mmHg increase will not be easily tolerated. The apparent discrepancy between the value of pulmonary capillary wedge and left ventricular end-diastolic pressure (LVEDP) is probably due to a substantial variance in a small population. We favor the direct measurement of LVEDP, since pulmonary capillary wedge pressure is considered an estimate of LVEDP.

References

  1. Shah H.R., Vaynblat M., Salciccioli L., Impellizzeri P., Cunningham J.N., Jr, Chiavarelli M. Composite cardiac binding in experimental heart failure. Ann Thorac Surg 2000;69:429-434.[Abstract/Free Full Text]
  2. Vaynblat M., Chiavarelli M., Grijalva G., et al. Cardiac binding in experimental heart failure. Circulation 1995;92(Suppl):I380.
  3. Shah H.R., Vaynblat M., Ramdev G., Cunningham J.N., Chiavarelli M. Experimental cardiomyopathy as a model of chronic heart failure. J Invest Surg 1997;10:387-396.[Medline]




This Article
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Right arrow Articles by Chiavarelli, M.
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Related Collections
Right arrow Cardiac - other
Right arrow Congestive Heart Failure

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