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• W2070804513 abstract "We have read the recent article of Shah and colleagues [1Shah H.R. Vaynblat M. Salciccioli L. Impellizzeri P. Cunningham Jr, J.N. Chiavarelli M. Composite cardiac binding in experimental heart failure.Ann Thorac Surg. 2000; 69: 429-434Abstract Full Text Full Text PDF PubMed Scopus (15) Google Scholar]. We also started a research study on the same subject in our Thoracic and Cardiovascular Unit in 1998 and our study still continues. There are several similarities between our study and this article. The aim of these studies is to obtain the “girdling” and “sparing” effects with a lesser invasive method. We have observed that some special aspects which we have considered, while defining the fundamental principles of our study, were neither taken into account nor stated by Shah and coworkers. 1.We firstly created a dilated cardiomyopathy in healthy subjects by an external cardiac pacemaker, and confirmed the dilated cardiomyopathy with echocardiography and pulmonary catheterization, then applied cardiac binding [2Oh J.H. Badhwar V. Mott B.D. Li C.M. Chiu R.C. The effects of prosthetic cardiac binding and a dynamic cardiomyoplasty in a model dilated cardiomyopathy.J Thorac Cardiovasc Surg. 1998; 116: 148-153Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar]. Shah and associates have firstly performed composite cardiac binding in healthy subjects, then created a dilated cardiomyopathy model. We think that it will be inconvenient to discuss the efficiency of cardiac binding by this method. As the main aim is to treat the patients with dilated cardiomyopathy, we think that more suitable results will be attained after applying the cardiac binding procedure to the unhealthy group.2.In this published study, both the ventricles and the atria and also vena cava superior and inferior were wrapped around with the composite membrane. Would it not lead to a situation like cardiac tamponade as the preload of the heart decreases by this method? In our study, as only the ventricles are wrapped around with the synthetic membrane, ventricular diastole is restricted. By protecting the atria and vena cavas from compression, the preload of the heart is saved from being increased. We think that myocardial oxygen consumption will be reduced more efficiently by restricting only the ventricular diastole.3.Their composite cardiac binding was with a wrap constructed with 90% synthetic membrane and 10% pericardium. Would not a vital pericardium (although it is 10%) lead to a decline in the compression pressure, as it can dilate with time? As it is necessary to lift the heart to stitch the synthetic membrane onto the posterior pericardium of the heart, we think that the surgical procedure will be difficult. In the first steps of our study, it was thought to decrease the pericardial volume in order to achieve the “girdling” and “sparing” effects, but this method was abandoned as mesenchymal tissues were hyperplastic in a defense against regression and as compression pressure decreased with time [3Ishihara T. Ferrans V.J. Jones M. et al.Histologic and ultra structural features of normal human parietal pericardium.Am J Cardiol. 1980; 46: 744-753Abstract Full Text PDF PubMed Scopus (85) Google Scholar]. In our study, we wrapped the membrane which is formed from 100% synthetic material only around the ventricles, without lifting the heart. By this method, we intend to have more effective results.4.In the study of Shah and associates, the magnitude of pressure (mmHg) by which the heart is compressed externally, is not mentioned. The diastole will be restricted according to the degree of dilatation in the subject. Thus, we think it will be impossible to standardize the study. In our study, the heart is compressed with a synthetic membrane with a pressure of 10 mmHg. Thus, the procedure was more effective as it did not block the preload of the heart [4Takagi H. Hirose H. Sasa E. et al.Effect of wrapping tightness on acute cardiac function in dynamic cardiomyoplasty.Ann Thorac Surg. 1997; 63: 1706-1712Abstract Full Text Full Text PDF PubMed Scopus (3) Google Scholar]. We regard our study as being a standardized (repeatable) one.5.In the study of Shah and coworkers, at weeks 0 and 12, while pulmonary capillary wedge pressures (PCWP) were measured with a Swan-Ganz catheter, left ventricular end-diastolic pressures (LVEDP) were obtained by direct puncture into the left ventricle, for the comparison between groups 1 (untreated) and 2 (cardiac binding). They observed that PCWP and LVEDP increased in untreated and cardiac binding groups, but while the increase in PCWP was not statistically significant in groups 1 and 2, the increase in LVEDP was significant in the cardiac binding group. If there is not a mitral valve lesion in the subject, PCWP shows LVEDP indirectly. Thus, it is difficult to interpret why the increase in LVEDP achieved statistical significance, while the increase in PCWP did not.6.We believe that Shah and colleagues will enlighten us about these subjects, and wish the continuation of their success. We have read the recent article of Shah and colleagues [1Shah H.R. Vaynblat M. Salciccioli L. Impellizzeri P. Cunningham Jr, J.N. Chiavarelli M. Composite cardiac binding in experimental heart failure.Ann Thorac Surg. 2000; 69: 429-434Abstract Full Text Full Text PDF PubMed Scopus (15) Google Scholar]. We also started a research study on the same subject in our Thoracic and Cardiovascular Unit in 1998 and our study still continues. There are several similarities between our study and this article. The aim of these studies is to obtain the “girdling” and “sparing” effects with a lesser invasive method. We have observed that some special aspects which we have considered, while defining the fundamental principles of our study, were neither taken into account nor stated by Shah and coworkers. 1.We firstly created a dilated cardiomyopathy in healthy subjects by an external cardiac pacemaker, and confirmed the dilated cardiomyopathy with echocardiography and pulmonary catheterization, then applied cardiac binding [2Oh J.H. Badhwar V. Mott B.D. Li C.M. Chiu R.C. The effects of prosthetic cardiac binding and a dynamic cardiomyoplasty in a model dilated cardiomyopathy.J Thorac Cardiovasc Surg. 1998; 116: 148-153Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar]. Shah and associates have firstly performed composite cardiac binding in healthy subjects, then created a dilated cardiomyopathy model. We think that it will be inconvenient to discuss the efficiency of cardiac binding by this method. As the main aim is to treat the patients with dilated cardiomyopathy, we think that more suitable results will be attained after applying the cardiac binding procedure to the unhealthy group.2.In this published study, both the ventricles and the atria and also vena cava superior and inferior were wrapped around with the composite membrane. Would it not lead to a situation like cardiac tamponade as the preload of the heart decreases by this method? In our study, as only the ventricles are wrapped around with the synthetic membrane, ventricular diastole is restricted. By protecting the atria and vena cavas from compression, the preload of the heart is saved from being increased. We think that myocardial oxygen consumption will be reduced more efficiently by restricting only the ventricular diastole.3.Their composite cardiac binding was with a wrap constructed with 90% synthetic membrane and 10% pericardium. Would not a vital pericardium (although it is 10%) lead to a decline in the compression pressure, as it can dilate with time? As it is necessary to lift the heart to stitch the synthetic membrane onto the posterior pericardium of the heart, we think that the surgical procedure will be difficult. In the first steps of our study, it was thought to decrease the pericardial volume in order to achieve the “girdling” and “sparing” effects, but this method was abandoned as mesenchymal tissues were hyperplastic in a defense against regression and as compression pressure decreased with time [3Ishihara T. Ferrans V.J. Jones M. et al.Histologic and ultra structural features of normal human parietal pericardium.Am J Cardiol. 1980; 46: 744-753Abstract Full Text PDF PubMed Scopus (85) Google Scholar]. In our study, we wrapped the membrane which is formed from 100% synthetic material only around the ventricles, without lifting the heart. By this method, we intend to have more effective results.4.In the study of Shah and associates, the magnitude of pressure (mmHg) by which the heart is compressed externally, is not mentioned. The diastole will be restricted according to the degree of dilatation in the subject. Thus, we think it will be impossible to standardize the study. In our study, the heart is compressed with a synthetic membrane with a pressure of 10 mmHg. Thus, the procedure was more effective as it did not block the preload of the heart [4Takagi H. Hirose H. Sasa E. et al.Effect of wrapping tightness on acute cardiac function in dynamic cardiomyoplasty.Ann Thorac Surg. 1997; 63: 1706-1712Abstract Full Text Full Text PDF PubMed Scopus (3) Google Scholar]. We regard our study as being a standardized (repeatable) one.5.In the study of Shah and coworkers, at weeks 0 and 12, while pulmonary capillary wedge pressures (PCWP) were measured with a Swan-Ganz catheter, left ventricular end-diastolic pressures (LVEDP) were obtained by direct puncture into the left ventricle, for the comparison between groups 1 (untreated) and 2 (cardiac binding). They observed that PCWP and LVEDP increased in untreated and cardiac binding groups, but while the increase in PCWP was not statistically significant in groups 1 and 2, the increase in LVEDP was significant in the cardiac binding group. If there is not a mitral valve lesion in the subject, PCWP shows LVEDP indirectly. Thus, it is difficult to interpret why the increase in LVEDP achieved statistical significance, while the increase in PCWP did not.6.We believe that Shah and colleagues will enlighten us about these subjects, and wish the continuation of their success. Different technical approaches on cardiac binding procedures: ReplyThe Annals of Thoracic SurgeryVol. 71Issue 5PreviewWe 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. Full-Text PDF" @default.
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