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Ann Thorac Surg 2000;69:434
© 2000 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery, McGill University Health Center, 1650 Cedar Ave, Room C9-169, Montreal, PQ H3G 1A4, Canada
e-mail: mdiu{at}musica.mcgill.ca
Invited commentary
Heart failure is initiated by various primary injuries, such as valvular incompetence, myocardial infarction and cardiomyopathies. In response to impaired cardiac function associated with increased myocardial stress, an adaptation process known as ventricular remodelling takes place. Acutely, increased myocardial tension results in fiber stretching, which improves contractile force in accordance with Frank-Starling’s Law. However, chronic stretching induces synthesis of new sarcomeres in series, elongating fiber length and causing ventricular dilatation. This allows for the preservation of individual sarcomere length and function. Furthermore, with a larger heart, stroke volume may be maintained in spite of reduced fiber shortening (ejection fraction). Thus remodelling may confer salutary effects in heart failure. Unfortunately, to maintain adequate perfusion pressure, an enlarged heart needs to generate even greater myocardial tension, as dictated by La Place’s Law. This in turn results in secondary myocardial injury, ie, a vicious cycle of further dilatation and progression of heart failure.
By interrupting this vicious cycle of cardiac dilatation with cardiac binding, the authors of this study reported that one may prevent such secondary injury, and improve outcome in heart failure. Various prosthetic materials and devices are being investigated by others to mechanically restrain ventricles from progressive enlargement. However, the authors’ claim in this article, that interposing a strip of pericardium in the prosthesis for cardiac binding will reduce risk of cardiac constriction, can not be validated without carrying out a proper comparative study, with and without pericardial strip, since the prosthetic membrane may become firmly adhered to the epicardium. Clearly, the effects of cardiac binding on long term diastolic function need to be further investigated.
The concept of surgically modulating the ventricular remodelling process in heart failure was an off-shoot from dynamic cardiomyoplasty experience, as pointed out by the authors. Dynamic cardiomyoplasty itself underwent rigorous clinical trials, progressing from Phase I to Phase II, then to the prospective randomized Phase III, with improvement in operative mortality from over 20%, to 12%, and then to less than 4% in each trial Phase. Unfortunately, in spite of the promising results in the first 103 patients randomized (unpublished data), the Phase III trial has been suspended due to slow recruitment of patients for randomization. Although other manufacturers of cardiomyostimulators are currently trying to fill the niche by offering devices improved with more recent experimental and clinical information, the future of this operation is uncertain. Nevertheless, in spite of the logistic and ethical difficulties often encountered in such trials [1], the new surgical procedures aimed at altering remodelling process do require rigorous clinical evaluation before they can be accepted into the surgical armamentarium for the management of heart failure.
References
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