Passive ventricular restaint

See article by Power et al. [4] (pages 549–555) in this issue. The importance of ventricular remodeling as a factor in the progression of heart failure has been a recent concept supported by an abundance of animal and human research. The serial echocardiographic measurements obtained in clinical studies in heart failure provide evidence for the occurrence of progressive remodeling and its direct relationship to clinical morbidity and mortality events. The ability of angiotensin converting enzyme inhibitors to modify this progressive remodeling has been the foundation of the medical therapy for heart failure during the last decade. Attempts to decrease left ventricular size or modify the remodeling process by mechanical or surgical intervention with procedures like dynamic cardiomyoplasty and ventricular reduction surgery have been less than successful. The effect of left ventricular cardiomyoplasty has had an uncertain success. Recent observations by Kass et al. indicate that the passive girdling effect of the heart by the latissimus dorsi muscle, rather than its contractile activity, appear to explain the benefit associated with this procedure [1]/ Ventricular reduction surgery generated considerable initial interest but has been associated with an unacceptable mortality and uncertain clinical benefit. One of the major factors that influences the clinical progression of heart failure is the development of mitral insufficiency which occurs as the left ventricle dilates and becomes more spherical. These changes are associated with dilatation of the mitral ring. Animal studies have demonstrated that mitral insufficiency occurs after the development of ventricular dilatation and can be prevented by angiotensin converting enzyme inhibitors [2]. The clinical success of mitral valve repair supports the importance, if not the central role, of mitral insufficiency in the progression of heart failure [3]. The studies presented in this issue of Cardiovascular Research provide a novel approach to the treatment of heart failure by restricting the remodeling and dilatation of the ventricle with a fabricated pericardial restraint [4]. This restraint not only limited further progression of the ventricular dilatation and left ventricular fractional shortening that occurred in this tachycardia induced heart failure model in sheep, but also limited the development of mitral regurgitation in this short four week period. Recently Sabbah et al. [5] have made similar observations in a canine model of heart failure produced by multiple coronary emboli using the same restraining device followed over a three month period. The restraint not only prevented remodeling of the ventricle but also was associated with an increase in left ventricular ejection fraction. The positive benefit of ventricular restraint is also supported by other observations on the restraining effects of cardiomyoplasty in both humans and animals [6,7]. Other approaches to ventricular restraints, although limited by methodology and using a variety of materials, also suggest that benefit can be achieved with this method of ventricular remodeling [8,9]. Not provided in these very preliminary studies is the effect of such a restraint on the myriad of neurohormonal associates of heart failure. It will also be of interest to learn what effect the restraints has on the morphologic changes of remodeling including cardiomyocyte size and the development of interstitial fibrosis, all of which are important morphologic correlates in ventricular remodeling. The studies reported in this issue are intriguing and represent a unique approach to the prevention of ventricular remodeling. Unfortunately the studies are short term and in a model of heart failure which does not fully simulate heart failure in man. Nevertheless the observations in this report are very provocative, and if shown to be effective over a longer period of implantation, could provide a relatively simple surgical method of ventricular reduction. Such a device could have a wide appeal to patients with left ventricular dilatation and could be coupled with other cardiosurgical procedures including mitral valve replacement and coronary by-pass surgery. Concern must be raised not only in regard to its long-term effciacy, but also the potential of producing significant pathologic diastolic restriction and restrictive pericarditis.