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Section of Cardiothoracic Surgery, The University of Chicago Medical Center, 5841 S. Maryland, Ste E-500, M/C 5040, Chicago, IL 60637
(Email: jraman1{at}uchicago.edu).
Behind every promising therapy that fails to realize its potential is an interesting story. Ventricular containment is a concept first described by Power and Raman in 1997, but crept into publication in 1999 [1]. This entailed wrapping ventricles predisposed to progressive dilatation by a passive constraining mesh. The impetus to try this radical and presumably counter-to-conventional teaching approach was based on emerging data from the dynamic cardiomyoplasty experience.
The early animal experiments used strips of polyester mesh (usually mesh used for hernia repair) sutured together. We demonstrated proof of concept with customized modified polyester meshes, showing that this was a worthwhile approach early in the phase of ventricular dilatation [2]. However, the future of this approach was contingent on the development of an improved device that would be well tolerated in patients for a long time if it was to be implanted early in the phase of heart failure progression. Unfortunately, in the rush to get to clinical trial and human implants, device development did not go beyond a polyester mesh with a customized weave that was "proprietary."
Polyester meshes used in hernia repair provoke a profound fibrous tissue reaction. A similar tissue reaction is seen in and around the heart in patients after a CorCap cardiac support device (Acorn Cardiovascular, St. Paul, MN) has been implanted. With this possibility in mind, our early clinical experience was geared toward a patient population that was unlikely to have undergone further cardiac surgical procedures [3].
Unfortunately, when the clinical trials were expanded in Europe and North America, they enrolled all-comers and also were pitched toward a patient population that had more advanced heart failure and consequently larger hearts. This was presumably based on a report on our experiments with animals where we showed survival benefit in advanced heart failure with the containment strategy [4]. However, that article also showed that the hemodynamic benefits with ventricular containment in large hearts were marginal, with only slight improvement in other indices like mitral regurgitation and fractional shortening.
This premise was used to construct clinical trials in patients. The negative results achieved by the experience reported by Rubino and colleagues [5], therefore, are not surprising. In addition, the control procedure (restrictive mitral valve annuloplasty for functional mitral regurgitation) also has a question mark hanging over it in terms of intermediate and long-term efficacy [6]. Furthermore, there is good evidence to show that restrictive annuloplasty improves mitral regurgitation but does little to alter the risk of heart failure-related death [7]. This is a tale of the combination of two therapies that held promise but were inappropriately applied. This may have contributed to the lack of significant effectiveness.
Rubino and colleagues should be congratulated for operating on a sick group of patients and getting very respectable perioperative results. They performed the trial in good faith and according to the guidelines set out by Acorn Cardiovascular Inc. The lack of efficacy of these treatment strategies is disappointing. This has become part of the course of medical progress.
Unlike drug trials, device trials involve an invasive surgical procedure with attendant morbidity and mortality. In that sense, the bar is already set high for achieving results that need to significantly overcome the expense and morbidity associated with these procedures. The conduct of the Acorn trial, although reasonable in terms of numbers and laudable in terms of the randomized, prospective nature, was flawed in the execution and selection of patients.
Finally, as we move forward, it is important to realize that as advocates for our patients, we have to make sure that whatever devices we implant are effective, safe, and provide a reasonable chance to the patient of fighting or limiting the underlying disease process.
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Related Article
This article has been cited by other articles:
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  M. Vaynblat and M. Chiavarelli Ventricular Constraint in Heart Failure Ann. Thorac. Surg., April 1, 2010; 89(4): 1344 - 1345. [Full Text] [PDF]
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A. S. Rubino, F. Onorati, and A. Renzulli Reply Ann. Thorac. Surg., April 1, 2010; 89(4): 1345 - 1345. [Full Text] [PDF]
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