The Coapsys Device: Technique and Results

Abstract

It is well known that functional mitral regurgitation (FMR) is a disease of the left ventricle in which the mitral valve (MV) is supposedly victimized while acting as an ‘innocent’ bystander. In ischemic FMR myocardial ischemia leads to regional left ventricular (LV) remodeling and mitral regurgitation (MR) that is a result of, rather than the cause of, such initial post infarction LV remodeling (Guy et al., J Am Coll Cardiol 43(3):377–383, 2004). Ventricular injury leads to mitral annular dilatation and posterior and inferior displacement of the postero-lateral papillary muscle (PLPM) resulting in tethering of the MV leaflets and diminution of leaflet coaptation (Timek et al., Circulation 108(Suppl 1):II122–II127, 2003) (Fig. 15.1) Yiu and colleagues found that the degree of FMR is dependent upon the interplay of several factors with the major determinant of an effective regurgitant orifice (ERO) being systolic mitral valvular tenting. Such tenting in turn is determined by papillary muscle (PM) displacement and the loss of systolic mitral annular contraction (Yiu et al., Circulation 102(12):1400–1406, 2000).

Unfortunately, in some subgroups, repair of FMR is associated with a 5 year survival rate of only 50 % and with a significant risk of recurrent MR (Miller, J Thorac Cardiovasc Surg 122(6):1059–1062, 2001). Mitral valve repair (MVr) has outcome benefits and is generally the technique preferred over MV replacement in select FMR patients less than 70 years old and with less than class IV heart failure (Gillinov et al., J Thorac Cardiovasc Surg 122(6):1125–1141, 2001; Grossi et al., J Thorac Cardiovasc Surg 122(6):1107–1124, 2001) Data from Dion and colleagues show that when FMR is treated early in its course, before the LV end diastolic diameter has increased beyond 6.5 cm, excellent outcomes can be achieved with subsequent positive ventricular remodeling (Braun et al., Ann Thorac Surg 85(2):430–436, 2008). Duran and colleagues, however, showed that ring annuloplasty does not protect against recurrent FMR in patients with severe displacement of the PLPM and that this papillary muscle displacement may predict annuloplasty failure (Matsunaga et al., J Heart Valve Dis 13(3):390–397, 2004). Although some studies have shown fewer congestive heart failure (CHF) episodes and hospitalizations with MVr (Shah et al., Ann Thorac Surg 80(4):1309–1314, 2005), no study has ever demonstrated an ultimate survival benefit from correcting FMR, and there is still controversy as to whether operating on end-stage FMR is even appropriate. Additionally, clinical controversy still exists as to the appropriate therapy for FMR. Currently the NIH sponsored Cardiothoracic Surgical Trials Network has finished enrolling patients with severe chronic FMR to randomization to either mitral repair or replacement in a study to address this issue (U.S. National Institutes of Health. Comparing the effectiveness of repairing versus replacing the heart’s mitral valve in people with severe chronic ischemic mitral regurgitation. [Internet]. Cited 15 Aug 2013. Available from: http://clinicaltrials.gov/ct2/show/NCT00807040, 2013).

While the above debate centers on whether or how to correct the ‘leaking valve’ of FMR, the Coapsys device was designed to instead address the MV insufficiency by treating the pathologic processes causing FMR. The Coapsys device works by reshaping the LV, restoring the position of the postlero-lateral subvalvular apparatus, and reducing the antero-posterior dimension of the MV annulus.