BACKGROUND AND AIM OF THE STUDY: The results of tricuspid annuloplasty to treat functional tricuspid regurgitation (FTR) are sometimes suboptimal, and alternative techniques are needed. In the absence of reliable FTR models, and in an effort to minimize the need for animal experiments, a reproducible bench-model was developed of FTR, that allowed the simulation of the anatomic features of the condition. METHODS: A fresh porcine heart was mounted on a rigid support that was placed into a basin filled with saline; a closed circuit was then created with a centrifugal pump, equipped with connection tubes. The inflow tube of the pump conveyed saline from the basin to the pump; the outflow cannula was inserted through the pulmonary artery, across the pulmonary valve, into the right ventricle. The pump was activated to pressurize the right ventricle, thus inducing tricuspid valve regurgitation (TVR). The regurgitant flow through the valve was quantified using a flow-meter. Radiopaque markers were sutured to the head of each papillary muscle and to the tricuspid annulus, in order to trace the geometric changes of the tricuspid valve at increasing pump rates, using fluoroscopy. The efficacy of the bench-model was validated with 10 hearts. RESULTS: The TVR was increased proportionally with the right ventricular pressure (RVP) (TVR = 0.089xRVP - 1.515; R2 = 0.89). The increase in TVR was associated with increases in the annular-to-papillary muscles distance (APML) (TVR = 0.059xAPML - 2.94; R2 = 0.96), of the inter-papillary muscles distance (PMD) (TVR = 0.058xPMD - 8.58; R2 = 0.94), and of the triscuspid annular dilatation (TAD) (TVR = 0.05xTAD - 1.85; R2 = 0.89). Of these parameters, APML was the strongest predictor of TVR. CONCLUSION: The porcine heart bench model represents a reproducible system to simulate the physiopathology of FTR, and has the potential to serve as a complementary method for the evaluation of new 'in vitro' technologies and therapies for FTR.
BACKGROUND AND AIM OF THE STUDY: The results of tricuspid annuloplasty to treat functional tricuspid regurgitation (FTR) are sometimes suboptimal, and alternative techniques are needed. In the absence of reliable FTR models, and in an effort to minimize the need for animal experiments, a reproducible bench-model was developed of FTR, that allowed the simulation of the anatomic features of the condition. METHODS: A fresh porcine heart was mounted on a rigid support that was placed into a basin filled with saline; a closed circuit was then created with a centrifugal pump, equipped with connection tubes. The inflow tube of the pump conveyed saline from the basin to the pump; the outflow cannula was inserted through the pulmonary artery, across the pulmonary valve, into the right ventricle. The pump was activated to pressurize the right ventricle, thus inducing tricuspid valve regurgitation (TVR). The regurgitant flow through the valve was quantified using a flow-meter. Radiopaque markers were sutured to the head of each papillary muscle and to the tricuspid annulus, in order to trace the geometric changes of the tricuspid valve at increasing pump rates, using fluoroscopy. The efficacy of the bench-model was validated with 10 hearts. RESULTS: The TVR was increased proportionally with the right ventricular pressure (RVP) (TVR = 0.089xRVP - 1.515; R2 = 0.89). The increase in TVR was associated with increases in the annular-to-papillary muscles distance (APML) (TVR = 0.059xAPML - 2.94; R2 = 0.96), of the inter-papillary muscles distance (PMD) (TVR = 0.058xPMD - 8.58; R2 = 0.94), and of the triscuspid annular dilatation (TAD) (TVR = 0.05xTAD - 1.85; R2 = 0.89). Of these parameters, APML was the strongest predictor of TVR. CONCLUSION: The porcine heart bench model represents a reproducible system to simulate the physiopathology of FTR, and has the potential to serve as a complementary method for the evaluation of new 'in vitro' technologies and therapies for FTR.
Authors: Maurizio Taramasso; Maximilian Y Emmert; Diana Reser; Andrea Guidotti; Nikola Cesarovic; Marino Campagnol; Alessandro Addis; Fabian Nietlispach; Simon P Hoerstrup; Francesco Maisano Journal: J Cardiovasc Transl Res Date: 2015-05-13 Impact factor: 4.132