Tricuspid Valvular Complex Remodeling in Ovine Tachycardia Induced Cardiomyopathy with Functional Tricuspid Regurgitation

B. Gaweda¹, M. Gaddam², T. Jazwiec³, A. Goodyke⁴, M. Lucyna. Piekarska⁵, M. Rausch⁶, K. Widenka⁷, T. Timek^8
1Division of Cardiothoracic Surgery, Corewell Health, Grand Rapids Michigan, USA, Department of Cardiac Surgery, Clinical District Hospital No. 2, Faculty of Medicine University of Rzeszow, Rzeszow, Poland, Grand Rapids, Michigan ²Department of Urology, Stanford University, USA, Stanford, California ³Department of Cardiac, Vascular and Endovascular Surgery and Transplantology, Silesian Centre for Heart Disease, Medical University of Silesia in Katowice, Zabrze, Poland, Zabrze, Slaskie ⁴Corewell Health Research Center, Grand Rapids, Michigan, USA, Grand Rapids, Michigan ⁵Division of Cardiothoracic Surgery, Department of Cardiovascular Research, Corewell Health, Grand Rapids, Michigan, USA, Grand Rapids, Michigan ⁶Aerospace Engineering & Engineering Mechanics, The University of Texas at Austin, USA, austin, Texas ⁷Department of Cardiac Surgery, Clinical District Hospital No. 2, Faculty of Medicine University of Rzeszow, Rzeszow, Poland, Tyczyn, Podkarpackie ⁸Division of Cardiothoracic Surgery, Corewell Health, Michigan State University College of Human Medicine, Grand Rapids, MI, USA, Grand Rapids, Michigan

Purpose: Functional tricuspid regurgitation (FTR) is associated with multilevel remodeling of the valvular apparatus, yet surgical repair is focused on isolated annular reduction. A more complete understanding of the entire tricuspid valvular complex remodeling in FTR may guide development of novel reparative techniques and enrich the surgical armamentarium.

Methods: FTR and biventricular dysfunction were induced in fourteen healthy sheep (FTR, n=14) by implantation of left ventricular (LV) epicardial electrode and rapid pacing at 200-240 bpm for a mean of 4 weeks. With pacer off, animals subsequently underwent cardiopulmonary bypass for implantation of sonomicrometry crystals on the tricuspid annulus (TA) (6), right ventricular (RV) free wall (14), and papillary muscle (PM) tips (3). Pressure sensors were placed in RV, LV, and right atrium. Ten healthy sheep served as controls (CTL, n=10). Simultaneous hemodynamic, sonomicrometry, and echocardiographic data were collected after weaning from CPB and hemodynamic stabilization. Crystal 3-D coordinates were used to calculate RV volume, TA area, PM area (triangular area enclosed by 3 PM tips), inter-papillary muscle distances, and distances from PM tips to annular plane and annular centroid. Parameters were calculated at maximum and minimum during the cardiac cycle. All animals were studied under open-chest conditions.

Results: Echocardiographically measured RV fractional area change (RVFAC) was 54±9 and 37±9% (p < 0.001) for CTL and FTR animals, respectively, while TA diameter increased from 2.5±0.3 to 3.1±0.1 cm (p=0.003). TR (0-4+) increased from 0.5±0.5 to 2.9±1 (p < 0.001). LV ejection fraction decreased from 57±4 to 33±8 % (p < 0.001) while mitral regurgitation (0-4+) increased from 0.1±0.3 to 2.2±0.8 (p < 0.001). These imagining findings confirmed biventricular failure with associated functional tricuspid and mitral regurgitation in our FTR animals reflective of advanced clinical cardiomyopathy. Hemodynamic parameters and sonomicrometry derived RV volumes and valvular complex geometry for CTL and FTR animals are summarized in Table 1. These data demonstrate significant annular dilation and associated displacement of anterior and posterior papillary muscles in FTR suggestive of subvalvular remodeling. Papillary muscle area increased significantly with FTR and is illustrated throughout the cardiac cycle in Figure 1.

Conclusion: Our ovine model of tachycardia induced cardiomyopathy resulted in biventricular failure and valvular insufficiency reflective of clinical cardiomyopathy. Significant papillary muscle displacement was associated with FTR reflective of subvalvular remodeling. Subvalvular procedures adjunctive to annular reduction may be needed to provide more durable valvular repair in cardiomyopathy with FTR.

Identify the source of the funding for this research project: The study was funded by internal grant from the Meijer Heart and Vascular Institute at Corewell Health and National Institute of Health NHLBI 1R01HL165251-01 (MKR and TAT).