Tricuspid valve regurgitation attributable to endomyocardial biopsies and rejection in heart transplantation

Tricuspid Regurgitation After Cardiac Transplantation: An Old Problem Revisited

“…10 Furthermore, the rate of rejection and donor heart weight were found to correlate with higher risk of TR, suggesting physiologic substrates that predispose to abnormal right heart remodeling and after-load, as well as allograft rejection with resultant right ventricular (RV) dysfunction to be important as well. 10,11 Anatomic TR TR may be caused directly by anatomic disruption of the valve apparatus, such as torn leaflet or ruptured chordae tendinae 12 ; the excessive leaflet motion is associated with severe prolapse or flail valve. In this respect, endomyocardial biopsy (EMB), performed to detect allograft rejection, is the single most important culprit.…”

Tricuspid Regurgitation After Cardiac Transplantation: How Many Biopsies Are Too Many?

“…[1][2][3][4] There are reports of a relationship between the number of EMBs performed and the development of flail tricuspid leaflets or chordal rupture. [5][6][7] It is hypothesized that inadvertent tearing of these structures by the jaws of the cardiac bioptome is what causes the TR. 5 Transthoracic echocardiography (TTE) can sometimes miss torn chordae tendinae and flail leaflets, and hence can underestimate the role of EMB in the pathogenesis of TR.…”

Tricuspid annuloplasty significantly reduces early tricuspid regurgitation after biatrial heart transplantation

“…Early TR may be the result of many factors, including inadequate right ventricular donor function or preservation, elevated PVR, and possibly the technique of implantation. [1][2][3][4] Several reports have suggested that the incidence of TR and need for a permanent pacemaker might be reduced by the technique of bicaval implantation. 5,6 Many programs, including ours, have been reluctant to embrace this technique because it potentially increases the complexity of operation, and its proposed benefit has yet to be conclusively demonstrated.…”

“…[1][2][3][4] It can delay recovery, further predispose the patient to late right ventricular decompensation, and ultimately reduce the functional benefit of transplantion. In our experience, the incidence of TR after cardiac transplantation has been unpredictable.…”