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      Late Tricuspid Regurgitation after Left-Sided Surgery in the Spotlight: Can We Really Assess the Matter?


      * , ,


      S. Karger AG

      Surgery, Tricuspid regurgitation

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          Secondary tricuspid regurgitation or dilatation: which should be the criteria for surgical repair?

          Secondary tricuspid dilatation may or not be accompanied by tricuspid regurgitation (TR). Tricuspid dilatation can be objectively measured whereas TR can vary according to the preload, afterload, and right ventricular function. The purpose of this prospective study was to determine whether surgical repair of the tricuspid valve based on tricuspid dilatation rather than TR could lead to potential benefits. Between 1989 and 2001, 311 patients underwent mitral valve repair (MVR). The tricuspid valve was examined in each patient. Tricuspid annuloplasty was performed only if the tricuspid annular diameter was greater than twice the normal size (> or = 70 mm) regardless of the grade of regurgitation. Patients in group 1 (163 patients; 52.4%) received MVR alone. Patients in group 2 (148 patients; 47.6%) received MVR plus tricuspid annuloplasty. Although not significant there was a difference with regard to hospital mortality (group 1 = 1.8%, group 2 = 0.7%) and actuarial survival rate (Kaplan-Meier: group 1 = 97.3%, 96.2%, and 85.5%; group 2 = 98.5%, 98.5%, and 90.3% at 3, 5, and 10 years, respectively). The New York Heart Association (NYHA) functional class was significantly improved in group 2 (group 1 = 1.59 +/- 0.84; group 2 = 1.11 +/- 0.31; p1). TR increased by more than two grades in 48% of the patients in group 1 and in only 2% of the patients in group 2 (p < 0.001). Remodeling annuloplasty of the tricuspid valve based on tricuspid dilation improves functional status irrespective of the grade of regurgitation. Considerable tricuspid dilatation can be present even in the absence of substantial TR. Tricuspid dilatation is an ongoing disease process that will, with time, lead to severe TR.
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            Conservative management of tricuspid regurgitation in patients undergoing mitral valve replacement.

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              Tricuspid regurgitation after successful mitral valve surgery.

              The tricuspid valve (TV) is inseparably connected with the mitral valve (MV) in terms of function. Any pathophysiological condition concerning the MV is potentially a threat for the normal function of the TV as well. One of the most challenging cases is functional tricuspid regurgitation (TR) after surgical MV correction. In the past, TR was considered to progressively revert with time after left-sided valve restoration. Nevertheless, more recent studies showed that TR could develop and evolve postoperatively over time, as well as being closely associated with a poorer prognosis in terms of morbidity and mortality. Pressure and volume overload are usually the underlying pathophysiological mechanisms; structural alterations, like tricuspid annulus dilatation, increased leaflet tethering and right ventricular remodelling are almost always present when regurgitation develops. The most important risk factors associated with a higher probability of late TR development involve the elderly, female gender, larger left atrial size, atrial fibrillation, right chamber dilatation, higher pulmonary artery systolic pressures, longer times from the onset of MV disease to surgery, history of rheumatic heart disease, ischaemic heart disease and prosthetic valve malfunction. The time of TR manifestation can be up to 10 years or more after an MV surgery. Echocardiography, including the novel 3D Echo techniques, is crucial in the early diagnosis and prognosis of future TV disease development. Appropriate surgical technique and timing still need to be clarified.

                Author and article information

                S. Karger AG
                November 2014
                14 November 2014
                : 129
                : 4
                : 240-241
                1st Cardiology Department, Hippokration Hospital, Athens, Greece
                Author notes
                *Constantina Aggeli, MD, FESC, 1st Cardiology Department, Hippokration Hospital, Vas Sophias, GR-11524 Athens (Greece), E-Mail dina.aggeli@gmail.com
                368891 Cardiology 2014;129:240-241
                © 2014 S. Karger AG, Basel

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