Tricuspid regurgitation and right ventricular function after mitral valve surgery with or without concomitant tricuspid valve procedure Ravi R. Desai, BE, a Lina Maria Vargas Abello, MD, b Allan L. Klein, MD, c Thomas H. Marwick, MD, PhD, c Richard A. Krasuski, MD, c Ying Ye, BS, a Edward R. Nowicki, MD, MS, b Jeevanantham Rajeswaran, MSc, d Eugene H. Blackstone, MD, b,d and G€ osta B. Pettersson, MD, PhD b Objectives: To study the effect of mitral valve repair with or without concomitant tricuspid valve repair on func- tional tricuspid regurgitation and right ventricular function. Methods: From 2001 to 2007, 1833 patients with degenerative mitral valve disease, a structurally normal tricuspid valve, and no coronary artery disease underwent mitral valve repair, and 67 underwent concomitant tricuspid valve repair. Right ventricular function (myocardial performance index and tricuspid annular plane systolic excursion) was measured before and after surgery using transthoracic echocardiography for ran- domly selected patients with tricuspid regurgitation grade 0, 1 þ , and 2 þ(100 patients for each grade) and 93 with grade 3 þ /4 þ , 393 patients in total. Results: In patients with mild ( < 3 þ ) preoperative tricuspid regurgitation, mitral valve repair alone was associated with reduced tricuspid regurgitation and mild worsening of right ventricular function. Tricuspid regurgitation of 2 þor greater developed in fewer than 20%, and right ventricular function had improved, but not to preoperative levels, at 3 years. In patients with severe (3 þ /4 þ ) preoperative tricuspid regurgitation, mitral valve repair alone reduced tricuspid regurgitation and improved right ventricular function; however, tricuspid regurgitation of 2 þ or greater returned and right ventricular function worsened toward preoperative levels within 3 years. Concom- itant tricuspid valve repair effectively eliminated severe tricuspid regurgitation and improved right ventricular function. Also, over time, tricuspid regurgitation did not return and right ventricular function continued to im- prove to levels comparable to that of patients with lower grades of preoperative tricuspid regurgitation. Conclusions: In patients with mitral valve disease and severe tricuspid regurgitation, mitral valve repair alone was associated with improved tricuspid regurgitation and right ventricular function. However, the improvements were incomplete and temporary. In contrast, concomitant tricuspid valve repair effectively and durably eliminated se- vere tricuspid regurgitation and improved right ventricular function toward normal, supporting an aggressive ap- proach to important functional tricuspid regurgitation. (J Thorac Cardiovasc Surg 2013;146:1126-32) Supplemental material is available online. The effect of surgery to relieve left-sided valve disease, with or without tricuspid valve repair (TVR), on right ventricular (RV) function in patients with functional tricuspid regurgi- tation (TR) is of great interest, but few studies have been published. In our companion study, we found that RV func- tion was markedly abnormal in patients with severe (grade 3 þ /4 þ ) TR. 1 This was true for the myocardial performance index (MPI), which reflects global RV systolic and diastolic function, and tricuspid annular plane systolic excursion (TAPSE), which reflects longitudinal systolic function. 2 Whether the TR was caused by RV dysfunction or vice versa remained unclear. The decreased function suggested by MPI and TAPSE, both being load-sensitive indexes, could reflect true RV dysfunction or altered pre- and afterload. 2 All these patients underwent mitral valve repair (MVR) to correct their mitral regurgitation (MR). Most patients with se- vere TR also underwent concomitant TVR; patients with less severe TR underwent only MVR. It is well known that MVR reduces pulmonary pressure and RV afterload; however, cor- recting TR increases RVafterload. Correcting MR could also influence the right heart by changing the atrial and ventricular septal positions from the shifting volume and pressure loads. From the Cleveland Clinic Lerner College of Medicine, a Cleveland, Ohio; Depart- ments of Thoracic and Cardiovascular Surgery b and Cardiovascular Medicine, c Heart and Vascular Institute, and Department of Quantitative Health Sciences, d Research Institute, Cleveland Clinic, Cleveland, Ohio. This study was supported in part by the Kenneth Gee and Paula Shaw, PhD, Chair in Heart Research (to Dr Blackstone), and the Peter and Elizabeth C. Tower and Fam- ily Endowed Chair in Cardiothoracic Research, James and Sharon Kennedy, the Slosburg Family Charitable Trust, Stephen and Saundra Spencer, and Martin Niel- sen (to Dr Pettersson). Disclosures: Authors have nothing to disclose with regard to commercial support. Received for publication Dec 7, 2011; revisions received July 30, 2012; accepted for publication Aug 23, 2012; available ahead of print Sept 24, 2012. Address for reprints: G€ osta B. Pettersson, MD, PhD, Department of Thoracic and Car- diovascular Surgery, Heart and Vascular Institute, Cleveland Clinic, 9500 Euclid Ave/Mail Stop J4-1, Cleveland, OH 44195 (E-mail: petterg@ccf.org). 0022-5223/$36.00 Copyright Ó 2013 by The American Association for Thoracic Surgery http://dx.doi.org/10.1016/j.jtcvs.2012.08.061 1126 The Journal of Thoracic and Cardiovascular Surgery c November 2013 ACD Acquired Cardiovascular Disease Desai et al