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Structural Heart
The Journal of the Heart Team
Volume 2, 2018 - Issue 4
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Original Research

Should Moderate or Less Functional Tricuspid Regurgitation be Repaired During Surgery for Degenerative Mitral Valve Disease?

, MD, , MD, , PhD, , MD, , MD, , MD, DPhil, , MD, , MD, PhD, , MD, , MD & , MD show all
Pages 305-313 | Received 15 Nov 2017, Accepted 26 Apr 2018, Published online: 21 May 2018
 

ABSTRACT

Background: It is unclear whether moderate or less functional tricuspid regurgitation (TR) should be repaired during surgery for degenerative mitral valve (MV) disease. We studied the natural course of unaddressed moderate or less TR and identified risk factors for TR progression after surgery for degenerative MV disease.

Methods: From 2001 to 2011, 2,982 patients with isolated degenerative MV disease and no evidence of coronary artery disease underwent MV surgery. To generate an enriched sample of patients with TR, by random selection 200 patients without TR, 197 with mild TR, and 177 with moderate TR were studied. A total of 1,150 echocardiograms were available for longitudinal analysis of TR progression after surgery in 550 of these 574 patients.

Results: Overall prevalence of severe TR was 1.1%, 2.2%, 3.6%, and 4.4% by 1, 3, 5, and 7 years, respectively. Patients with moderate preoperative TR were more likely to progress to severe TR by 7 years (8.6%) than those with mild TR (3.2%) or no TR (1.3%) preoperatively (< 0.001). Other risk factors for progression to severe TR included larger diastolic tricuspid valve diameter (= 0.03), shorter right ventricular base-to-apex length (= 0.0004), smaller tethering area (= 0.01), older age, and preoperative heart failure. During follow-up, no patient underwent TV intervention.

Conclusion: Routine repair of moderate or less functional TR during surgery for degenerative MV disease does not appear to be warranted, because progression to severe TR is uncommon. Instead, we suggest a tailored approach, reserving TR repair during surgery for degenerative MV disease for patients with known risk factors.

Acknowledgments

We are grateful to Lina Maria Vargas Abello, MD, Ravi Desai, MD, and Ying (Amy) Ye, MD, for carrying out the echocardiographic measurements.

Disclosure statements

Dr. Sabik: North American principal investigator for the Abbott Laboratories–sponsored left main coronary disease randomized trial (EXCEL). Society of Thoracic Surgeons board of directors. Scientific advisory board of Medtronic.

Dr. Gillinov: Consultant to Edwards Lifesciences, Medtronic, Abbott, CryoLife, and AtriCure. Research support from Abbott.

Dr. Suri: Clinical Steering Committee member, Abbott COAPT trial. National principal investigator, Perceval trial. Patents–Sorin, Perceval trial. Publications Committee, PARTNER trial.

Others: None of the other authors report any conflicts of interest.

Supplemental data

Supplemental data for this article can be accessed on the

publisher’s website.

Additional information

Funding

This study was funded in part by the Gus P. Karos Registry Fund; the Kenneth Gee and Paula Shaw, PhD, Chair in Heart Research; the Judith Dion Pyle Endowed Chair in Heart Valve Research; the Peter and Elizabeth C. Tower and Family Endowed Chair in Cardiothoracic Research; the Sheikh Hamdan bin Rashid Al Maktoum Distinguished Chair in Thoracic and Cardiovascular Surgery; and James and Sharon Kennedy, the Slosburg Family Charitable Trust, Stephen and Saundra Spencer, and Martin Nielsen. Sajjad Raza, MD, is a Clinical Research Scholar as part of the Cardiothoracic Surgical Trials Network (CTSN), and his Master of Management–Healthcare is being funded by NIH/National Heart, Lung and Blood Institute grant UM1HL088955.

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