LAUSR

Tricuspid annuloplasty (TA) for moderate to severe tricuspid regurgitation (TR) (Class I, IIb) is the current standard of practice to restore the normal tricuspid annular dimension and function. The current controversy in atrioventricular surgery concerns the indication for concomitant TA in patients with moderate TR and significant annular dilatation of at least ≥40mm or at least 21mm/m indexed for body surface area (Class IIb) during mitral valve surgery (MVS) proposed by the American Heart Association/American College of Cardiology and European Society of Cardiology. It is reported that 65%–85% of the population present with trivial to moderate TR which remains asymptomatic until it is discovered in an echocardiogram for preoperative cardiac evaluation or routine cardiovascular checkup. Moderate to severe TR occurs in patients with right‐ and left‐sided congenital and acquired diseases and may be associated with bi‐ventricular failure, increased risk for associated morbidity such as pulmonary arterial hypertension, hepato‐renal syndrome, and mortality. It is recognized that 14%–35% of the patients with rheumatic heart disease (RHD) have mild‐to‐moderate functional TR who have an incremental risk of developing severe TR. The patients have a low survival at a mean follow‐up of 5 years if they remain untreated without concomitant TA during MVS. The editorial will discuss the paper of Arafat and colleagues with references to recently reported similar topics. The article published in this edition of Journal of Cardiac Surgery, Arafat and colleagues discuss the results of their 10‐year clinical experience of concomitant TA for moderate to severe TR during MVS in patients with rheumatic (RMVD n=345; 61% had mitral regurgitation and 39% mitral valve stenosis) and degenerative (DMVD n=135) mitral valve diseases. The objective of the observational nonrandomized trial was to identify predictors of the durability of TA for moderate to severe TR in patients with RMVD and DMVD undergoing mitral valve repairs and replacements. Valve repair was feasible in 12% in the RMVD group as compared to 52% in the DMVD group. TheTA was performed with flexible, rigid prostheses, and the de Vega suture technique. The mean ages of the two groups (RMVD and DMVD) were 51 and 56 years, respectively. The demography of the RMVD group represents an age shift from juvenile RHD to a stage of a burn‐out RHD in which the structural deterioration process of the rheumatic mitral valve has ceased and stabilized. The pathology of the mitral valve apparatus is presented with annular dilatation or mixed lesion. In the absence of calcification, valve repair is feasible in experienced hands, otherwise replacement is inevitable. The endpoints of the study by Arafat and colleagues were 30‐day mortality, long‐term survival, freedom from Grade II or higher tricuspid valve regurgitation, change in the degree of TR during follow‐up, and tricuspid valve reinterventions. The Kaplan–Meier method was used to calculate survival at 1, 5, and 7 years, cumulative incidence for recurrent TR, and reintervention. Follow‐up was 97.8% complete. The median follow‐up time was 53 months (25–85 months). The cumulative incidence of death in Arafat et al. series at 7 years was 4.8%. Similar studies were conducted by Farooq and Bernal and their colleagues in younger patients at a mean age of 41–46 years; the 30‐day mortality was 4.5%–5.9%. The Kaplan–Meier survival probability in the series of Bernal and colleagues was 74.4% at 10 years and age > 65 years was the only predictor of late mortality. Progression of moderate TR from the baseline was similarly observed in rheumatic and degenerative populations at a median follow‐up of 53 months at 1, 5, and 7 years. It was 15.6%, 33.8%, and 39.3% in the RHD group and 16.1%, 30.4%, and 36.02% in the degenerative group, respectively. In contrast to mitral valve repair versus replacement plus TA, progression of moderate TR was less in the MV repair group (SHR: 1.69 [1.03–2.78]; p = .038). In a similar study by Farooq and colleagues on TA plus mitral valve replacement, there was no progression of TR reported at 3 years. Recently reported randomized controlled trial by Gammie and colleagues showed much lesser progression of moderate TR at 2 years (0.6% vs. 6.1% control group, relative risk, 0.09; 95% CI, 0.01 to 0.69). Bernal and colleagues reported progression of TR during their 15.8 years mean follow‐up in 23.5% of the RHD population caused by recurrent rheumatic disease. Progression of TR in the rheumatic endemic region is recognized as an important clinical event, which is a sequela of rheumatic fever caused by streptococcal infection of the throat (Strept‐Throat). Consequently, long‐term penicillin prophylactic therapy against recurrent RHD as recommended by the World Health Organization should be included in the protocol for optimal medical therapy for TA‐MV repair. The authors should be congratulated for their laudable clinical studies and for sharing the results with the global cardiovascular community. Although it is a single‐center observational trial like others, which they admit, their data provide valuable information that stimulates discussions in the clinical practice, which encourages an early aggressive approach for concomitant TA plus MVS in rheumatic populations. A multicenter randomized controlled trial to provide predictive power of the resultant data is required for developing a surgical strategy for TA and MVS in rheumatic patients. Pacemaker implantation was not an issue in their series as well as Farooq and Bernal and their colleagues, but it is a global concern as