Abstract OBJECTIVES Limited literature is available on the best management strategy for tricuspid valve (TV) disease in adults. We sought to review our long-term outcomes of TV surgery with regard to survival and reoperation. METHODS A retrospective analysis of all patients ≥18 years of age [n = 2541, aged 67 ± 13years, 1433 (56%) females] who underwent first-time TV surgery between January 1993 and December 2013 was done. There were 1735 patients who received TV repair and 806 patients underwent replacement. A gradient boosting machine model was used to derive a propensity score for predicting replacement using 27 preoperative characteristics. Four hundred and eighteen propensity-matched pairs of TV repair and replacement were identified. Cox proportional hazard regression was used on the matched subset to determine the effect of replacement. RESULTS Functional TV regurgitation was present in 54% (n = 1369). A bioprosthesis was used in 84% (n = 680) of replacements, while 54% (n = 934) of TV repairs were ring annuloplasties. Operative mortality was 8% (n = 212). Overall survival was 54%, 29% and 13% at 5, 10 and 15 years, respectively. After propensity score matching, replacement was significantly associated with increased mortality [hazard ratio (HR) 1.54, 95% confidence interval (CI) 1.18–2.00; P = 0.001]. The cumulative incidence of TV reoperation was similar between the 2 groups when accounting for the competing risk of death [Fine–Gray HR 1.56, 95% CI 0.9–2.8; P = 0.144]. CONCLUSIONS TV surgery is associated with poor outcomes due to multiple patient comorbidities. TV repair results in better survival compared to replacement in patients with similar comorbidities with no increased risk of getting a reoperation.
Mitochondrial Morphology, Dynamics, and Function in Human Pressure Overload or Ischemic Heart Disease With Preserved or Reduced Ejection Fraction
Circulation: Heart Failure | February 12, 2019 | Volume: 12 | Issue: 2 | Pages: No page available
Background: The FOXO3a (forkhead box O3a)-BNIP3 (B-cell lymphoma 2/adenovirus E1B 19kDa interacting protein 3) pathway modulates mitochondrial dynamics and function and contributes to myocardial remodeling in rodent models of heart failure. We sought to investigate the expression of this pathway along with the expression of mitochondrial biogenesis (PGC-1α [peroxisome proliferator-activated receptor-γ coactivator-1α]), dynamics (DRP-1 [dynamin-related protein 1], OPA-1 [optic atrophy 1], and MFN 2 [mitofusin 2]), and oxidative phosphorylation (citrate synthase and electron transport chain complexes) markers and COX IV (cytochrome C oxidase) activity in myocardium from patients with valvular or ischemic heart disease and heart failure with preserved ejection fraction (HFpEF) or heart failure with reduced ejection fraction (HFrEF). Methods and Results: Subepicardial left ventricular biopsies (10×1×1 mm 3 ) were obtained at aortic valve replacement (HFpEF AVR , n=5; and HFrEF AVR , n=4), coronary artery bypass grafting (HFpEF CABG , n=5; and HFrEF CABG , n=5), or left ventricular assist device implantation (HFrEF LVAD , n=4). Subepicardial biopsies from patients with normal left ventricular function (n=2) and from donor hearts (n=3) served as controls (normal). Relative to normal, mitochondrial fragmentation and cristae destruction were evident, and mitochondrial area was decreased in HFpEF; 1.00±0.09 versus 0.71±0.08; P =0.016. These mitochondrial morphological changes were more pronounced in HFrEF (0.54±0.06); P =0.002 HFpEF versus HFrEF. BNIP3 (monomer+dimer) expression was increased in HFpEF (3.99±2.44) and in HFrEF (5.19±1.70) relative to normal; P =0.004 and P <0.001, respectively. However, BNIP3 monomer was increased in HFrEF (4.32±1.43) compared with normal (0.99±0.06) and HFpEF (1.97±0.90); P =0.001 and 0.004, respectively. The HFrEF group uniquely showed increase in DRP-1 expression (1.94±0.38) and decreases in PGC-1α expression (0.61±0.07) and COX IV activity (0.70±0.10) relative to normal; P =0.013, P <0.001, and P <0.001, respectively, with no significant change in electron transport chain complexes expression. Conclusions: These findings in human myocardium confirm studies in rodents where contractile dysfunction is associated with activation of the FOXO3a-BNIP3 pathway and altered mitochondrial dynamics, biogenesis, and function.
Vasopressor magnitude predicts poor outcome in adults with congenital heart disease after cardiac surgery
AbstractWe present a case of a 7‐year‐old boy with a history of multiple mitral valve interventions and subsequent Melody valve placement in the mitral position, who presented with acute mitral stenosis due to complete fracture of the Melody stent. He was born early with severe mitral and tricuspid insufficiency due to valvular dysplasia, and ended up with 4 sternotomies before the age of 2 due to mitral valve dysfunction and recurrent prosthetic valve thrombosis. He then developed mixed stenosis and regurgitation at age 6, and to avoid another sternotomy, valve‐in‐valve therapy with off‐label use of a 20‐mm Melody valve was done with hybrid procedure via trans‐apical approach. Eight months later he presented with acutely worsened mitral stenosis (mean gradient 20 mm Hg), due to fracture of the proximal stent. While the safety and efficacy of the Melody valve has been well established especially in the pulmonary position, stent fracture is a known and potentially serious complication. As with any novel valve therapy, close follow‐up and frequent imaging may be warranted to watch for loss of stent integrity, particularly if clinical symptoms of valve dysfunction occur.
Intramyocardial Hematoma After Radiofrequency Catheter Ablation
The World Society for Pediatric and Congenital Heart Surgery (WSPCHS) is the largest professional organization in the world dedicated to pediatric and congenital heart surgery. The purpose of this article is to document the first decade of the history of WSPCHS from its formation in 2006, to summarize the current status of WSPCHS, and to consider the future of WSPCHS. The WSPCHS was incorporated in Canada on April 7, 2011, with a head office in Montreal, Canada. The vision of the WSPCHS is that every child born anywhere in the world with a congenital heart defect should have access to appropriate medical and surgical care. The mission of the WSPCHS is to promote the highest quality comprehensive cardiac care to all patients with congenital heart disease, from the fetus to the adult, regardless of the patient’s economic means, with an emphasis on excellence in teaching, research, and community service.
A Letter to the Resident Starting My Service…
World Journal for Pediatric and Congenital Heart Surgery | June 26, 2018 | Volume: 9 | Issue: 4 | Pages: 381-382
Response by Nguyen et al to Letter Regarding Article, “Early Outcomes of Repair of Left Ventricular Apical Aneurysms in Patients with Hypertrophic Cardiomyopathy”