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Purpose Prophylactic beta-blockers are recommended to prevent postoperative atrial fibrillation (POAF) after coronary artery bypass grafting (CABG). Polymorphisms in the beta-1 adrenergic receptor (ADRB1) and G protein-coupled receptor kinase 5 (GRK5) genes are associated with variable responses to beta-blockers. The aim of this study was to determine the clinical and genetic factors that influence the response to beta-blockers for POAF prophylaxis after CABG. Methods Patients undergoing isolated CABG and receiving prophylactic beta-blockers (n = 249) were prospectively recruited and followed up for 6 postoperative days. Genotyping of ADRB1 rs1801253, and 3 GRK5 SNPs (rs3740563, rs10787959, and rs17098707) was performed. Results Of the 249 patients, 52 patients (20.8%) experienced POAF. Age, hypertension, vasopressor use, calculated POAF risk score, GRK5 rs2230345 T-allele, and GRK5 rs3740563 A-allele were associated with POAF despite beta-blocker prophylaxis. The multivariate analysis revealed that age [odds ratio (OR) 1.06, 95% CI 1.02–1.11, p = 0.003] and GRK5 rs2230345 T-allele [OR 2.81, 95% CI 1.39–5.67, p = 0.004] were independent predictors of POAF after CABG despite beta-blocker prophylaxis. Conclusion GRK5 rs2230345 T-allele carriers were less responsive than AA genotype carriers to prophylactic beta-blockers for the prevention of POAF after CABG. The study was registered on http://clinicaltrials.gov in March 2019, with trial registration number (TRN): NCT03871647.

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Background Patient-prosthesis mismatch after mitral valve replacement has an unfavorable postoperative hemodynamic outcome, which underlines the importance of identifying and preventing prosthesis- and patient-related risk factors. This study was conducted to determine the incidence and identify possible predictors of patient-prosthesis mismatch. Methods A prospective study was conducted on 715 patients with a mean age of 42 ± 11 years who underwent mechanical mitral valve replacement between 2013 and 2017. The effective orifice area of the prostheses was estimated by the continuity equation, and a mismatch was defined as an effective orifice area index ≤1.2 cm2·m−2. The mean clinical and echocardiographic follow-up was 26.74 ± 11.58 months. Multivariate regression analysis was performed to identify predictors of patient-prosthesis mismatch. Results Patient-prosthesis mismatch was detected in 382 (53.4%) patients. A small mechanical prosthesis (<27 mm) was inserted in 54.3%. Mortality during follow-up was 9% (65 patients). Patient-prosthesis mismatch was identified in patients with preoperative rheumatic mitral valve pathology, associated tricuspid regurgitation, higher New York Heart Association class, preoperative atrial fibrillation, mitral stenosis, and small preoperative left ventricular dimensions. Multivariate analysis identified mitral stenosis, preoperative atrial fibrillation, and small postoperative left ventricular end-diastolic dimension as risk factors for patient-prosthesis mismatch. Conclusion Patient-prosthesis mismatch is a common sequela after mechanical mitral valve replacement. Identification of predictors of patient-prosthesis mismatch can help so that a preoperative strategy can be implemented to avoid its occurrence.

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