BackgroundSystemic inflammation is a strong predictor of atrial fibrillation. A key role for electrical remodeling is increasingly recognized, and experimental data suggest that inflammatory cytokines can directly affect connexins resulting in gap‐junction dysfunction. We hypothesized that systemic inflammation, regardless of its origin, promotes atrial electric remodeling in vivo, as a result of cytokine‐mediated changes in connexin expression.Methods and ResultsFifty‐four patients with different inflammatory diseases and elevated C‐reactive protein were prospectively enrolled, and electrocardiographic P‐wave dispersion indices, cytokine levels (interleukin‐6, tumor necrosis factor‐α, interleukin‐1, interleukin‐10), and connexin expression (connexin 40, connexin 43) were measured during active disease and after reducing C‐reactive protein by >75%. Moreover, peripheral blood mononuclear cells and atrial tissue specimens from an additional sample of 12 patients undergoing cardiac surgery were evaluated for atrial and circulating mRNA levels of connexins. Finally, in vitro effects of interleukin‐6 on connexin expression were studied in HL‐1 mouse atrial myocytes. In patients with active inflammatory diseases, P‐wave dispersion indices were increased but rapidly decreased within days when C‐reactive protein normalizes and interleukin‐6 levels decline. In inflammatory disease patients, both P‐wave dispersion indices and interleukin‐6 changes were inversely associated with circulating connexin levels, and a positive correlation between connexin expression in peripheral blood mononuclear cells and atrial tissue was demonstrated. Moreover, interleukin‐6 significantly reduced connexin expression in HL‐1 cells.ConclusionsOur data suggest that regardless of specific etiology and organ localization, systemic inflammation, via interleukin‐6 elevation, rapidly induces atrial electrical remodeling by down‐regulating cardiac connexins. Although transient, these changes may significantly increase the risk for atrial fibrillation and related complications during active inflammatory processes.

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Objective: To highlight the main target points covered by clinical studies on the Perceval sutureless valve for surgical aortic valve replacement (SAVR) and raise a point of discussion for further expansion of its use when compared with stented bioprostheses (SB) and transcatheter aortic valve replacement (TAVR).Methods: We reviewed clinical trials and retrospective studies published up to date and compared the outcomes in terms of mortality, myocardial infarction (MI) stroke, paravalvular leak (PVL), permanent pacemaker implantation (PPI), bleeding and long-term outcomes.Results: Clinical studies showed that 30-day mortality ranged from 0–4% for Perceval and 2.9–7% for TAVR. The incidence of PVL (Perceval 1.9–19.4 vs. TAVR 9–53.5%), PPI (Perceval 2–11.2 vs. TAVR 4.9–25.5%), stroke (Perceval 0 vs. TAVR 0–2.8%), MI (Perceval 0 vs. TAVR 0–3.5%), were all higher in the TAVR group. Compared to other SB, mortality ranged from 0–6.4% for Perceval and 0–5.9% for SB. The incidence of PVR (Perceval 1–19.4 vs. SB 0–1%), PPI (Perceval 2–10.7 vs. SB 1.8–8.5%), stroke (Perceval 0–3.7 vs. SB 1.8–7.3%) and MI (Perceval 0–7.8 vs. SB 0–4.3%) were comparable among the groups. In patients with a bicuspid aortic valve, mortality rate was (0–4%) and PVL incidence was (0–2.3%). However, there was a high incidence of PPI (0–20%), and stroke (0–8%). Long-term survival ranged between 96.7–98.6%.Conclusions: The Perceval bioprosthesis has proved to be a reliable prosthesis for surgical aortic valve replacement due to its implantation speed, the reduced cardiopulmonary bypass time, the reduced aortic cross-clamp time and the shorter intensive care unit and hospital length of stay.

Background: Equipoise exists between the use of leaflet resection and preservation for surgical repair of mitral regurgitation caused by prolapse. We therefore performed a randomized, controlled trial comparing these 2 techniques, particularly in regard to functional mitral stenosis. Methods: One hundred four patients with degenerative mitral regurgitation surgically amenable to either leaflet resection or preservation were randomized at 7 specialized cardiac surgical centers. Exclusion criteria included anterior leaflet or commissural prolapse, as well as a mixed cause for mitral valve disease. Using previous data, we determined that a sample size of 88 subjects would provide 90% power to detect a 5–mm Hg difference in mean mitral valve gradient at peak exercise, assuming an SD of 6.7 mm with a 2-sided test with α=5% and 10% patient attrition. The primary end point was the mean mitral gradient at peak exercise 12 months after repair. Results: Patient age, proportion who were female, and Society of Thoracic Surgeons risk score were 63.9±10.4 years, 19%, and 1.4±2.8% for those who were assigned to leaflet resection (n=54), and 66.3±10.8 years, 16%, and 1.9±2.6% for those who underwent leaflet preservation (n=50). There were no perioperative deaths or conversions to replacement. At 12 months, moderate mitral regurgitation was observed in 3 subjects in the leaflet resection group and 2 in the leaflet preservation group. The mean transmitral gradient at 12 months during peak exercise was 9.1±5.2 mm Hg after leaflet resection and 8.3±3.3 mm Hg after leaflet preservation ( P =0.43). The participants had similar resting peak (8.3±4.4 mm Hg versus 8.4±2.6 mm Hg; P =0.96) and mean resting (3.2±1.9 mm Hg versus 3.1±1.1 mm Hg; P =0.67) mitral gradients after leaflet resection and leaflet preservation, respectively. The 6-minute walking distance was 451±147 m for those in the leaflet resection versus 481±95 m for the leaflet preservation group ( P =0.27). Conclusions: In this adequately powered randomized trial, repair of mitral prolapse with either leaflet resection or leaflet preservation was associated with similar transmitral gradients at peak exercise at 12 months postoperatively. These data do not support the hypothesis that a strategy of leaflet resection (versus preservation) is associated with a risk of functional mitral stenosis. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier NCT02552771.