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Introduction Surgical management of atrial fibrillation (AF) is a well‐established method of preventing complications and late mortality in patients presenting with AF before mitral valve (MV) surgery. However, despite a substantial body of evidence and a Class I recommendation to apply surgical ablation (SA) concomitant to MV surgery, the utilization of SA remains low. Methods In this study, we sought to summarize the current trends in the SA of AF during MV surgery and update the medical community on its advantages, including perioperative mortality and morbidity, freedom from AF, as well as long‐term survival and stroke rates. Results The data indicate that SA can be added with no increased risk (and perhaps a reduction in perioperative risk) and improved late survival compared to patients with AF left untreated during MV surgery. Discussion Inconsistent application of SA may be related to inaccurate perceptions regarding the complexity of the procedure itself, extended cross‐clamp and bypass times with attendant increased risks, views that it is ineffective, and increased need for an early pacemaker. Conclusion Education in the proper performance of SA, including careful placement of the lesions and attainment of the full transmural effect, contributes to procedure success. Propagating the safety and positive outcomes may also address the concerns.

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We tested the hypothesis that isoform shifts in sarcomeres of the immature heart modify the effect of cardiac myosin-directed sarcomere inhibitors and activators. Omecamtiv mecarbil (OM) activates tension and is in clinical trials for the treatment of adult acute and chronic heart failure.Mavacamten (Mava) inhibits tension and is in clinical trials to relieve hyper-contractility and outflow obstruction in advanced genetic hypertrophic cardiomyopathy (HCM) linked commonly to mutations in sarcomeric proteins. To address the effect of these agents in developing sarcomeres we isolated heart fiber bundles, extracted membranes with Triton X-100, and measured tension developed over a range of Ca 2+ concentrations with and without OM or Mava treatment. We made measurements in fiber bundles from hearts of adult non-transgenic controls (NTG) expressing cardiac troponin I (cTnI), and from hearts of transgenic mice (TG-ssTnI) expressing the fetal/neonatal form, slow skeletal troponin I (ssTnI). We also compared fibers from 7+14-day-old NTG mice expressing ssTnI and cTnI. These studies were repeated with 7+14-day old transgenic mice (TG-cTnT-R92Q) expressing a mutant form of cardiac TnT (cTnT) linked to HCM. OM increased Ca 2+ -sensitivity and decreased cooperative activation in both ssTnI-and cTnI-regulated myofilaments with a similar effect reducing sub-maximal tension in immature and mature myofilaments. Although Mava decreased tension similarly in cTnI-and ssTnI-regulated myofilaments controlled either by cTnT or cTnT-R92Q, its effect involved a depressed Ca 2+ -sensitivity in the mature cTnT-R92-myofilaments. Our data demonstrate an influence of myosin and thin filament-associated proteins on the actions of myosin-directed agents such as OM and Mava. Significance StatementThe effects of myosin-targeted activators and inhibitors on Ca 2+ -activated tension in developing cardiac sarcomeres presented here provide novel, ex-vivo evidence as to their actions in earlystage cardiac disorders. These studies advance understanding of the molecular mechanisms of This article has not been copyedited and formatted. The final version may differ from this version.