Catheter ablation (CA) is a procedure commonly used to restore sinus rhythm in patients with atrial fibrillation (AF). However, AF recurrence after CA remains a relevant clinical issue. We tested the effects of an oral anti-oxidant treatment (α-lipoic acid, ALA) on AF recurrence post-CA. Patients with paroxysmal AF have been enrolled in a randomized, prospective, double blind, controlled placebo trial. Following CA, patients have been randomly assigned to receive ALA oral supplementation (ALA group) or placebo (control group), and evaluated at baseline and after a 12-month follow-up: 73 patients completed the 12-month follow-up (ALA: 33; control: 40). No significant difference has been detected between the two groups at baseline. Strikingly, one year after CA, ALA therapy significantly reduced serum markers of inflammation. However, there was no significant difference in AF recurrence events at follow-up when comparing ALA to placebo group. Multivariate analysis revealed that the only independent prognostic risk factor for AF recurrence post-CA is age. In conclusion, ALA therapy reduces serum levels of common markers of inflammation in ablated patients. Nevertheless, ALA does not prevent AF recurrence after an ablative treatment.

Introduction: Minimally invasive extracorporeal circulation (MiECC) reduced inflammatory burden, leading to best clinical outcomes in patients treated with coronary artery bypass grafting (CABG). Despite this, the patients with type 2 diabetes mellitus (T2DM) vs those without T2DM (non-T2DM) have a worse prognosis, caused by over-inflammation and modulated by sodium-glucose transporter 2 receptors. However, we evaluated the inflammatory burden and clinical outcomes in non-T2DM vs T2DM patients under sodium-glucose transporter 2 inhibitors (SGLT2-I users) vs non-SGLT2-I users at 5 years of follow-up post-CABG via MiECC.Materials and methods: In a multicenter study, we screened consecutive patients with indications to receive CABG. The study endpoints were the inflammatory burden (circulating serum levels of tumor necrosis factor-alpha (TNF-α), interleukin 1 and 6 (IL-1 and IL-6), C-reactive protein (CRP), and leucocytes count) and the clinical outcomes at follow-up of 5 years in non-T2DM vs SGLT2-I users, in non-T2DM vs non-SGLT2-I users, and SGLT2-I users vs non-SGLT2-I users.Results: At baseline, and at one year and 5 years of follow-up, the non-T2DM vs SGLT2-I users, non-T2DM vs non-SGLT2-I users, and SGLT2-I users vs non-SGLT2-I users had the lowest values of IL-1, IL-6, and TNF-α (p < 0.05). At one year of follow-up, SGLT2-I users vs non-T2DM and non-SGLT2-I users vs non-T2DM users had a higher rate of all deaths, cardiac deaths, re-myocardial infarction, repeat revascularization, and stroke, and of the composite endpoint (p < 0.05). In a multivariate Cox regression analysis, the composite endpoint was predicted by IL-1 [2.068 (1.367–3.129)], TNF-α [1.989 (1.081–2.998)], and SGLT2-I [0.504 (0.078–0.861)].Conclusion: In T2DM patients, the SGLT2-I significantly reduced the inflammatory burden and ameliorated clinical outcomes at 5 years of follow-up post-CABG via MiECC.

In secondary mitral regurgitation, the concept that the mitral valve (MV) is an innocent bystander, has been challenged by many studies in the last decades. The MV is a living structure with intrinsic plasticity that reacts to changes in stretch or in mechanical stress activating biohumoral mechanisms that have, as purpose, the adaptation of the valve to the new environment. If the adaptation is balanced, the leaflets increase both surface and length and the chordae tendineae lengthen: the result is a valve with different characteristics, but able to avoid or to limit the regurgitation. However, if the adaptation is unbalanced, the leaflets and the chords do not change their size, but become stiffer and rigid, with moderate or severe regurgitation. These changes are mediated mainly by a cytokine, the transforming growth factor-β (TGF-β), which is able to promote the changes that the MV needs to adapt to a new hemodynamic environment. In general, mild TGF-β activation facilitates leaflet growth, excessive TGF-β activation, as after myocardial infarction, results in profibrotic changes in the leaflets, with increased thickness and stiffness. The MV is then a plastic organism, that reacts to the external stimuli, trying to maintain its physiologic integrity. This review has the goal to unveil the secret life of the MV, to understand which stimuli can trigger its plasticity, and to explain why the equation "large heart = moderate/severe mitral regurgitation" and "small heart = no/ mild mitral regurgitation" does not work into the clinical practice.

Background and Aim of the Study The outcome of mitral valve (MV) repair for chronic ischemic mitral regurgitation (IMR) is suboptimal, due to the high recurrence rate of moderate or severe mitral regurgitation (MR) during follow‐up. The MV adapts to new MR increasing its area to cover the enlarged annular area (mitral plasticity). As this process is often incomplete, we aimed to evaluate if augmenting the anterior leaflet (AL) and cutting the second‐order chords (CC) together with restrictive mitral annuloplasty, a strategy we call “surgical mitral plasticity,” could improve the midterm results of MV repair for IMR. Materials and Methods From November 2017 to October 2019, 22 patients with chronic IMR underwent surgical mitral plasticity. Mean age was 73 ± 7 years and six were female. Mean ejection fraction was 32% ± 11%, IMR grade was moderate in 10 and severe in 12. Mean clinical and echocardiographic follow‐up was 12 ± 6 months. Results There was no early death, and one patient died 6 months after surgery. Ejection fraction improved from 32% ± 15% to 40% ± 6% (P = .031). IMR was absent or mild in all patients, and none showed recurrent moderate or more IMR. Tenting area decreased significantly from 2.5 ± 0.5 to 0.5 ± 0.3 cm² and coaptation length increased from 1.9 ± 0.7 to 7.8 ± 1.6 mm. All patients were in New York Heart Association class I or II. Conclusions Mitral plasticity, if uncomplete, is ineffective in preventing IMR to become significant. Surgical mitral plasticity, by completing incomplete process of MV adaptation, has a strong rationale, which however needs to be validated with longer follow‐up.

Background and Aim Second‐order chord tethering of the anterior leaflet is a risk factor for failure of posterior leaflet prolapse repair. Materials and Methods We describe two cases of second‐order chord tethering of the anterior leaflet associated with severe mitral regurgitation due to prolapse or chordal rupture of the anterior leaflet, causing early and late failure of repair. Results We described two cases where this phenomenon happened. Conclusions Our cases demonstrate that the second‐order chords of the prolapsing AL can be tethered and that this aspect should be carefully evaluated before surgery, as it can progress over time, affecting the results of surgical repair.