Background: The main dietary source of omega-3 polyunsaturated fatty acids (n-3 PUFA) is fish, which contains eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). In the present manuscript, we aimed to review the current evidence regarding the clinical role of n-3 PUFA in the prevention of atrial fibrillation (AF) and the possible underlying mechanisms. Methods: A literature search based on PubMed listings was performed using “Omega-3 fatty acids” and “atrial fibrilation” as key search terms. Results: n-3 PUFA have been shown to attenuate structural atrial remodeling, prolong atrial effective refractory period through the prevention of reentry and suppress ectopic firing from pulmonary veins. Dietary fish intake has been found to have no effect on the incidence of AF in the majority of studies. Circulating DHA has been consistently reported to be inversely associated with AF risk, whereas EPA has no such effect. The majority of studies investigating the impact of n-3 PUFA supplementation on the incidence of AF following cardiac surgery reported no benefit, though most of them did not use n-3 PUFA pretreatment for adequate duration. Studies using adequate four-week pretreatment with n-3 PUFA before cardioversion of AF showed a reduction of the AF incidence. Conclusions: Although n-3 PUFA have antiarrhythmogenic properties, their clinical efficacy on the prevention of AF is not consistently supported. Further well-designed studies are needed to overcome the limitations of the existing studies and provide robust conclusions.

Myocardial infarction often leads to progressive structural and electrophysiologic remodeling of the left ventricle. Despite the widespread use of β-adrenergic blockade and implantable defibrillators, morbidity and mortality from chronic-phase ventricular tachyarrhythmias remains high, calling for further investigation on the underlying pathophysiology. Histological and functional studies have demonstrated extensive alterations of sympathetic nerve endings at the peri-infarct area and flow-innervation mismatches that create a highly arrhythmogenic milieu. Such accumulated evidence, along with the previously well-documented autonomic dysfunction as an important contributing factor, has stirred intense research interest for pharmacologic and non-pharmacologic neuromodulation in post-infarction heart failure. In this regard, aldosterone inhibitors, sacubitril/valsartan and sodium-glucose cotransporter type 2 inhibitors have shown antiarrhythmic effects. Non-pharmacologic modalities, currently tested in pre-clinical and clinical trials, include transcutaneous vagal stimulation, stellate ganglion modulation and renal sympathetic denervation. In this review, we provide insights on the pathophysiology of ventricular arrhythmogenesis post-myocardial infarction, focusing on sympathetic activation.

Background: Obesity is invariably accompanied by autonomic dysfunction, although data in pediatric populations are conflicting. Methods: We conducted a systematic review and meta-analysis of 12 studies (totaling 1102 participants) comparing obese and normal-weight subjects (5–18 years of age), defined as body mass index >95th or <85th percentile, respectively. Using a random-effects model, we report the standardized mean differences (SMD) of sympathetic and vagal indices of heart rate variability. Results: Autonomic dysfunction was present in the obesity group, based on the average SMD in the standard deviation of sinus intervals (at −0.5340), and on the ratio of low (LF)- to high (HF)-frequency spectra (at 0.5735). There was no difference in sympathetic activity, but the heterogeneity among the relevant studies weakens this result. SMD in HF (at 0.5876), in the root mean square of successive differences between intervals (at −0.6333), and in the number of times successive intervals exceeded 50 ms divided by the total number of intervals (at −0.5867) indicated lower vagal activity in the obesity group. Conclusions: Autonomic dysfunction is present in obese children and adolescents, attributed to lower vagal activity. Further studies are needed in various pediatric cohorts, placing emphasis on sympathetic activity.

Transcatheter Aortic Valve Implantation (TAVI) has revolutionized the treatment of severe aortic stenosis in high-risk and inoperable patients. Despite significant advancements in patient selection, techniques, and the evolution of TAVI devices, stroke persists as a consistent adverse event over time, presenting a devastating complication of TAVI procedures and exerting a significant negative prognostic impact. Both acute and subsequent strokes following TAVI continue to pose significant challenges, with substantial implications for patient morbidity and mortality. This paper reviews the incidence, mechanisms, risk factors, and preventive strategies for stroke in TAVI, highlighting recent advancements, particularly in current protective devices, and ongoing challenges in minimizing this adverse outcome.