The autonomic nervous system (ANS) is known to play an important role in the genesis and maintenance of atrial fibrillation (AF). Biomolecular and genetic mechanisms, anatomical knowledges with recent diagnostic techniques acquisitions, both invasive and non‐invasive, have enabled greater therapeutic goals in patients affected by AF related to ANS imbalance. Catheter ablation of ganglionated plexi (GP) in the left and right atrium has been proposed in varied clinical conditions. Moreover interesting results arise from renal sympathetic denervation and vagal nerve stimulation. Despite all this, in the scenario of ANS modulation translational strategies we necessary must consider the treatment or correction of dynamic factors such as obesity, obstructive sleep apnea, lifestyle, food, and stress. Finally, new antiarrhythmic drugs, gene therapy and “ablatogenomic” could be represent exciting future therapeutic perspectives.

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For several years, the autonomic nervous system has played a central role in the pathophysiological mechanism of atrial fibrillation (AF), so much so that it has been considered one of the cornerstones of Coumel’s triangle. The clinical and therapeutic management of AF secondary to sympatho–vagal imbalance represents one of the most important examples of how precision medicine should be applied. Increasing knowledge of this kind of arrhythmias has made it possible to select specific antiarrhythmic drugs and to diversify their use according to vagal or adrenergic AF forms. Ablative strategies, such as cardioneuroablation and non-direct cardiac neuromodulation methods (such as renal denervation and peripheral vagal stimulation), have gradually emerged. In the possibly near future, there will be a development of new acquisitions regarding new pharmacological therapeutic strategies and gene therapy. Finally, finding an AF in patients experiencing syncopal episodes opens a whole chapter regarding interesting, but also complex, diagnostic and therapeutic strategies, ranging from neurally mediated forms to convulsive seizure that could also increase the risk of sudden death.

Background Lipoprotein(a) [Lp(a)] is a liver–derived lipoprotein with genetically determined concentrations. High level of lipoprotein(a) is a common risk factor for cardiovascular disease and stroke. Higher plasma Lp(a) concentrations are associated with an increased risk of atherosclerotic cardiovascular disease (ASCVD), through mechanisms associated with increased atherogenesis, inflammation, and thrombosis. Methods The study enrolled patients ≤ 55 years of age referred to Cardiology Department of Policlinico Casilino with acute coronary syndrome (ACS). In order to identify patients with high cardiovascular risk, we measured, according to current guidelines, Lp(a) value. Results A total of 73 patients (84% males, mean age 47±7 years old) were enrolled from July 2020 to March 2022. Mean Lp(a) level was 50.9± 46.7 mg/dL. High Lp(a) > 50 mg/dL was documented in 31.5 % of patients, while the interim grey zone of elevated Lp (a) (30–50 mg/dL) in 27.4%. Conclusion In our experience, elevated levels of Lp(a) was documented in more than half of patients, presenting with ACS at a relatively young age. This support recent guidelines recommendation to measure Lp (a) at least once in adults, preferably in the first lipid profile, to identify patients with high cardiovascular risk of recurrence. This result focus on the potential use in clinical practice of efficacious Lp(a)–lowering drugs.

Levosimendan increases the sensitivity of the heart to calcium and consequently exerts positive inotropic effects. Levosimendan is indicated in acutely decompensated severe congestive heart failure. We report that levosimendan infusion may induce myocardial ischemia in patients with acute heart failure.