Low-density lipoprotein cholesterol (LDL-C) plays a crucial role in the development of atherosclerosis. Statin therapy is the standard treatment for lowering LDL-C in primary and secondary prevention. However, some patients do not reach optimal LDL-C target levels or do not tolerate statins, especially when taking high doses long-term. Combining statins with different therapeutic approaches and testing other new drugs is the future key to reducing the burden of cardiovascular disease (CVD). Recently, several new cholesterol-lowering drugs have been developed and approved; others are promising results, enriching the pharmacological armamentarium beyond statins. Triglycerides also play an important role in the development of CVD; new therapeutic approaches are also very promising for their treatment. Familial hypercholesterolemia (FH) can lead to CVD early in life. These patients respond poorly to conventional therapies. Recently, however, new and promising pharmacological strategies have become available. This narrative review provides an overview of the new drugs for the treatment of dyslipidemia, their current status, ongoing clinical or preclinical trials, and their prospects. We also discuss the new alternative therapies for the treatment of dyslipidemia and their relevance to practice.

The interventional treatment of coronary artery disease (CAD) has undergone significant improvements thanks to technological innovations. Nowadays, percutaneous coronary intervention (PCI) with drug-eluting stent (DES) implantation is the standard of care for the treatment of CAD. Nevertheless, the non-negligible incidence of in-stent restenosis (ISR) and suboptimal results in various anatomical settings has led to the development of drug-coated balloons (DCBs). DCBs are catheter-based balloons whose surface is coated with an anti-proliferative drug (mainly Paclitaxel or Sirolimus) loaded onto the balloon surface with different technologies and dose concentrations. In the beginning, these devices were used for the treatment of ISR showing an excellent efficacy profile in the inhibition of intimal hyperplasia. Subsequently, several studies evaluated their use in other angiographical and clinical contexts such as de novo lesions, small vessel disease, diffuse coronary disease, bifurcation lesions, acute coronary syndromes, high-bleeding risk and diabetic patients. This comprehensive review aims to describe the main DCB platforms on the market, their fields of application with the main supporting studies and their future perspectives.

Background: The prevalence of coronary artery disease (CAD) considerably varies by ethnicity. High-risk populations include patients from Eastern Europe (EEP), the Middle East and North Africa (MENAP) and South Asia (SAP). Methods: This retrospective study aims to highlight cardiovascular risk factors and specific coronary findings in high-risk immigrant groups. We examined the medical records and coronary angiographies of 220 patients from the above-mentioned high-risk ethnic groups referred for Acute Coronary Syndrome (ACS) and compared them with 90 Italian patients (IP) from 2016 to 2021. In the context of high-risk immigrant populations, this retrospective study aims to shed light on cardiovascular risk factors and particular coronary findings. We analyzed the medical records of 220 patients from the high-risk ethnic groups described above referred for ACS and compared them with 90 IPs between 2016 and 2021. In addition, we assessed coronary angiographies with a focus on the culprit lesion, mainly evaluating multi-vessel and left main disease. Results: The mean age at the first event was 65.4 ± 10.2 years for IP, 49.8 ± 8.5 years for SAP (Relative Reduction (ReR) 30.7%), 51.9 ± 10.2 years for EEP (ReR 26%) and 56.7 ± 11.4 years for MENAP (ReR 15.3%); p < 0.0001. The IP group had a significantly higher prevalence of hypertension. EEP and MENAP had a lower prevalence of diabetes. EEP and MENAP had a higher prevalence of STEMI events; SAP showed a significant prevalence of left main artery disease (p = 0.026) and left anterior descending artery disease (p = 0.033) compared with other groups. In SAP, we detected a higher prevalence of three-vessel coronary artery disease in the age group 40–50. Conclusions: Our data suggest the existence of a potential coronary phenotype in several ethnicities, especially SAP, and understate the frequency of CV risk factors in other high-risk groups, supporting the role of a genetic influence in these communities.

Background and Clinical Significance: Early loss of pacing capture after pacemaker generator replacement is an uncommon but potentially life-threatening event, especially in pacemaker-dependent patients. In this setting, device malfunction is often initially attributed to intrinsic lead damage, prompting consideration of invasive lead revision or extraction. However, not all early failures reflect true structural lead dysfunction. Careful interpretation of device interrogation findings, particularly in relation to pacing configuration, may uncover reversible causes and support a more targeted diagnostic and management approach; Case Presentation: A 61-year-old man with complete atrioventricular block presented with recurrent syncope six days after elective pacemaker generator replacement. The electrocardiogram showed absence of effective ventricular pacing with a slow escape rhythm. Device interrogation revealed loss of ventricular capture in bipolar configuration associated with markedly elevated impedance, initially raising concern for lead malfunction. However, switching to unipolar pacing restored effective capture with normal electrical parameters, suggesting preserved lead integrity and prompting reconsideration of the underlying mechanism. Further diagnostic evaluation, including imaging and intraoperative assessment, was therefore undertaken to clarify the cause and guide management; Conclusions: Early pacing failure should not automatically be equated with lead damage. Beyond documenting a reversible lead–header interface problem, this case highlights the diagnostic value of a stepwise approach integrating pacing configuration behavior, targeted imaging, and intraoperative header-independent testing. Such an approach may facilitate rapid localization of reversible defects and help avoid unnecessary lead revision.

Obesity, sleep-disordered breathing (SDB), and epicardial adipose tissue (EAT) are increasingly recognized as interconnected contributors to cardiometabolic and cardiovascular disease, although they are often addressed as distinct clinical conditions. This narrative review aims to integrate current evidence on the reciprocal pathophysiological interactions linking these entities and their contribution to cardiovascular remodeling. A comprehensive literature search up to May 2025 was performed, focusing on clinical, imaging, and mechanistic studies examining obesity, SDB, EAT, and cardiovascular outcomes. Available data indicate that obesity promotes visceral and epicardial fat expansion, systemic inflammation, and altered cardiopulmonary mechanics, thereby facilitating the development of SDB. In turn, intermittent hypoxia and sympathetic activation associated with SDB further aggravate adipose tissue dysfunction and inflammatory activation of EAT. As a metabolically active fat depot in direct anatomical continuity with the myocardium and coronary arteries, EAT contributes to myocardial fibrosis, atrial remodeling, diastolic dysfunction, and coronary atherosclerosis through paracrine inflammatory and neurohumoral pathways. The convergence of these mechanisms delineates a high-risk cardiometabolic phenotype associated with atrial fibrillation, coronary artery disease, and heart failure with preserved ejection fraction. Recognizing obesity, SDB, and EAT as components of an integrated cardiometabolic system may support improved phenotypic stratification and inform more comprehensive approaches to residual cardiovascular risk.