Positive airway pressure (PAP) therapy is widely used to manage both acute and chronic respiratory failure and plays an increasingly important role in cardiology, particularly in treating patients with respiratory comorbidities. PAP, including continuous positive airway pressure and noninvasive ventilation, significantly impacts hemodynamics by altering intrathoracic pressure, affecting preload, afterload, and stroke volume. These changes are crucial in conditions such as acute cardiogenic pulmonary edema, where PAP can enhance gas exchange, reduce the work of breathing, and improve cardiac output. PAP reduces the left ventricular afterload, which in turn increases stroke volume and myocardial contractility in patients with left-sided heart failure. However, the role of PAP in right ventricular function and its effects on venous return and cardiac output are critical in the cardiac intensive care setting. While PAP provides respiratory benefits, it must be used cautiously in patients with right heart failure or preload-dependent conditions to avoid adverse outcomes. Additionally, in recent years, the use of PAP has expanded in the treatment of severe obstructive sleep apnea and obesity hypoventilation syndrome, both of which significantly influence cardiovascular events and heart failure. This review provides an in-depth analysis of the hemodynamic effects of PAP in cardiovascular disease, focusing on its impact on ventricular function in both acute and chronic conditions. Evaluating clinical studies, guidelines, and recent advancements offers practical insights into the physiological mechanisms and key clinical considerations. Furthermore, this review aims to serve as a helpful guide for clinicians, assisting in decision-making processes where PAP therapy is applied.

Heart failure (HF) remains a leading cause of morbidity and mortality worldwide. Despite significant advances in pharmacological therapies, responses to treatment vary widely among patients. Growing evidence suggests that genetic factors play a crucial role in influencing individual responses to HF therapies. Genetic variations, including single-nucleotide polymorphisms (SNPs), gene expression profiles, and epigenetic modifications, have been shown to affect drug metabolism, receptor sensitivity, and the molecular pathways involved in HF progression. These genetic determinants may not only predict the efficacy of common therapeutic agents such as angiotensin-converting enzyme inhibitors, beta-blockers, mineralocorticoid receptor antagonists, and sodium-glucose cotransporter-2 inhibitors, but also help identify patients at risk of adverse drug reactions. As personalized medicine continues to advance, a deeper understanding of the genetic basis of drug response in HF could enable more tailored treatment strategies, improving clinical outcomes and minimizing adverse effects. This review explores the current evidence on the genetic underpinnings of response to HF treatment and discusses its potential implications in clinical practice, highlighting current knowledge gaps.

Dyslipidemia is a leading risk factor for cardiovascular diseases. Nutraceuticals for the management of dyslipidemia are gaining growing attention. Derived from food sources, they represent a promising adjunctive or alternative therapeutic option in specific clinical contexts, particularly in individuals with mild dyslipidemia or those who fail to achieve lipid targets despite optimal pharmacological treatment. Bergamot—alongside its lipid-lowering effects—has demonstrated multiple additional properties, including anti-inflammatory, antioxidant, and vascular benefits. While lipid effects are supported by several clinical studies, evidence for vascular and inflammatory pathways is based mainly on preclinical studies. This review summarizes the mechanisms of action and available clinical evidence and outlines potential indications for bergamot use in selected patient subgroups.

Extensive evidence now confirms Lipoprotein(a) [Lp(a)] as a causal, independent risk factor for atherosclerotic cardiovascular disease. Elevated Lp(a) levels are detected in approximately 20% of the global population, positioning it as a major contributor to residual cardiovascular risk. Circulating Lp(a) levels are determined predominantly by genetic factors, so they are largely unresponsive to lifestyle modifications or conventional lipid-lowering therapies. Therefore, multiple international guidelines now endorse a one-time, lifetime measurement of Lp(a), as lowering Lp(a) concentrations is expected to have a positive impact on the reduction of cardiovascular risk. Currently, the therapeutic landscape of Lp(a) lowering drugs is rapidly evolving. Some RNA-based therapies (antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs)) have been demonstrated to reduce plasma Lp(a) concentrations by up to 98% in early-phase clinical trials. The efficacy and safety of these compounds are currently being evaluated in large-scale cardiovascular outcome trials. The results of these studies will be critical in validating the “Lp(a) hypothesis”: specific reduction of Lp(a) levels can lead to a measurable decrease in cardiovascular events. The purpose of this narrative review is to examine and discuss the available evidence on the role of Lp(a) as a risk factor and pharmacological target to provide a practical tool for decision-making in clinical practice.