Lipoprotein(a) (Lp(a)) is a low-density lipoprotein (LDL) cholesterol-like particle bound to apolipoprotein(a). Increased Lp(a) levels are an independent, heritable causal risk factor for atherosclerotic cardiovascular disease (ASCVD) as they are largely determined by variations in the Lp(a) gene (LPA) locus encoding apo(a). Lp(a) is the preferential lipoprotein carrier for oxidized phospholipids (OxPL), and its role adversely affects vascular inflammation, atherosclerotic lesions, endothelial function and thrombogenicity, which pathophysiologically leads to cardiovascular (CV) events. Despite this crucial role of Lp(a), its measurement lacks a globally unified method, and, between different laboratories, results need standardization. Standard antilipidemic therapies, such as statins, fibrates and ezetimibe, have a mediocre effect on Lp(a) levels, although it is not yet clear whether such treatments can affect CV events and prognosis. This narrative review aims to summarize knowledge regarding the mechanisms mediating the effect of Lp(a) on inflammation, atherosclerosis and thrombosis and discuss current diagnostic and therapeutic potentials.

Shock is traditionally classified according to its primary etiology—septic, hypovolemic, obstructive, or cardiogenic—yet these syndromes frequently converge on a common feature: disturbances of cardiac performance, ventricular loading, and tissue perfusion. Despite distinct initiating mechanisms, altered preload and afterload, ventricular interdependence, vascular dysfunction, maladaptive neurohormonal responses, and, in selected states, impaired myocardial contractility may ultimately reduce effective forward flow and tissue perfusion. Echocardiography provides a rapid, noninvasive bedside tool for characterizing these evolving cardiovascular effects. It enables assessment of left and right ventricular function, cardiac filling, preload responsiveness, pulmonary and systemic venous congestion, fluid tolerance, and broader hemodynamic profiles while facilitating recognition of reversible causes such as cardiac tamponade, acute pulmonary embolism, or severe hypovolemia. This allows clinicians to move beyond static etiologic classifications toward a physiology-based assessment of shock. Beyond diagnosis, echocardiography can inform fluid resuscitation and vasoactive or inotropic therapy. Serial assessment also permits evaluation of therapeutic response and evolving hemodynamic phenotypes. This review synthesizes the mechanisms of cardiac involvement across shock syndromes and highlights echocardiography as a unifying tool for their evaluation and management. By integrating pathophysiology, bedside imaging, and hemodynamic treatment, we propose a physiology-based framework that complements traditional shock classification and may improve diagnostic precision and individualized management in critically ill patients.

Introduction: Wearable Activity Trackers (WATs) offer real-time feedback on activity levels. We assessed the impact of WAT usage on physicians’ exercise habits. Methods: Physicians from the Athens Medical Association, Greece (n = 742) responded to a self-administered questionnaire evaluating usage of WAT, demographic characteristics, specialty, and physical exercise habits. WHO guidelines recommend at least 150 min/week of moderate-intensity exercise in all healthy adults. Subjects were divided in Users of WATs (Group A), and Non-Users of WATs (Group B). This is an observational, cross-sectional study. Results: There was no difference in baseline characteristics between the two groups (age, sex, body mass index). WATs were used by 38%. Between Group A and B, there was difference in mean exercise training time (302 ± 304 min vs. 210 ± 268 min, p < 0.001), higher percentage of WHO goal achievement (66.3% vs. 50.7%, p < 0.001), and greater awareness of WHO Guidelines (59.9% vs. 47.4%, p < 0.001). WATs were mostly used by four main specialties, with higher use from Cardiologists: Cardiology (47%), Endocrinology (44%), Surgery (35%) and Internal Medicine (25%), with a p = 0.045. Finally, users of WATs compared to non-users showed higher willingness to reduce body weight (58.5% vs. 48%, p = 0.01), apply dietary restrictions (36.5% vs. 29.6%, p = 0.05), and greater motivation for weekly physical exercise (74.1% vs. 32.4%, p < 0.001); Conclusion: Physicians using WATs demonstrate increased exercise training time, greater awareness of WHO guidelines and a higher propensity to implement dietary restrictions compared to non-users. Variations in WAT usage across medical specialties emphasize the need for targeted interventions to promote physical activity and enhance healthcare professionals’ health.

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD), the hepatic manifestation of cardiometabolic dysfunction, is closely linked to atherosclerosis, heart failure, and adverse cardiovascular outcomes. This review summarizes current evidence on the biological basis of the MASLD–heart axis, with particular emphasis on vascular injury and adverse cardiac remodeling. Methods: A narrative review of contemporary literature was conducted, including experimental studies, observational cohorts, meta-analyses, randomized clinical trials, and current guideline recommendations addressing the cardiohepatic axis. Results: The interaction between the liver and the heart involves interconnected mechanisms, including insulin resistance, lipotoxicity, oxidative stress, chronic inflammation, endothelial dysfunction, and neurohormonal activation. Experimental and translational evidence supports biologically plausible links between MASLD-related metabolic and inflammatory pathways and vascular or myocardial injury, while clinical studies consistently associate MASLD with arterial stiffness, microvascular dysfunction, atherosclerotic disease, adverse cardiac remodeling, heart failure, atrial fibrillation, and cardiovascular events. Several of these associations persist after adjustment for conventional cardiometabolic risk factors, although residual confounding and shared risk determinants limit causal inference. Non-invasive tools, including the Fibrosis-4 (FIB-4) score and transient elastography, may help identify patients at higher risk of advanced fibrosis and cardiometabolic complications. Lifestyle interventions remain the cornerstone of management, while glucagon-like peptide-1 receptor agonists, sodium-glucose cotransporter-2 inhibitors, and fibroblast growth factor-21 analogs may provide combined hepatic and cardiovascular benefits. Conclusions: The cardiohepatic axis is an important component of cardiometabolic disease, linking hepatic dysfunction with vascular and myocardial injury through shared biological pathways. Incorporating hepatic assessment into cardiovascular risk evaluation may support earlier identification of high-risk patients.