Christina Chrysohoou

Background: Acute effects of pulsed field ablation (PFA) on passive atrial mechanical properties have not hitherto been assessed by reconstruction of pressure–volume relationship using invasive intracavitary pressure measurements. Methods: In a cohort of 38 first‐time atrial fibrillation ablation patients, submitted to pulmonary vein isolation, we studied the effects of PFA and cryoballoon ablation on the left atrial elastic constant and passive elastic chamber stiffness constant, expressing baseline left atrial conditions and quantifying passive left atrial stiffness, respectively. Left atrial pressure was invasively measured immediately pre‐ and post‐procedurally, while volume values were obtained echocardiographically. Results: No differences were noted in passive elastic chamber stiffness constant values, pre‐ and post‐procedurally in either group. No differences were noted between CBA and PFA groups. There were no observable associations between Δ α and Δ b and either AF duration or preprocedural left atrial volume. Conclusions: Based on the above, CBA and PFA demonstrated comparable effects on left atrial mechanical properties in the acute post‐ablation setting.

Aims: Elevated levels of lipoprotein(a) [Lp(a)] and fibrinogen are known risk factors for atherosclerotic cardiovascular disease (ASCVD), and their combined elevation in high-risk individuals may amplify risk. However, the long-term impact of this combination on ASCVD incidence in a primary prevention setting remains unclear. This study sought to examine the association between the combination of Lp(a) and fibrinogen with long-term ASCVD risk, in apparently healthy adults from the general population. Methods and results: A cohort of 3042 CVD-free adults residing in greater Athens, Greece, was recruited in 2002. A 20-year follow-up was conducted in 2022, comprising n = 2169 participants, of which n = 1988 had complete data for cardiovascular disease incidence. Participants were divided into four groups, using a recommended threshold of 30 mg/dL for Lp(a) and the median value of 303 mg/dL for fibrinogen. In the overall cohort, fibrinogen was associated with higher ASCVD risk [hazard ratio (HR) per 10 mg/dL: 1.040, 95%CI:1.009–1.072]. Upon stratification by Lp(a) levels, the significant association was retained and amplified only in individuals with elevated Lp(a) levels (HR 1.083, 95%CI:1.009–1.162) (P for interaction=0.041). Participants with both elevated Lp(a) and fibrinogen levels demonstrated the highest 20-year ASCVD risk (HR 1.904, 95%CI [1.023, 3.547]). Path analysis revealed a mediating role of fibrinogen in the inflammation [i.e. interleukin-6 (IL-6)]–ASCVD risk association, which become more pronounced at higher Lp(a) concentrations. Conclusion: In this general population study, elevated levels of Lp(a) and fibrinogen jointly conferred a higher long-term risk of ASCVD than either marker alone, potentially through the complex involvement of inflammation.

Background: Diagnoses of transthyretin amyloid cardiomyopathy (ATTR-CM) have increased in recent years, with a growing proportion of patients being identified at earlier disease stages. However, temporal trends in ATTR-CM diagnosis and survival during the tafamidis era in the Greek population remain largely unknown. Methods: This retrospective study included 75 patients with ATTR-CM treated with tafamidis. Baseline demographic, clinical, laboratory, and echocardiographic characteristics were assessed, and survival outcomes were subsequently evaluated. Results: Among 75 tafamidis-treated patients, 14 deaths (19%) occurred during a median follow-up of 20 months [IQR 10.0–30.5] with an estimated 30-month survival of 75%. Kaplan–Meier analysis demonstrated significantly poorer survival among patients aged ≥80 years (log-rank p = 0.013), those with NYHA class III–IV (log-rank p = 0.018), and across progressively more advanced NAC stages I–III (global log-rank p < 0.001). In contrast, survival did not differ significantly according to LVEF p = 0.863) or maximal wall thickness ≥15 mm versus p = 0.801). After Holm correction across five comparisons, only NAC stage remained statistically significant (adjusted p < 0.001). Conclusions: In this real-world Greek cohort of patients with ATTR-CM treated with tafamidis, the estimated 30-month all-cause mortality was 25% and more advanced NAC stage was associated with poorer survival.

Background/Objectives: Diet quality is a potentially modifiable determinant of heart failure (HF), yet evidence regarding its long-term association with HF incidence remains limited. This study examined the association between baseline diet quality and 20-year incident HF in the population-based ATTICA cohort. Methods: Among 3042 adults free of cardiovascular disease at baseline (2001–2002), HF status was available for 2159 participants in 2022, of whom 241 (11.2%) developed HF. Diet quality, including the relative contributions of healthy and unhealthy food groups, was assessed using the Global Diet Quality Score (GDQS), derived from a validated food-frequency questionnaire. Logistic regression models were sequentially adjusted for age, sex, body mass index, education, physical activity, smoking burden, hypertension, diabetes, and hypercholesterolemia. Results: HF incidence was 20.7%, 5.1%, and 6.6% among participants with low, intermediate, and high diet quality, respectively (p < 0.001). In the fully adjusted analysis (n = 1973), better overall diet quality was associated with lower odds of HF (odds ratio [OR] per 1-point increment, 0.97; 95% confidence interval [CI], 0.94–0.99). A greater contribution of healthy foods was also inversely associated with HF (OR, 0.96; 95% CI, 0.93–0.98), whereas the unhealthy-food component was not independently associated with the outcome (OR, 1.04; 95% CI, 0.96–1.13). Conclusions: Better diet quality, particularly greater consumption of health-promoting foods, was independently associated with lower 20-year HF incidence in a Mediterranean population.

Heart failure with preserved ejection fraction (HFpEF) represents a heterogeneous clinical syndrome characterized by complex pathophysiological mechanisms and substantial diagnostic and prognostic challenges. Recently, circulating biomarkers have emerged as potential tools for improving risk stratification and disease characterization in this population. Among these biomarkers, soluble suppression of tumorigenicity-2 (sST2) and galectin-3 (Gal-3) have gained particular attention due to their association with myocardial fibrosis, inflammation, and adverse cardiac remodeling. This scoping review aimed to evaluate the current evidence on the diagnostic and prognostic roles of sST2 and Gal-3 in patients with HFpEF. A literature search was conducted in PubMed and ScienceDirect to identify studies investigating the clinical significance of these biomarkers in HFpEF. Titles and abstracts were screened, and eligible studies were assessed through full-text review according to predefined inclusion criteria. Ultimately, 11 studies were included in the qualitative synthesis. Evidence from the available literature suggests that both sST2 and Gal-3 are associated with markers of myocardial fibrosis, inflammation, and disease severity in HFpEF. Elevated circulating levels of these biomarkers have been linked to poorer clinical outcomes, including an increased risk of hospitalization and mortality. However, variability across studies in study populations, biomarker thresholds, and methodological approaches limits the direct translation of these findings into routine clinical practice. Overall, sST2 and Gal-3 appear to hold promise as complementary biomarkers for risk stratification in HFpEF. Nonetheless, further large-scale prospective studies are needed to clarify the clinical utility of these biomarkers and determine the subsequent integration into multimarker strategies for the management of patients with HFpEF.

Cardiovascular (CV) health is influenced not only by biological factors but also by the environments in which people live. The environment comprises interconnected built, living, and social domains that shape health behaviours, psychosocial well-being, environmental exposures, and access to resources. Within this framework, the built environment, the human-made settings that structure daily life, plays a key role in influencing physical activity, dietary behaviours, social interactions, safety, and overall well-being. Neighbourhoods are embedded within historical, legal, political, cultural, and economic contexts that shape the social determinants of health and contribute to CV health. Growing evidence indicates that characteristics of the living environment substantially influence cardiovascular disease (CVD) and related disorders, through multiple pathways. These include access to healthcare, air and noise pollution, availability of healthy foods and green spaces, physical activity, social cohesion, and chronic psychosocial stress. Potential mechanisms include inflammation, oxidative stress, neuroendocrine dysregulation, unhealthy lifestyle behaviours, and persistent stress responses that promote cardiometabolic dysfunction and vascular disease. This expert opinion examines challenges and opportunities related to nutrition, physical activity, environmental quality, community engagement, and occupational as well as social dimensions of the living environment from a public health perspective. This document highlights the importance of designing healthier communities that support CV health and reduce disease burden. Furthermore, neighbourhoods may serve as measurable units for monitoring CVD and broader health outcomes by integrating environmental characteristics with CV metrics, electronic health records, geospatial data, and neighbourhood-level social risk indicators. Addressing environmental determinants across multiple scales supports targeted public health strategies in Europe and globally.

Acute coronary syndrome (ACS) remains a leading cause of cardiovascular morbidity and mortality worldwide. Although traditional cardiovascular risk factors remain central to ACS development, recreational drug use is increasingly recognized as a clinically relevant trigger, particularly in younger patients with fewer conventional risk factors. This narrative review synthesized evidence identified through searches of PubMed/MEDLINE and Scopus up to June 2026, including clinical guidelines, systematic reviews, observational studies, mechanistic investigations, and clinically informative case-based evidence. Cannabis, cocaine, amphetamines, methamphetamine, 3,4-methylenedioxymethamphetamine (MDMA), opioids, lysergic acid diethylamide (LSD), synthetic cannabinoids, and polysubstance use may promote myocardial ischemia and infarction through overlapping mechanisms, including sympathetic activation, coronary vasospasm, endothelial dysfunction, oxidative stress, inflammation, platelet activation, thrombosis, arrhythmogenesis, and myocardial oxygen supply–demand mismatch. Clinical presentation may be typical or atypical and may overlap with intoxication, withdrawal, anxiety, neurological symptoms, or non-cardiac chest pain, making diagnosis challenging. Underreporting of recreational drug use is common, and targeted toxicology screening may improve diagnostic accuracy and risk stratification, particularly in patients younger than 50 years, those with few traditional cardiovascular risk factors, or those presenting with otherwise unexplained ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), coronary vasospasm, arrhythmias, or cardiac arrest. Acute management should generally follow standard ACS guidelines, while considering drug-specific issues such as stimulant-induced vasospasm, sympathetic excess, cautious use of beta-blockers during acute intoxication, and preference for primary percutaneous coronary intervention when fibrinolysis carries increased risk. Long-term care should combine evidence-based secondary prevention with substance-use counseling, addiction medicine referral, cardiac rehabilitation, and behavioural interventions. This review summarizes the pathophysiology, clinical manifestations, epidemiology, treatment considerations, preventive strategies, and knowledge gaps related to recreational drug-associated ACS.

Pulmonary arterial hypertension (PAH) is a progressive and life-threatening condition characterized by elevated pulmonary vascular resistance eventually causing right ventricular failure and premature death. Despite advances in targeted therapies, morbidity and mortality levels remain high, highlighting the need for additional treatment strategies that address the disease’s multifactorial pathophysiology. Attention has recently centred on two pharmacological groups with proven roles in other cardiovascular settings: sodium–glucose cotransporter 2 inhibitors (SGLT2i) and mineralocorticoid receptor antagonists (MRAs). SGLT2 inhibitors have demonstrated robust clinical benefits in heart failure (HF), type 2 diabetes mellitus (T2DM), and chronic kidney disease (CKD), extending survival and reducing hospitalizations. Although their primary actions involve renal glucose and sodium handling, accumulating evidence suggests they may also exert favourable effects on the pulmonary vasculature, endothelial function, and right ventricular performance. In parallel, elevated aldosterone levels have been implicated in vascular remodelling, inflammation, and fibrosis in PAH, suggesting a potential therapeutic role for MRAs. However, the strength and clinical significance of these associations remain under investigation. The aim of this review is to synthesize and critically appraise the current evidence regarding the potential role of SGLT2 inhibitors and MRAs in the treatment of pulmonary arterial hypertension, exploring their mechanistic rationale, preclinical findings, and available clinical data to determine whether these agents may offer additional therapeutic benefit in PAH management.

Background: Cognitive impairment (CI) affects a significant percentage of heart failure (HF) patients, reducing adherence and worsening outcomes. Routine cognitive assessment remains limited. Objectives: To evaluate cognitive assessment practices, identify barriers, and examine associations between knowledge, attitudes, and clinical behaviours among clinicians managing HF patients. Methods: An anonymous cross-sectional survey was distributed to 120 cardiologists across 68 clinics in the Hellenic Heart Failure Clinics Network (May–June 2025). The 13-question survey examined knowledge on cognitive decline, personal opinions on screening, assessment methods, and implementation obstacles. Associations were examined using Pearson’s chi-square. Results: Fifty-one cardiologists completed the survey, corresponding to a response rate of 42.5%. Among respondents 80% reported awareness of the high prevalence of cognitive decline, 14% systematically screened for CI presence. Main barriers reported were lack of time (76%) and inadequate familiarity with assessment tools (50%). Screening frequency was not associated with HF patient volume (χ2 = 4.75, P = .58). Significant correlations were demonstrated between (i) knowledge on CI and frequency of screening (V = 0.37, P = .04); (ii) frequency of screening and support of establishing screening as routine practice (V = 0.50, P < .001); and (iii) frequency of screening and referral of patients to specialists (V = 0.39, P = .007). All respondents expressed interest in further education. Conclusion: There is a gap between awareness of and testing for CI in HF patients, with the latter not being affected by clinicians’ patient load. Since there is universal interest in learning, integrating screening tools into daily routines and creating clear referral pathways may help in addressing this evidence-practice gap.