Paradoxical low-flow, low-gradient aortic stenosis (pLF-LG AS) represents a distinct phenotype of severe aortic stenosis characterized by a reduced aortic valve area with low transvalvular gradients despite preserved left ventricular ejection fraction and reduced forward flow. It is associated with concentric remodeling, impaired longitudinal systolic function, and diastolic dysfunction, resulting in reduced stroke volume and potential underestimation of disease severity. This state-of-the-art review synthesizes evidence from registries, observational studies, randomized trial subgroup analyses, guideline recommendations, and mechanistic investigations. Diagnosis requires an integrative multimodality approach combining Doppler echocardiography, low-dose dobutamine stress echocardiography, and computed tomography-based aortic valve calcium scoring to differentiate true-severe from pseudo-severe disease. In symptomatic patients with confirmed severe pLF-LG AS, aortic valve replacement is associated with improved survival, although the magnitude of clinical benefit remains variable. Transcatheter aortic valve implantation represents an effective treatment option in selected patients; however, phenotype-specific comparative data versus surgical valve replacement remain limited. Overall, pLF-LG AS requires accurate diagnostic confirmation and individualized, heart team-guided management to optimize clinical outcomes.

Background ST-segment elevation on electrocardiography is classically associated with acute transmural myocardial ischemia due to coronary artery occlusion and is central to the diagnosis of ST-segment elevation myocardial infarction. However, persistent ST-segment elevation may also reflect nonischemic structural heart disease. Case Summary A 62-year-old woman presented with chest pain and widespread ST-segment elevation with T-wave inversion. Coronary angiography showed no obstructive disease. Echocardiography and cardiac magnetic resonance revealed midventricular hypertrophic cardiomyopathy with systolic midcavity obstruction and a left ventricular apical aneurysm. Nonsustained ventricular tachycardia was documented, and an implantable cardioverter-defibrillator was placed for primary prevention. Discussion This case illustrates a rare, high-risk hypertrophic cardiomyopathy phenotype in which persistent ST-segment elevation mimics acute myocardial infarction. Take-Home Messages Midventricular hypertrophic cardiomyopathy with apical aneurysm can present with persistent ST-segment elevation and T-wave inversion, mimicking myocardial infarction. Electrocardiography is a valuable diagnostic and surveillance tool in this phenotype, as characteristic ST-segment abnormalities may precede or complement imaging findings.

Cardiovascular disease is the leading cause of death in Greece, despite substantial reductions in age-standardized mortality over recent decades. These improvements have been largely confined to older populations, while the burden of cardiometabolic risk remains high. The Greek cardiovascular landscape has also evolved under the combined influence of population aging, the COVID-19 pandemic, persistent socioeconomic pressures, and increasingly stringent European Society of Cardiology targets for lipid and blood pressure control. Traditional determinants, particularly dyslipidemia, hypertension, diabetes, obesity, unhealthy dietary patterns, smoking, and physical inactivity, remain prevalent and frequently suboptimally controlled. Against this background, residual risk and emerging determinants of disease are increasingly recognized as clinically relevant contributors to cardiovascular burden. This narrative review summarizes recent evidence on the role of non-traditional risk factors in the Greek population, including lipoprotein(a), inflammation, metabolic dysfunction-associated steatotic liver disease, chronic kidney disease, chronic obstructive pulmonary disease, sleep disturbances, infections and vaccination, environmental exposures, mental health, and social determinants of health. Overall, the available evidence supports a broader cardiovascular prevention framework that extends beyond conventional risk-factor assessment. Integrating selected non-traditional determinants into clinical practice and prevention policy may improve risk stratification, support individualized care, and help address the evolving cardiovascular burden in Greece.

miR-27a-3p targets several proteins on the coagulation cascade. The potential effect of direct oral anticoagulants (DOACs) treatment on miR-27a-3p expression and their broader regulative effect on anticoagulation is unknown. Fifty-nine atrial fibrillation patients treated with rivaroxaban ( n = 19), apixaban ( n = 27) or dabigatran ( n = 13), were included in the study. miR-27a-3p expression was analyzed at baseline and after 7 days of DOAC therapy by using a predesigned TaqMan assay. Relative quantitation of miR-27a-3p expression was calculated and compared in pooled population and in different sample groups. DOAC therapy did not alter miR-27a-3p expression (0.80 fold-change, p = 0.486, pooled population; 0.839 fold-change, p = 0.706, rivaroxaban; 0.921 fold-change, p = 0.800, apixaban; 0.733 fold-change, p = 0.540, dabigatran). miR-27a-3p expression did not differ between controls and bleeding cases (0.833 fold-change, p = 0.588, baseline). Female patients had a trend towards increased baseline expression (1.564 fold-change, p = 0.177) and reduced expression after DOAC treatment (0.683 fold-change, p = 0.243) compared to male patients. Despite the regulatory role of miR-27a-3p on coagulation cascade, treatment with DOACs did not alter its expression. However, additional studies in different ethnic groups are necessary to fully elucidate the effect, if any, of DOACs on miR-27a-3p expression. Graphical Abstract

Catheter ablation of slow pathway (SP) is the treatment of choice for symptomatic patients with episodes of atrioventricular nodal reentry tachycardia (AVNRT). We sought to evaluate a new technique to identify and ablate SP by using late activation mapping with CARTO 3 (CARTO PRIME V7, Biosense Webster). We obtained Koch triangle 3D activation map in 76 patients (65.8% females, mean age 51.4± 14.4 years) using THERMOCOOL SMARTTOUCH SF ablation catheter (Biosense Webster©, Inc., Irvine, CA, USA). His potential and coronary sinus ostium were accurately marked. During sinus rhythm we generated endocardial voltage gradient and late activation time (LAT) maps. A conventional decapolar catheter was positioned in the CS and a quadripolar on the His bundle. A window of interest (WOI) was set from −200 to +30 ms relatively to P wave using CS ARA (Advanced Reference Annotation). The point where the latest atrial activation was identified at the LAT map, was considered as SP position and was targeted for ablation. The low-voltage bridge was obtained from the voltage gradient map. The mean total time of procedure was 66.4 ± 24.9 minutes and the mean mapping time was 27.1 ± 6.3 minutes. The mean RF ablation time was 73.8 ± 59 seconds and the mean RF applications were 3.7 ± 2.7. The mean ablation index was 374 ± 86. The mean contact force was 7 ± 2.2 grams and the mean resistance drop was 8.6 ± 3.7 Ω. No patient experienced any complications during the procedure, and there was no recurrence during the 12-month follow-up. SP ablation using 3D activation mapping via CARTO3 V7 system is an innovative, safe, effective and fast alternative for AVNRT ablation. The use of this technique allows SP ablation with minimal radiation, a very small number of energy applications and zero complications from conduction system damage, due to its clear mapping and delineation.Late activation and low voltage SP map

INTRODUCTION:Cardiac sarcoidosis (CS) is a complex inflammatory cardiomyopathy resulting from myocardial granulomatous inflammation. Its variable clinical presentation and lack of a single definitive test make diagnosis challenging. CS causes significant morbidity and mortality through conduction abnormalities, ventricular arrhythmias, heart failure (HF), and sudden cardiac death (SCD). This review synthesizes current knowledge on CS epidemiology, pathophysiology, diagnosis, and management. MATERIALS AND METHODS:A comprehensive, non-systematic literature search was performed using PubMed/MEDLINE, Embase, and Google Scholar for English-language articles focusing on publications from January 2010 to May 2025. Original research, systematic reviews, meta-analyses, consensus statements, and guidelines were included. RESULTS:Recent evidence indicates a paradigm shift in CS diagnosis, with advanced cardiac imaging gaining central place in international algorithms. Cardiac magnetic resonance (CMR), 18F-fluorodeoxyglucose positron emission tomography (FDG-PET), and hybrid CMR/FDG-PET have revolutionized CS diagnosis and management. Histological confirmation of sarcoidosis, when pursued, is obtained via extracardiac biopsy; cardiac involvement is then established using clinical and imaging criteria. Endomyocardial biopsy is reserved for select cases. Immunomodulation, primarily corticosteroids, remains the therapeutic cornerstone, with adjunctive steroid-sparing agents and biologics. Implantable cardioverter-defibrillators are indicated in high-risk patients to prevent ventricular arrhythmias and SCD. HF management follows guideline-directed therapy, reserving advanced therapies for CS-related advanced HF. CONCLUSION:CS is "the cardiomyopathy of a thousand faces". International consensus emphasizes advanced imaging and multidisciplinary approaches for timely diagnosis and management. While immunomodulation and device therapy have improved outcomes, knowledge gaps persist regarding optimal treatment strategies. Future research should refine diagnostic algorithms, identify CS-specific biomarkers, and develop optimal and novel therapeutics to improve CS management.

Introduction: Chronic kidney disease (CKD) affects roughly 10% of the global population and significantly increases cardiovascular risk. While renin–angiotensin system inhibitors (RASi) remain a therapeutic mainstay, recent evidence supports the renoprotective value of sodium–glucose cotransporter-2 inhibitors (SGLT2i) and finerenone. This study evaluated the real-world use of guideline-directed medical therapy (GDMT) among patients with cardiorenal disease in Greece and explored factors influencing prescribing patterns. Methods: The Hellenic Cardiorenal Morbidity Snapshots (HECMOS 1 and 2) enrolled all cardiology inpatients across Greece on 3 March, 2022, and 5 June, 2024. Comorbidities and medication data were based on self-report and chart review. CKD patients eligible for SGLT2i and finerenone were identified per guideline criteria. Multivariable logistic regression was used to identify predictors of SGLT2i use. Results: From a total of 923 and 1222 patients enrolled in HECMOS 1 and 2, CKD was present in 26% and 27%, respectively. SGLT2i use prior to hospitalization rose from 15% in HECMOS 1 to 30.4% in HECMOS 2. In HECMOS 1, diabetes mellitus was the strongest predictor of SGLT2i use (OR 12.01, 95% CI 3.31–45.56, p < 0.001), while heart failure predicted use in HECMOS 2 (OR 4.10, 95% CI 1.70–9.88, p = 0.002). Finerenone was prescribed in only 1.7% of eligible patients in HECMOS 2. RASi usage among CKD patients remained stable across both cohorts (42.1% vs. 41.7%), with renal dysfunction showing no impact on prescribing patterns. Conclusions: SGLT2i use in patients with CKD and cardiovascular disease doubled over 2 years, indicating progress in implementing GDMT. However, overall use of disease-modifying therapies remains suboptimal, underscoring the need for further improvement in real-world care.

The mortality rates and the incidence of cardiac remodeling and subsequent heart failure remain high, despite ongoing advancements in the management of patients with ST-segment elevation myocardial infarction (STEMI). Most of the adjunctive therapies aiming to further reduce myocardial infarction (MI) size have failed to apply in daily clinical practice. In this context, new promising therapeutic approaches aiming to enhance myocardial salvage have emerged. Recent studies have suggested that thyroid hormone (TH) may have regenerative effects on ischemic myocardium. Immediate treatment with TH appears to trigger repair and the regeneration process in the injured myocardium, especially in patients with large infarct sizes. The aim of this narrative review is to summarize the most recent advances in the use of TH for salvaging ischemic myocardium following STEMI and place it among the most promising cardioprotective therapies. Emphasis is placed on preclinical and clinical data that highlight the favorable effects of TH in enhancing myocardial recovery and improving outcomes after acute myocardial ischemia.

Direct oral anticoagulants (DOACs) are the standard treatment for thromboembolic protection in atrial fibrillation (AF) patients. Epigenetic modifications, such as DNA methylation and microRNAs, have emerged as potential biomarkers of AF. The epigenetics of DOACs is still an understudied field. It is largely unknown whether epigenetic modifications interfere with DOAC response or whether DOAC treatment induces epigenetic modifications. To fill this gap, we started the miR-CRAFT (Circulating microRNAs and DNA methylation as regulators of Direct Oral Anticoagulant Response in Atrial Fibrillation) research study. In miR-CRAFT, we follow, over time, changes in DNA methylation and microRNAs expression in naïve AF patients starting DOAC treatment. The ultimate goal of miR-CRAFT is to identify the molecular pathways epigenetically affected by DOACs, beyond the coagulation cascade, that are potentially mediating DOAC pleiotropic actions and to propose specific microRNAs as novel circulating biomarkers for DOAC therapy monitoring. We herein describe the study design and briefly present the progress in participant enrolment.

Aims: The impact of newly detected diabetes mellitus (NDDM) on metabolic parameters and extent of myocardial necrosis in patients with acute coronary syndrome (ACS) is not fully explored. We examined the impact of NDDM on cardiometabolic characteristics and myocardial necrosis in ACS patients. Methods: CALLINICUS-Hellas Registry is an ongoing prospective multicenter observational study evaluating the adherence to lipid-lowering therapy (LLT) among ACS patients in Greece. Three groups were created: a) patients with NDDM (abnormal fasting glucose, HbA1c >= 6.5 % and no previous history of DM), b) patients without known DM and HbA1c < 6.5 % (non-DM) and c) patients with prior DM. Results: The prevalence of NDDM among 1084 patients was 6.9 %. NDDM patients had lower HDL-C [38 (32-45) vs 42 (36-50) mg/dL] and higher triglycerides levels [144 (104-231) vs 115 (87-152) mg/dL] compared to non- DM patients (p < 0.05). NDDM patients featured both higher body mass index [29.5 (26.4-34.3) vs 27.1 (24.9-29.9) kg/m(2)] and waist circumference [107 (100-114) vs 98 (91-106) cm] compared to non-DM patients (p < 0.05). In addition, NDDM patients had more extensive myocardial necrosis than patients with prior DM. Conclusions: ACS patients with NDDM have an adverse cardiometabolic profile similar to patients with prior DM and have more extensive myocardial insult.

A 51-year-old female patient presented to the emergency department (ED) with worsening shortness of breath and fatigue over the past two weeks.However, she denied experiencing palpitations and chest pain.The patient has been diagnosed with stage IV anaplastic lymphoma kinase-positive non-small-cell lung cancer (NSCLC) with multiple metastatic deposits in the liver, bone, and central nervous system.Furthermore, she was receiving lorlatinib for the neoplasm, along with rivaroxaban for deep vein thrombosis (DVT) and pulmonary embolism (PE), diagnosed two months before this admission.At that time, a small mobile mass measuring 2.7x2.3 cm in the right atrium (RA) was identified by chest computed tomography (CT) and transthoracic echocardiogram (TTE).It was designated and treated as a thrombus.

Background: Current guidelines recommend a rhythm control strategy in patients with symptomatic atrial fibrillation (AF) while catheter ablation has been shown to be a safer and more ef ficacious approach than antiarrhythmic medications. Methods: HECMOS was a nationwide snapshot survey of cardiorenal morbidity in hospitalized cardiology patients. In this sub-study, we included 276 cases who had a history of AF, particularly on the rhythm strategy, and catheter ablation procedures had been performed before the index admission. Results: Among 276 AF patients (mean age: 76.4 +/- 11.5 years, 58 % male), 60.9 % (N = 168) had persistent AF and 39.1 % (N = 108) had paroxysmal AF. Heart failure was the main cause of admission in 54.3 % (N = 145) of the patients, while 14.1 % (N = 39) were admitted due to paroxysmal AF, 7.3 % (N = 20) due to bradyarrhythmic reasons, and 6.5 % (N = 18) suffered from acute coronary syndrome. Most importantly, heart failure with reduced ejection fraction was present in 76 (27 %) patients. Only 10 patients out of the total (3 %, mean age 59.7 years) had undergone AF ablation while electrical cardioversion had been attempted in 37 (13.4 %) patients. Interestingly, in this AF population with heart failure, 3.6 % (N = 10) had a de fibrillator implanted (4 single-chamber), and only 1.5 % (N = 4) had a cardiac resynchronization therapy de fibrillator (CRT-D). Conclusion: High prevalence of persistent AF was detected in hospitalized patients, with heart failure being the leading cause of admission and main co-morbidity. Rhythm control strategies are notably underused, along with CRT -D implantation in patients with AF and heart failure.

BackgroundThyroid hormone (TH) appears to have a reparative action on the postinfarcted myocardium. This novel action was recently tested in a pilot, randomized, double-blind, placebo-controlled trial (ThyRepair). The present study performed a post-hoc analysis of data from the ThyRepair study to provide further insights into the novel actions of TH on the human postischemic myocardium.MethodsData from 41 patients participating in the ThyRepair study (n = 20 placebo and n = 21 LT3) were included in the analysis. LT3 treatment started after stenting and continued intravenously for 48 h. All patients had cardiac magnetic resonance (CMR) at hospital discharge; left ventricular (LV) ejection fraction (LVEF%), LV end-diastolic volume index (LVEDVi; mL/m2), LV end-systolic volume index (LVESVi; mL/m2), infarct volume (IV), left ventricular mass index (LVMi) as edema index, and microvascular obstruction (MVO) were assessed. Patients were divided into two groups based on the median value of the IV: patients with IV ≤ 20% of the LV (group A) and patients with IV > 20% (group B). CMR measurements at discharge are expressed as mean ± SD.ResultsIn group A, the placebo and T3-treated groups had similar LVEF% (56.8 ± 10.2 vs. 52.2 ± 10.5), LVEDVi (90.9 ± 19.8 vs. 92.8 ± 14.5), and LVESVi (40.8 ± 18.2 vs. 44.9 ± 14.1) at discharge. In group B, LVEDVi and LVESVi were 112 ± 23.8 and 68.3 ± 21.5 for placebo vs. 91.8 ± 18.6 and 49.0 ± 14.0 for the T3-treated group, respectively, p < 0.05. LVEF% was significantly increased in the T3-treated group vs. placebo, 47.3 ± 6.5 vs. 39.9 ± 8.7, p < 0.05. In group B, CMR LVMi was lower in T3-treated patients vs. placebo but did not reach statistical significance (p = 0.1). MVO was 1.95 ± 2.2 in placebo vs. 0.84 ± 0.9 in the LT3-treated group, p = 0.15.ConclusionThe present study suggests that acute LT3 treatment may exert more favorable effects on the recovery of cardiac function in patients with large infarct size. Furthermore, it signals a potential effect of LT3 on myocardial edema and microvascular obstruction. These novel findings merit further investigation in large trials.