Abstract A 58-year-old female patient with a medical history of dyslipidemia and pleural tuberculosis and a significant family history of cardiovascular disease, presented to the Emergency Department with a two-week history of dizziness. She denied syncope, angina, heart failure symptoms, or use of any medications. Her family history included a brother with dilated cardiomyopathy with biventricular involvement, who underwent heart transplantation at the age of 40; a first-degree cousin with a history of sudden cardiac death (not autopsied); and both parents with heart failure. Initial evaluation revealed a sinus rhythm electrocardiogram with a heart rate of 40 bpm and a 2:1 atrioventricular block. Transthoracic echocardiography showed preserved global systolic function (left ventricular ejection fraction of 63% by biplane Simpson). The patient was admitted to the Cardiology Department for pacemaker implantation. Given the patient’s relatively young age, significant family history, and symptomatic atrioventricular block without any identifiable secondary cause, further investigation was conducted during hospitalization and follow-up. Autoimmune screening was negative. Cardiac magnetic resonance imaging showed preserved biventricular systolic function, no segmental wall motion abnormalities and a small area of mid-myocardial fibrosis in the basal anterior interventricular septum. Genetic testing in the patient identified a variant of uncertain significance, while subsequent testing in her brother revealed a probably pathogenic gene mutation, both in the Lamin (LMNA) gene. Over a follow-up period of approximately one year and a half, serial echocardiograms showed progressive left ventricular systolic dysfunction. The latest assessment demonstrated a slightly dilated left ventricle with normal wall thickness, abnormal septal motion, and mildly reduced left ventricular ejection fraction (45% by biplane Simpson, 46% by 3D). The patient was referred for cardiac resynchronization therapy – defibrillator implantation. This case describes a 58-year-old woman with significant family history of dilated cardiomyopathy with a probably pathogenic LMNA gene mutation in her brother and sudden cardiac death, who initially presented with symptomatic 2:1 atrioventricular block, requiring pacemaker implantation, followed by progressive left ventricular dysfunction and genetic confirmation of a LMNA mutation, identified per now as variant of uncertain significance. The LMNA gene is associated with dilated cardiomyopathy and conduction system disease, conferring a high risk of sudden cardiac death. This case highlights the importance of a high index of suspicion and timely genetic testing, as well as the correlation with clinical findings, that allow an early diagnosis and tailored management of these patients.

Abstract Introduction Although acute myocarditis is often linked to viral causes, recent studies suggest a predisposing genetic component. Case A 42-year-old woman with a history of hypertension experienced suspected acute myocarditis at age 25, complicated by cardiogenic shock, left ventricular (LV) systolic dysfunction, and complete atrioventricular block (CAVB), requiring inotropes and temporary pacing. She was treated with non-steroidal anti-inflammatory therapy and later corticosteroids, with recovery of LV function and sinus rhythm at discharge. Serological and immunological studies were negative, and she remained asymptomatic without LV or conduction abnormalities. At the time cardiac MRI and endomyocardial biopsy were not performed. There was no family history of sudden cardiac death, cardiomyopathy, or early device implantation. Seventeen years later, after a respiratory infection, she developed exertional fatigue and pleuritic chest pain. On admission, she was stable (118/85 mmHg, afebrile). ECG showed CAVB with ventricular escape at 68 bpm. Echocardiography revealed septal hypertrophy (∼15 mm) and mild global LV dysfunction (LVEF 50%). Laboratory tests showed elevated C-reactive protein 18 mg/L (ref <5), hs-troponin T 1032 pg/ml (ref <14) and NT-proBNP 2457 pg/ml (ref <450). Coronary angiography excluded obstructive disease. She improved with high-dose aspirin; serologies and immunology remained negative. By day 7, she recovered sinus rhythm. Cardiac MRI supported myocarditis, showing mildly dilated LV (End Diastolic LV Volume 100 ml/m²), LVEF 51%, septal hypertrophy (∼14 mm), subtle T2 hyperintensity, and subepicardial/intramural late gadolinium enhancement. Endomyocardial biopsy revealed lymphocytic myocarditis with viral PCR positive for Epstein–Barr virus. Genetic testing showed two variants of uncertain significance: CACNA1C c.76G>A p.(Ala26Thr) and CTNNA3 c.2493G>T p.(Lys831Asn), the latter with potential functional impact. Discussion This case highlights the challenge of differentiating viral myocarditis from an underlying cardiomyopathy. Genetic testing can be decisive and guide management, but often, as here, reveals variants of uncertain significance that do not explain the phenotype and instead raise questions for patient and family follow-up. The variants detected lack sufficient evidence to be considered causative. This underscores the need for long-term surveillance, periodic reassessment of genetic data, and a multidisciplinary approach. Ultimately, both viral and genetic contributions should be considered, with close monitoring to determine whether such episodes represent isolated myocarditis or early inherited cardiomyopathy.

Abstract Left ventricular hypertrabeculation is a heterogeneous phenotype that may overlap with dilated cardiomyopathy and conduction disease. We report a family with a pathogenic NKX2-5 variant, illustrating the role of genetic testing in diagnosis, risk stratification, and screening. The clinical case describes a 39-year-old female with a personal history of atrial septal defect (ASD) surgically repaired at the age of 4. She was referred to our center with a diagnosis of dilated cardiomyopathy and mild left ventricular systolic dysfunction. At the time she was asymptomatic, and physical examination revealed no signs of congestion. Initial investigations included: 12-lead electrocardiogram showing sinus rhythm, first-degree atrioventricular block (PR 335 ms), and complete left bundle branch block; transthoracic echocardiogram demonstrating a dilated left ventricle with trabeculation of the inferior, posterior and lateral walls, with an ejection fraction of 52%; Holter monitoring revealing episodes of second-degree atrioventricular block Mobitz I, nocturnal idioventricular rhythm and non-sustained ventricular tachycardia (NSVT); routine laboratory testing with NT-proBNP of 346 pg/mL. Cardiac magnetic resonance imaging (MRI) was performed for morpho-functional assessment. It showed evident hypertrabeculation of the apical and lateral regions, but did not fulfil the formal criteria for non-compaction phenotype. No focal myocardial fibrosis or necrosis was identified. Given the conduction disturbances, arrhythmic episodes, congenital heart disease and imaging findings, genetic testing was pursued. A likely pathogenic variant in the NKX2-5 gene was identified. Variants in this gene are well described in association with atrial septal and conduction defects, often accompanied by cardiomyopathies, including dilated cardiomyopathy and cardiomyopathy with left ventricular hypertrabeculation. The diagnosis was therefore established as dilated cardiomyopathy with a phenotype of left ventricular hypertrabeculation, associated with congenital heart disease, conduction system disorder and ventricular arrhythmia. Prognostic-modifying therapy was initiated with an SGLT2 inhibitor and an MRA antagonist. After multidisciplinary discussion involving imaging cardiologists, electrophysiologists and geneticists, implantation of a subcutaneous implantable cardioverter-defibrillator (S-ICD) for primary prevention was performed, given the described risk of sudden death in patients carrying this mutation. Familial screening was conducted: one daughter tested positive for the same variant and already demonstrates a phenotype of left ventricular hypertrabeculation, documented by echocardiography and cardiac MRI fulfilling non-compaction criteria, as well as conduction abnormalities on Holter monitoring. Despite being asymptomatic, she is under specialized follow-up. This case highlights the importance of genetic testing not only in diagnosing cardiomyopathies but also in guiding therapy and preventive strategies. The identification of a pathogenic NKX2-5 variant had direct implications for management, including the decision to implant an S-ICD for primary prevention and to initiate family screening, underlining the relevance of precision medicine in inherited cardiomyopathies.

Abstract Background Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a disorder that predisposes individuals to ventricular arrhythmias and sudden cardiac death. When medical therapy is inadequate, catheter ablation, including epicardial ablation, can be an effective treatment. This case describes successful epicardial ablation of ventricular tachycardia (VT) in an 18-year-old male with biventricular ARVC. Case Report An 18-year-old male, previously healthy and active in sports, had a syncopal event in September 2021. One week later, during exercise, he had pre-syncope with palpitations, which resolved after 5 minutes. Initial assessment revealed global hypokinesia of the left ventricle and right ventricular dysfunction on echocardiography. Holter monitoring under bisoprolol therapy showed frequent polymorphic PVCs (4875 events). Cardiac MRI revealed severe biventricular dilation with LVEF of 42% and RVEF of 34%. Myocardial edema was noted in the right ventricle, especially in the mid-inferior septum, along with extensive late gadolinium enhancement on the anterior-lateral and inflow regions of the left ventricle, distal anterior segment, and right ventricle (inferior and lateral walls), sparing the subendocardial layer, consistent with biventricular ARVC. Genetic testing was negative, and the patient was treated with ramipril and bisoprolol. In January 2022, sustained monomorphic VT was documented, and he was started on amiodarone, with an implantable cardioverter-defibrillator (ICD) placed for secondary prevention. Device monitoring showed stability, but in March 2024, pre-syncope recurred, and non-sustained VT was detected by ICD interrogation, despite maximum titration of bisoprolol and amiodarone therapy. On October 22, 2024, the patient underwent epicardial VT ablation at Hospital de Santa Maria. The procedure successfully eliminated the arrhythmic focus, and amiodarone dosage was reduced. Since the procedure, the patient has remained asymptomatic, with no recurrence of VT. Conclusion Epicardial ablation is an effective treatment for refractory VT in biventricular ARVC. It can reduce the arrhythmic burden and improve clinical outcomes when medical therapy fails.

Abstract Genetic characterization in dilated cardiomyopathy (DCM) can be decisive for therapeutic management and prognosis definition. We report a case of a 54-year-old woman with a history of complete left bundle branch block (LBBB, QRS 160ms), identified in 2016. At that time, a transthoracic echocardiogram (TTE) revealed mild left ventricular (LV) dysfunction, and bisoprolol 2.5mg/day was initiated. In 2019, she underwent a myocardial perfusion scintigraphy, which was negative for myocardial ischemia. In January 2021, she presented to the emergency department (ED) with palpitations. The initial ECG showed regular wide-complex tachycardia with LBBB pattern and a heart rate of 202 bpm, interpreted as supraventricular tachycardia (SVT) with aberrant conduction. Pharmacological cardioversion was performed, restoring sinus rhythm (SR), and she was referred to the Arrhythmology Consultation At the consultation in March 2021 , the family history was revealed: her mother had LV dilation, and her mother, maternal aunt, and maternal cousin had pacemaker implantation at ages 44, 60, and 54, respectively. The ECG showed SR with LBBB (QRS 200ms), and the TTE showed mild LV dilation, intraventricular (IV) dyssynchrony, and a left ventricular ejection fraction (LVEF) of 45–50%. Prognosis-modifying therapy was initiated, and an electrophysiological study was performed, which did not induce any supraventricular or ventricular arrhythmias. A cardiac magnetic resonance imaging (CMR) performed in 2022 showed mild LV dilation, global hypokinesia, and IV dyssynchrony, with LVEF of 40% and no late gadolinium enhancement. Follow-up showed recovery of LVEF and absence of arrhythmic events. In November 2024, genetic testing was requested when she began follow-up in the Cardiomyopathies Consultation. In January 2025, she returned to the ED with palpitations. A regular SVT with aberrant conduction was identified and chemically cardioverted to SR. Over the following 48 hours, she had paroxysmal episodes of atrial fibrillation and atrial tachycardia. Initial treatment with amiodarone was chosen. At discharge, LVEF was estimated at 50–55%, and a CMR was requested (pending). Genetic testing identified a likely pathogenic variant, c.3010_3022delTGCATTGCCACCC; p.(Cys1004Profs*136), in heterozygosity, in the SCN5A gene, previously reported in the ClinVar database. This genetic variant leads to the formation of a premature termination codon, which may result in a truncated, non-functional protein. This clinical case highlights the relevance of an integrative approach in DCM, emphasizing the critical role of genetic testing in understanding clinical manifestations. Variants in the SCN5A gene, classically associated with supraventricular arrhythmias, conduction system disease, and Brugada syndrome, were first linked to DCM in 2004. Subsequent studies identified these variants in approximately 1.7% of cases, often associated with SV arrhythmias and conduction system disturbances.

BackgroundTransradial access (TRA) is increasingly preferred over transfemoral access (TFA) for coronary procedures due to its safety profile. However, uptake varies across clinical settings, particularly in complex and high-risk patients.ObjectiveTo assess arterial access site utilization (TRA vs TFA) and associated clinical and procedural factors in patients undergoing coronary procedures performed by a single operator at a tertiary center.MethodsWe conducted a retrospective review of 250 patients who underwent coronary procedures between September 2024 and February 2025, all performed by a single operator. Demographic, clinical, and procedural data were analyzed to evaluate factors associated with arterial access choice. Logistic regression models were used to determine predictors of access site.ResultsTFA was used in 52.8% and TRA in 47.2% of procedures. TRA was more common in stable patients and for diagnostic angiography (68% vs 32%), while TFA was preferred in emergencies, LV dysfunction, and complex multivessel disease. Independent predictors of TFA included older age (OR 1.021; p = 0.049), mild/moderate LV dysfunction (ORs 2.93 and 3.16, respectively), and prior CABG (p = 0.01). TRA was associated with fewer complications and was never used in unstable patients. Access site choice was also significantly associated with coronary disease burden and treated vessel complexity.ConclusionDespite global trends favoring TRA, TFA remains predominant in high-risk and complex cases in our setting. Tailoring access strategies based on patient risk and procedural complexity remains essential.

BackgroundAsymptomatic left ventricular systolic dysfunction (LVSD) is a well-established precursor of overt heart failure (HF), yet it often remains undiagnosed in the general population. Artificial intelligence–enabled electrocardiogram (ECG) analysis offers a scalable approach for early detection.ObjectivesThe purpose of this study was to evaluate the diagnostic performance of an artificial intelligence–enabled ECG model (AiTiALVSD) for identifying asymptomatic LVSD in a large health screening population.MethodsIn this retrospective, single-center study, we evaluated the AiTiALVSD model among 40,713 self-referred adults who underwent a total of 60,711 ECG-transthoracic echocardiography (TTE) pairs between 2011 and 2023. LVSD was defined as a left ventricular ejection fraction ≤40%. Model discrimination was assessed using the area under the receiver-operating characteristic curve (AUROC) and the area under the precision–recall curve (AUPRC), and diagnostic performance metrics were compared with established HF risk scores.ResultsAmong 60,711 ECG–TTE pairs, 32 cases (0.054%) met the criteria for LVSD. The AiTiALVSD model demonstrated excellent discrimination (AUROC 0.973; AUPRC 0.328), with a sensitivity of 90.6%, specificity of 99.4%, positive predictive value of 7.7%, and a negative predictive value of 100%. Established HF risk scores, including the MESA (Multi-Ethnic Study of Atherosclerosis) 5-year HF score and Pooled Cohort Equations to Prevent HF score, showed inferior discrimination (AUROC: 0.696 and 0.672, respectively). The MESA score was not designed to detect prevalent LVSD and was calculated without natriuretic peptide data, which may have disadvantaged its performance in this comparison. Simulation analyses suggested that approximately 1,841 ECGs and 13 confirmatory TTEs would be required to detect one case of LVSD.ConclusionsIn a real-world screening population with an extremely low prevalence of LVSD, the AiTiALVSD model demonstrated high diagnostic accuracy, supporting its potential role as a rule-out screening tool for HF prevention. Prospective validation is warranted.

BACKGROUNDAn echocardiogram is an essential tool in the evaluation of potential kidney transplant recipients (KTRs). Despite cardiac clearance, potential KTRs still have structural and functional abnormalities. Identifying the prevalence of these abnormalities and understanding their predictors is vital for optimizing pre-transplant risk stratification and improving post-transplant outcomes.AIMTo determine the prevalence of left ventricular hypertrophy (LVH), left ventricular systolic dysfunction (LVSD), diastolic dysfunction (DD), pulmonary hypertension (PH), and their predictors, and to assess their impact on graft function in pre-transplant candidates.METHODSThe study included all successful transplant candidates older than 14 who had a baseline echocardiogram. Binary logistic regression models were constructed to identify factors associated with LVH, LVSD, DD, and PH.RESULTSOut of 259 patients, LVH was present in 64% (166), 12% (31) had LVSD, 27.5% (71) had DD, and 66 (25.5%) had PH. Independent predictors of LVH included male gender [odds ratio (OR): 2.51; 95%CI: 1.17–5.41 P = 0.02], PH (OR = 2.07; 95%CI: 1.11–3.86; P = 0.02), DD (OR: 2.47; 95%CI: 1.29–4.73; P = 0.006), and dyslipidemia (OR = 1.94; 95%CI: 1.07–3.53; P = 0.03). Predictors for LVSD included patients with DD (OR = 3.3, 95% CI: 1.41–7.81; P = 0.006) and a family history of coronary artery disease (OR = 4.50, 95%CI: 1.33–15.20; P = 0.015). Peritoneal dialysis was an independent predictor for DD (OR = 10.03; 95%CI: 1.71-58.94, P = 0.011). The presence of LVH (OR = 3.32, 95%CI: 1.05–10.55, P = 0.04) and mild to moderate or moderate to severe mitral regurgitation (OR = 4.63, 95%CI: 1.45–14.78, P = 0.01) were significant factors associated with PH. These abnormalities had no significant impact on estimated glomerular filtration at discharge, 6 months, 1 year, or 2 years post-transplant.CONCLUSIONSignificant echocardiographic abnormalities persist in a potential transplant candidate despite cardiac clearance, although they don’t affect future graft function. Understanding the risk factors associated with these abnormalities may help clinicians address these factors pre- and post-transplant to achieve better outcomes.

Left ventricular (LV) dysfunction is a known risk factor for adverse outcomes in patients with repaired tetralogy of Fallot (rTOF). While cardiovascular magnetic resonance (CMR) is the reference standard for LV assessment, two-dimensional echocardiography (2DE) remains the most accessible tool for surveillance. The accuracy of commonly used 2DE methods, Simpson's biplane (SiBP) and 5/6 area-length (AL), in the setting of right ventricular (RV) dilation and altered interventricular septum configuration remains uncertain. We conducted a retrospective analysis of pediatric patients with rTOF seen between 2013 and 2023 who underwent both CMR and 2DE within a 90-day interval. Patients were excluded if an intervention occurred between studies. LV end-diastolic volume (EDV), end-systolic volume (ESV), and ejection fraction (EF) were measured using SiBP and AL methods and compared to CMR values. Agreement was compared using standard agreement metrics, with subgroup analyses stratified by RV dilation severity. 2DE reproducibility was assessed using intraclass correlation coefficient (ICC). Of 154 patients (2013-2023), 62 met inclusion criteria based on image quality. Median age at CMR was 15 years, with median indexed RVEDV of 137 mL/m2. Both 2DE methods underestimated LVEDV and LVEF compared to CMR, with SiBP method performing slightly worse than AL (LVEDV percent error: 19% vs. 4%; LVEF percent error: 8% vs. 6%). Increasing RV dilation was associated with worsening percent error for LVEDV but not EF (p ≤ 0.04). Both techniques showed excellent reproducibility. In pediatric patients with rTOF, the AL method showed slightly better agreement with CMR than SiBP for LVEDV and was comparable for LVEF. These findings indicate that the AL method is a practical alternative for LV assessment in rTOF despite altered LV geometry. Increasing RV dilation adversely affects LV volume assessment by 2DE. This study underscores the importance of CMR for LV assessment in rTOF.

Pulmonary hypertension (PH) is a group of diseases characterized by progressive increase in pulmonary vascular resistance, which leads to development of right ventricular failure and an unfavorable prognosis of life. There are 5 groups in the clinical classification, mainly based on the cause and pathophysiological changes in the pulmonary vessels. PH in patients with chronic kidney disease (CKD) is a common and severe complication and belongs to group 5 in the classification. PH is diagnosed in 21 % of patients with CKD who are not on dialysis and in 50–60 % of patients with end-stage kidney disease. On the other hand, development of CKD in patients with pulmonary hypertension doubles the risk of mortality, and with end-stage CKD it triples. In most patients in this group, the main causes of PH are volume overload and left ventricular dysfunction. However, many other factors both enhance and offset the effect of volume overload on PH. These factors include the effects of vascular access for dialysis, anemia, respiratory disorders and hypoxemia, inflammation, and changes in mineral metabolism. In addition, CKD can directly affect the blood vessels of the lungs through the action of nitric oxide, endothelin-1, prostacyclin. Catheterization of the right heart, as the basis for the diagnosis of PH, provides insight into the potential hemodynamic profile of pulmonary hypertension associated with CKD. The article summarizes current data undelying new theoretical mechanisms of pathogenesis of PH associated with CKD.

Background: Speckle tracking echocardiography (STE) is a well-established tool in human cardiology for detecting subtle myocardial dysfunction using strain indices. In cats with hypertrophic cardiomyopathy (HCM), STE has been applied in several studies and has identified myocardial deformation abnormalities. This study aimed to identify sensitive echocardiographic markers of myocardial dysfunction in cats with HCM by comparing global strain and strain rate parameters with those of healthy cats. Methods: Sixty cats were examined, including 31 healthy controls and 29 HCM-affected cats. Echocardiographic assessments included global circumferential strain (GCS), global radial strain (GRS), global longitudinal strain (GLS), their corresponding strain rates (GCSR, GRSR, and GLSR), left atrial ejection fraction (LAEF), and atrial reservoir strain (RS). Results: GLS and GRS were significantly lower in HCM cats than in controls, while GCS showed no significant difference. Among strain rate parameters, only GRSR was significantly reduced in the HCM group. Additionally, both LAEF and RS were markedly decreased, suggesting atrial dysfunction associated with HCM. Conclusions: These findings indicate that GLS and GRS are reliable indicators of left ventricular dysfunction in feline HCM and that GRSR may offer additional insight into myocardial deformation dynamics. Overall, STE provides a useful, non-invasive tool for improving the diagnosis and clinical evaluation of feline HCM.

Left ventricular reverse remodeling (LVRR) is a key objective of contemporary heart failure (HF) therapies and is characterized by reversal of left ventricular (LV) dilation and dysfunction. To report the incidence and clinical impact of early (30-day) LVRR patients with primary (PMR) and secondary mitral regurgitation (SMR) treated with mitral transcatheter edge-to-edge repair (M-TEER), and to identify independent associations with early LVRR. The EXPANDed cohort includes 2205 patients treated with M-TEER from the EXPAND and EXPAND G4 studies. Patients were classified as having early LVRR if they demonstrated a >10% reduction in LV dimension or volume from baseline to 30 days. All LV measurements were assessed by independent echocardiographic core laboratories. Among 527 SMR patients, 338 patients (64.1%) experienced early LVRR after M-TEER. At 1 year, SMR patients with early LVRR had significantly lower rates of death or HF hospitalizations compared to those without (early LVRR: 24.7% vs no early LVRR: 35.9%, p=0.009), despite similar MR reduction (both ≥93% in both groups) and comparable improvements in functional status (NYHA≤II ≥78%) and quality of life (∼20-points improvement per KCCQ-OS). Independent associations with early LVRR included hypertension (OR=1.96, p=0.004), absence of prior cardiac surgeries (OR=0.51, p=0.002), and smaller LV end-systolic volume (OR=0.81, p=0.002).Among 536 PMR patients, 391 (73.0%) experienced early LVRR at 30 days. At 1 year, PMR patients with early LVRR group had similar clinical (composite all-cause mortality or HF hospitalization: early LVRR: 14.5% vs no early LVRR: 17.1%, p=0.47) and symptomatic outcomes (≥83% NYHA≤II; ∼19-point improvement per KCCQ-OS) compared to those without. However, among PMR patients with dilated ventricles, early LVRR group was associated with significantly lower all-cause mortality (early LVRR: 3.8%, no Early LVRR: 14.0%, p=0.028). Regardless of etiology, most patients experienced early LVRR after M-TEER with significant MR reduction and symptom relief. In SMR patients, early LVRR was associated with lower rates of HF hospitalization and death.

The purpose is to study the prevalence of coronary heart disease and the structure of rhythm disturbances in overweight and obese men of working age, as well as to establish the relationship between the presence of arrhythmias and coronary heart disease, depending on various clinical, laboratory and instrumental risk factors. Material and methods . The study included 184 male patients aged 25 to 64 years [44.4 ± 8.0] who applied for routine medical examination and treatment. The patients were divided into 3 groups depending on body mass index (BMI), followed by a comprehensive clinical, laboratory and instrumental examination and analysis of the results in groups. Statistical processing was performed using parametric and nonparametric analysis methods on a personal computer using statistical programs in the environment Exel 97.0 and Statistica for Windows 6.0. The differences were considered statistically significant at p < 0.05. Results . Three groups of patients were examined depending on the BMI value: group I — 40 people with normal body weight (BW), average BMI of 23.3 ± 1.3 kg/m 2 ; group II — 46 people with excess BW, average BMI of 27.3 ± 1.5 kg/m 2 ; group III — 98 people with obesity 1–3 degrees, average BMI 34.9 ± 5.0 kg/m 2 . It was found that an increase in BW is associated with an increase in the frequency of coronary artery disease (CAD): with normal BW — 10% of patients had CAD, with excessive BW — 50.0%, with obesity — 58.2% (I–II p < 0.001; I–III p < 0.001; II–III p < 0.604), and in the group of patients with CAD was not observed before the age of 35, among patients aged 35-50 years, its frequency was 23.9%, over 50 years-52.9% (pχ 2 < 0.001). It has been shown that the increase in BW is accompanied by a statistically significant increase in the frequency of paired supraventricular extrasystoles ( SVES), ventricular extrasystoles ( VES) > 200 per day, allorhythmic VES and atrial fibrillation (AF). Moreover, the risk of arrhythmias, depending on BMI, increases only with associated CAD, the presence of which significantly increases the relative risk (RR) of VES in general by 3.78 times (p < 0.001), high-grade VES by 2.18 times (p < 0.002), frequent VES by 3.3 times (p = 0.017), allorhythmic VES by 4.13 times (p = 0.007). In the development of VES, such potentiating factors in the study group may play a role as: left ventricular hypertrophy (LVH) (p = 0.038), LV diastolic dysfunction (p = 0.032), low serum high density lipoprotein cholesterol (HDL) (p = 0.029), as well as an exceeding the reference values content of adiponectin (А), which directly correlated with the daily number of VES (r = +0.34, p = 0.043). Conclusion . There is a relationship between increased BW and the frequency of arrhythmias such as SVES, VES, allorhythmic VES and AF as the age of patients increases. However, this pattern is peculiar only to persons with CAD, the presence of which in case of obesity and excessive BW plays the role of a significant risk factor for the development of ventricular arrhythmias, which has not been revealed with respect to supraventricular (AF, SVES) rhythm disturbances. Among the risk factors associated with the development of ventricular arrhythmias in CAD and obesity, left ventricular diastolic dysfunction (LVDD), left ventricular hypertrophy (LVH), low serum high density lipoprotein cholesterol (HDL) and hyper adiponectinemia should be noted.

Comparative study of lead placement in the right ventricular apex vs. right ventricular outflow tract: effects on left ventricular systolic dysfunction, dilatation, and myocardial performance - a single-center experience

There are limited data on mortality in patients with moderate mixed aortic valve disease (MAVD), defined as the combination of moderate aortic stenosis (AS) and moderate aortic regurgitation (AR). Consequently, current guidelines lack specific recommendations for aortic valve replacement (AVR) in this population. This study aims to compare survival between moderate MAVD and isolated severe AS or severe AR, and to evaluate the impact of symptoms or left ventricular ejection fraction (LVEF) < 50%, as current criteria for AVR in severe AS or AR. Overall, 1926 patients were included from four centers: 527 with moderate MAVD, 413 with severe AR, and 986 with severe AS. The primary endpoint was all-cause mortality. Over a median follow-up of 7.2 (interquartile range 3.4-11.3) years, 748 patients died. After adjusting for clinical and echocardiographic variables (including New York Heart Association [NYHA] class, LVEF < 50%, and AVR as time-dependent covariate), moderate MAVD patients showed 10-year survival similar to severe AS but worse than severe AR (62%, 55%, and 79%, respectively; P < .001). Symptomatic moderate MAVD patients showed adjusted mortality comparable to symptomatic severe AS, while asymptomatic moderate MAVD patients had adjusted mortality similar to severe AR (symptomatic and asymptomatic). Moderate MAVD patients with LVEF < 50% had adjusted mortality comparable to severe AS with LVEF < 50%, while those with LVEF ≥ 50% showed mortality similar to severe AR (regardless of left ventricular dysfunction). In moderate MAVD, the presence of symptoms or LVEF < 50% is associated with increased mortality, comparable to isolated severe AS under similar conditions. Therefore, patients with moderate MAVD should benefit from AVR in the presence of symptoms or left ventricular dysfunction.

Type A aortic dissection (TAAD) is a life-threatening condition that often presents diagnostic challenges, particularly when mimicking acute myocardial infarction (AMI). This case report describes a 31-year-old male with a history of fever and no cardiovascular history who presented with acute chest pain and rapidly developed hemodynamic instability. Initial assessments revealed mild aortic regurgitation (AR) and ascending aortic dilation but no aortic dissection was reported. ECG showed ST-segment changes, yet coronary angiography ruled out obstructive coronary disease. Serial daily echocardiograms demonstrated rapid progression of AR from mild to severe within 72 h, accompanied by worsening left ventricular dysfunction. Reassessment of aortic CT confirmed TAAD with left main coronary artery involvement. Different elements of his presentation suggested possible other diagnoses, including TAAD, AMI and myocarditis. We discuss how evaluating these other diagnostic possibilities led to the correct diagnosis. This case underscores the diagnostic pitfalls of TAAD masquerading as AMI, it demonstrates the need to consider aortic dissection in patients with AMI and/or emerging diastolic murmurs of AR.

Sepsis remains a leading cause of mortality, and optimizing treatment is challenging due to patient heterogeneity. Identification of cardiac phenotypes may inform precision medicine approaches and guide resuscitation. We performed a clustering analysis of patients with sepsis using echocardiographic data without using any a priori definitions of cardiac dysfunction or outcomes to establish the subgroups. This was a retrospective cohort study of patients admitted to the hospital with sepsis at a single academic center. Patients were identified using sepsis-related ICD codes, and those who had echocardiogram performed within 14days of admission underwent chart review to ensure sepsis-3 criteria were met. Those with preexisting heart disease were excluded. Clustering by echocardiographic variables was performed using latent profile analysis. Clinical features such as patient characteristics, laboratory studies, sepsis source, and outcomes were compared across the clusters. There were 2,071 patients included in the analysis. Our cluster analysis yielded five phenotypes: cluster 1, elevated mean E/e' 24.5 (SD 9.6); cluster 2, reduced ejection fraction, mean 33.1% (SD 10.6), and cardiac index 2.6 L/min/m2 (SD 0.9); cluster 3, right ventricular dilation with right ventricular basal diameter 4.5cm (SD 0.9) and elevated tricuspid regurgitation gradient 60.0mmHg (SD 13.5); cluster 4, hyperdynamic with mean left ventricular ejection fraction 75% (SD10.9) and mean cardiac index 6.6 L/min/m2 (SD 2.6); and lastly cluster 5, normal echocardiographic parameters. Group 3 had the highest mortality compared to the normal group (36.9% vs. 19.6%, p = 0.002), with an odds ratio of 2.3 (95%CI 1.4-3.9). Using an unsupervised clustering analysis, we identified five phenotypes of cardiac function in sepsis based on commonly recorded echocardiographic data: diastolic dysfunction, left ventricular systolic dysfunction with low cardiac index, right ventricular dilation with elevated tricuspid regurgitation gradient, hyperdynamic cardiac function, and normal. The right ventricular dilation group had the highest mortality. Future research should explore mechanisms and potential treatment implications for these groups.

Sepsis, the leading cause of death among critically ill patients worldwide, can induce sepsis-induced cardiomyopathy (SICM), which is characterized by reversible acute impairment of biventricular systolic and diastolic functions. SICM has a high incidence in sepsis patients and significantly increases mortality, and it has emerged as one of the key factors contributing to death in septic shock.[1] The pathological manifestations of SICM are highly heterogeneous, encompassing various forms such as left ventricular systolic dysfunction and diastolic dysfunction, which pose significant challenges to early identification and treatment. Fluid resuscitation serves as the cornerstone of sepsis treatment, yet there remains ongoing controversy regarding its optimal volume and timing.[2] Meanwhile, mechanical circulatory support technologies such as venoarterial extracorporeal membrane oxygenation (VA-ECMO) have been successfully applied in refractory septic shock.[3] These 2 approaches exert a synergistic effect based on complementary hemodynamic regulation mechanisms. Fluid resuscitation optimizes preload to improve cardiac filling while mechanical support directly replaces cardiac pump function to reduce afterload. This bidirectional regulation is particularly crucial in patients with mixed shock (septic combined with cardiogenic) as it helps resolve the contradiction between fluid resuscitation and diuretic therapy.[4] In current clinical practice, controversies including the lack of individualized volume standards for fluid resuscitation, no consensus on the timing of mechanical support intervention, and difficulties in balancing fluid administration and diuresis in mixed shock states highlight the evidence gap in this field and the urgency for further research. The pathogenesis of SICM involves multiple molecular abnormalities, such as the release of inflammatory mediators, mitochondrial dysfunction, and calcium homeostasis imbalance. Mechanisms like toll-like receptor-mediated pyroptosis further exacerbate myocardial injury, ultimately leading to hemodynamic changes, including reduced cardiac output and ventricular dilatation.[5] The hemodynamic effects of fluid resuscitation exhibit a double-edged sword property. During the initial phase, fluid infusion increases preload to enhance cardiac output, but excessive resuscitation can exceed the compensatory range of the Frank–Starling curve. This not only aggravates myocardial oxygen consumption and interstitial edema but may also worsen right heart dysfunction.[2] Among mechanical circulatory support modalities, VA-ECMO exerts a compensatory role by maintaining systemic perfusion pressure, reducing cardiac workload, and protecting end-organ perfusion. It is more suitable for patients with biventricular dysfunction compared with venovenous-ECMO, though it may also introduce new challenges, such as increased left ventricular afterload.[6] Evidence-based studies indicate that lactated Ringer’s solution may be superior to normal saline for initial resuscitation.[7] After the implantation of mechanical circulatory support devices, dynamic indicators such as stroke volume variation should be used to assess fluid responsiveness, and hemodynamic parameters should be interpreted in conjunction with a multiparameter monitoring system.[8] Treatment timing directly affects prognosis. Early fluid resuscitation within 8 hours of onset can improve mortality, but large-volume resuscitation may increase risks when mechanical ventilation resources are limited. The association between SICM and mortality, as well as its dynamic changes, also needs to be incorporated into prognostic assessments.[9] Currently, the treatment of SICM still lacks high-quality evidence-based individualized protocols. Key issues such as the optimal support strategy for different hemodynamic subgroups and the balance between fluid administration and diuresis in mixed shock states remain unclear.[4] Precision therapy guided by biomarkers is limited by insufficient mechanistic research. For instance, the mechanisms underlying the impact of diabetes on SICM have not been fully elucidated.[10] Monitoring technologies face multiple bottlenecks. The predictive value of traditional parameters decreases during mechanical circulatory support, and there is a lack of bedside quantitative tools for assessing microcirculatory function.[8] Multicenter studies have poor result comparability due to inconsistent definitions of SICM and varied resource accessibility, and most evidence comes from single-center studies with insufficient follow-up on long-term cardiac function recovery.[11] Future efforts should focus on developing intelligent decision support systems that integrate multimodal data to resolve contradictions in mixed shock treatment and optimize the judgment of optimal intervention timing for mechanical support. They should also explore biomarker combinations that distinguish pathological subtypes to guide the prediction of fluid resuscitation response and sequential application of treatments. Additionally, studies on the timing optimization of mechanical support and pharmacotherapy are needed to clarify the microcirculatory effects of different support modalities and the principles of fluid management after device implantation.[2] At the same time, unified diagnostic criteria for SICM should be established to reduce research heterogeneity. Conflict of interest statement The authors declare no conflict of interest. Author contributions Meng C and Sun J conducted searches of the scientific literature and developed the draft of the manuscript. Miao G provided contributions to the conception and design of the study, in addition to revising the manuscript with a focus on critical intellectual content. All authors reviewed and approved the final version of the manuscript. Funding This study was funded by the National Key R&D Program of China (2023YFC3011904). Ethical approval of studies and informed consent Not applicable. Acknowledgements None.

Background: Late cardiotoxicity is a recognized complication in survivors of childhood cancer treated with potentially cardiotoxic agents, particularly anthracyclines. These therapies may cause progressive myocardial injury through mechanisms involving oxidative stress, mitochondrial dysfunction, and cardiomyocyte apoptosis. Over time, this process can lead to ventricular remodeling, dilated cardiomyopathy, and heart failure. Advanced ventricular dilation frequently results in functional mitral and tricuspid regurgitation, further worsening hemodynamic burden and clinical outcomes. Case summary: We report the case of a 42-year-old man with a history of non-Hodgkin lymphoma diagnosed in childhood and treated with chemotherapy, without subsequent cardiologic follow-up. From the age of 29, he developed progressive heart failure symptoms. Transthoracic echocardiography revealed severe functional mitral regurgitation with mixed mechanism (Carpentier type I due to annular dilation and type IIIa due to leaflet restriction) and massive tricuspid regurgitation, associated with severe atrial dilation, grade III diastolic dysfunction, and pulmonary hypertension. Left ventricular systolic dysfunction was documented with an ejection fraction of 36% and markedly reduced global longitudinal strain (−11%), consistent with non-ischemic dilated cardiomyopathy. The patient underwent mitral valve replacement and tricuspid valve repair but developed intraoperative cardiac arrest and postoperative mixed shock. Persistent severe ventricular dysfunction (LVEF 26%, GLS −8%) and multiple complications were observed. Conclusion: This case highlights the importance of long-term cardiovascular surveillance in childhood cancer survivors and the role of strain imaging in detecting chemotherapy-related cardiomyopathy.

Heart failure (HF) is a prevalent cardiovascular condition among the elderly population, with an incidence rate that continues to rise annually, highlighting the urgent need for effective therapeutic interventions. Sustained activation of Toll-like receptor 4 (TLR4) may contribute to left ventricular dysfunction and adverse cardiac remodeling through the induction of myocardial inflammation and oxidative stress - pathological processes that closely align with the hallmark features of HF. Preclinical studies in animal models have demonstrated that TLR4 deficiency improves cardiac function in aged mice; however, the precise role and underlying mechanisms of TLR4 in human HF remain poorly understood. This study aims to test the central hypothesis that TLR4 serves as a critical molecular link between chronic inflammation and the pathophysiology of HF. HF was induced in 18-month-old male C57BL/6J mice via continuous subcutaneous infusion of isoproterenol (ISO, 30 mg/kg/day) over a period of 3 weeks. Thereafter, mice received daily intraperitoneal injections of the TLR4 inhibitor TAK-242 (2 mg/kg), deoxyribonuclease I (DNase I, 5 mg/kg), or the peptidylarginine deiminase 4 (PAD4) inhibitor GSK484 (4 mg/kg) for 7 consecutive days. Cardiac function was assessed using a ultrasound imaging system. HE staining and Masson staining were employed to evaluate myocardial pathological changes and collagen deposition. ELISA was performed to measure serum levels of myeloperoxidase-DNA (MPO-DNA), neutrophil elastase-DNA (NE-DNA), cTnI, NT-proBNP, IL-1beta, IL-6 and TNF-alpha. Immunofluorescence staining was performed to detect the co-localization levels of Ly6G with myeloperoxidase (MPO) and citrullinated histone H3 (cit-H3) in myocardial tissue, in order to assess the formation level of neutrophil extracellular traps (NETs). Western blot were utilized to determine the expression level of TLR4 protein. The expression of TLR4 was significantly upregulated in the myocardial tissue of aged HF mice. Inhibition of TLR4 not only markedly improved cardiac function but also alleviated pathological damage to myocardial tissue and reduced collagen fiber deposition. Concurrently, it also decreased the serum levels of MPO-DNA, NE-DNA, NT-proBNP, cTnI, and inflammatory factors. Moreover, the colocalization levels of Ly6G with MPO or cit-H3 in myocardial tissue was also diminished. These findings were consistent with the effects observed following DNase I and GSK484 interventions. Targeting TLR4 can mitigate inflammatory responses and enhance cardiac function in HF mice by inhibiting NETs formation. Key words Heart failure " Cardiac function " Inflammation " Toll-like receptor 4 " Neutrophil extracellular traps.