Search Results (628)

Background and Objectives: Cardiac myxoma (CM) is the most common primary benign neoplasm of the heart. This study’s objective was to analyse diagnostic features of CM, surgical data and postoperative courses of patients over a 20-year period in a single institution. Materials and Methods: We conducted a retrospective analysis of patients with diagnosed and pathologically confirmed CM who underwent surgical resection in our hospital from 1 January 2004 to 1 January 2024. Data was assessed and analysed from medical records. Results: The study included 76 patients (mean age, 61.7 ± 12.6 years; 60.5% female). The majority of patients (93.7%) had symptoms, most commonly presenting with dyspnoea (64.5%), chest pain (39.5%) and arrhythmias (35.5%). Myxomas were found in the left atrium (89.5%), right atrium (9.2%) and left ventricle (1.3%). Isolated tumour extirpation surgery was performed in 50 patients (65.8%). During the early postoperative period, arrhythmias were the most common complication (n = 16, 21.1%). Early in-hospital mortality occurred in two patients due to cardiopulmonary failure. In the late postoperative period, 11 deaths (14.9%) were observed 4 to 17.5 years after surgery. No recurrence of CM was found in any patient during the follow-up period, yet tumours of other localisations were detected in nine patients. Conclusions: Surgery is the first-line treatment for CM, with a good prognosis. Although during the late postoperative period no cardiac tumour recurrence was observed in our study, 12.2% patients were newly diagnosed with non-cardiac neoplasms. Therefore, we suggest monitoring patients not only for cardiac disorders but also for the occurrence of extracardiac tumours. Full article

Pulmonary arterial hypertension (PAH) is a devastating cardiovascular disorder caused by right heart failure leading to premature death. The TGFBR2 and BMPR-II receptors, which are members of the TGF-β receptor family, are considered promising targets for developing novel drugs in PAH. Lupeol and ψ-taraxasterol, naturally occurring triterpene molecules with proven anti-inflammatory, anti-cancer, and cardioprotective activities, hold considerable potential in the treatment of PAH. Hence, the present study aimed to evaluate the impacts of lupeol and ψ-taraxasterol isolated from Cirsium sintenisii Freyn on the TGF-β and BMP pathways, aiming to determine their therapeutic values in PAH. The effects of the compounds were extensively investigated using both in silico and wet lab experiments, including reporter assays, RT-PCR/QPCR, Western blots, and cell proliferations assays. Both lupeol and ψ-taraxasterol demonstrated interactions with the majority of components of these signaling pathways, including the TGFBR2 and BMPR-II receptors, suggesting that both compounds were capable of modulating the BMP and TGF-β pathways. Data derived from reporter assays, RT-PCR/QPCR, and Western blots demonstrated that lupeol and ψ-taraxasterol inhibited the TGF-β signaling pathway by reducing the phosphorylation of the SMAD3 protein and the expression of pai-1 transcripts. Additionally, ψ-taraxasterol enhanced BMP signaling via regulating the phosphorylation of SMAD1/5 proteins and upregulated the expression of id-1 transcripts. Finally, lupeol and ψ-taraxasterol inhibited abnormal proliferation of mutant-type (bmpr2^R899X+/-) PAMSCs stimulated with the TGF-β1 ligand with no discernible effects on wild-type cells. This is the first comprehensive report outlining the potential therapeutic effects of lupeol and ψ-taraxasterol in PAH, which may have immediate experimental and clinical applications not only in PAH but also other BMP- and TGF-β-associated disorders. Full article

Distributive shock and acute respiratory distress syndrome (ARDS) are syndromes of profound pathophysiological complexity, each independently associated with high morbidity and mortality. When coexistent, they create a state of synergistic cardiopulmonary failure where conventional, protocolized management approaches are often insufficient. This review synthesizes current mechanistic insights into heart–lung interactions in distributive shock with ARDS, highlighting the central role of right ventricular–pulmonary arterial coupling and the dual impact of altered lung mechanics and vascular dysregulation. We examine the distinct hemodynamic implications of pulmonary versus extrapulmonary ARDS phenotypes, including their divergent effects on transpulmonary pressure, venous return, and right ventricular afterload, and emphasize the clinical relevance of mixed phenotypes. Advanced monitoring modalities—esophageal manometry, echocardiography, and, in select cases, pulmonary artery catheterization—are presented as essential tools for dynamic phenotyping and individualized titration of ventilatory and hemodynamic strategies. Building on these principles, we outline phenotype-directed approaches to ventilation, fluid and vasoactive therapy, and adjunctive interventions such as proning and extracorporeal support. Finally, we discuss knowledge gaps and future directions, underscoring the need for integrative technologies and phenotype-stratified trials to refine precision management. The nuanced integration of cardiopulmonary physiology into bedside decision-making represents a paradigm shift toward individualized, physiology-guided care for this high-risk population. Full article

Cardiovascular diseases in dogs have diverse causes and may progress rapidly to life-threatening complications. This review outlines the relevant pathological conditions involving the cardiovascular system in dogs, especially the myocardium, including myocarditis caused by canine parvovirus (CPV-2), heartworm disease (Dirofilaria immitis), hemangiosarcoma, and polyarteritis nodosa (PAN). CPV-2 affects the myocardium of puppies during the early weeks of life, leading to necrosis, fibrosis, and congestive heart failure. Heartworm disease is caused by adult D. immitis residing mainly in the pulmonary arteries, inducing pulmonary hypertension, right ventricular overload, and vascular damage, with the severity being related to the worm burden and duration of infestation. Hemangiosarcoma is a malignant vascular tumor, most frequently originating in the spleen or right atrium, often diagnosed at an advanced stage, with widespread metastases. Polyarteritis nodosa in dogs is a necrotizing, systemic vasculitis of medium-sized arteries that may affect the coronary arteries of the heart. Its pathogenesis is still unclear, though an immune-mediated mechanism is suspected. By presenting these lesions, the review underscores the many factors that can trigger cardiovascular diseases in dogs, as well as the clinical significance and the need for further research into their pathogenesis and treatment. Full article

Background: Heart failure (HF) with pulmonary hypertension due to left-sided heart disease (PH-LHD) is associated with poor prognosis. Dapagliflozin showed benefits in terms of ejection fraction (EF); meanwhile, sildenafil improved pulmonary pressures and right ventricular function in PH -LHD in recent clinical studies. This study assesses the potential additive effects of dapagliflozin and sildenafil on cardiac function and pulmonary hemodynamics in this population. Methods: In this prospective, randomized, controlled trial, 93 participating patients with HF and PH-LHD were randomly assigned to receive dapagliflozin (control group, n = 48) or dapagliflozin plus sildenafil 25 mg/day (test group, n = 45) in addition to conventional therapy for HF for 12 weeks. The primary outcomes were assessing changes in echocardiographic hemodynamic parameters. Secondary outcomes included outcomes, changes in cardiac enzyme (troponin), kidney function (serum creatinine), and lipid profile. Results: The average baseline median left ventricular ejection fraction (LVEF) for both groups was 30%, and the Pulmonary Artery Systolic Pressure (PASP) median was 50 mmHg. At follow-up, PASP had declined, and EF had improved compared to baseline. However, there were no statistically noticeable variations between the groups (p = 0.458, 0.331, respectively). No notable changes were observed in secondary and safety outcomes, including hospitalization rate, number of deaths, kidney function, and cardiac enzymes (p = 0.524, 1, 0.923, and 0.574, respectively). Conclusions: Addition of sildenafil to dapagliflozin did not demonstrate any significant clinical or hemodynamic benefit over dapagliflozin monotherapy in HF patients and PH-LHD. Further studies are warranted to evaluate the effects over the long term. Full article

Background/Objectives: Pacemaker-induced cardiomyopathy (PICM) develops in up to 30% of patients with chronic right ventricular pacing. While biventricular (BIV) upgrade is the conventional strategy, conduction system pacing (CSP) offers a physiologic alternative recently endorsed by the 2025 ESC/EHRA Consensus Statement. However, comparative evidence in PICM is limited. Therefore, we aimed to compare outcomes of PICM patients undergoing CSP versus BIV upgrade. Methods: This retrospective analysis included consecutive PICM patients who were upgraded to CSP or BIV between 2022 and 2024 at a single, experienced center. Follow-up averaged >19 months. Clinical outcomes, lead performance, echocardiographic parameters, complications, and quality of life (QoL) were evaluated. Results: Sixty-three patients were included (CSP: 26; BIV: 37). Mean age and sex distribution were similar; both groups had wide paced QRS complexes and a high ventricular pacing burden. Baseline left ventricular ejection fraction (LVEF) was lower in BIV patients (29 ± 7% vs. 35 ± 6%, p = 0.01). Procedure duration was comparable, but fluoroscopy was shorter with CSP. QRS duration narrowed significantly in both groups (CSP: 163 ± 28→132 ± 12 ms; BIV: 171 ± 23→140 ± 18 ms; both p < 0.05). During follow-up, LVEF improved (CSP: 41 ± 8%; p = 0.008; BIV: 39 ± 8%, p = 0.0001), as did NYHA class, with no significant intergroup differences. The rates of heart failure hospitalization, all-cause mortality, and QoL were similar. Notably, 34.6% of CSP patients retained their existing generator, suggesting procedural and economic benefits. Conclusions: CSP is a feasible and potentially cost-efficient alternative to BIV upgrade in PICM, with comparable improvements in ventricular function, symptoms, and clinical outcomes. Larger prospective trials are warranted. Full article

Cardiogenic shock (CS) is a complex, life-threatening syndrome characterized by inadequate tissue perfusion due to impaired cardiac function. Acute myocardial infarction (AMI) and acute decompensated heart failure are the leading causes, with mortality remaining high despite advances in revascularization and supportive care. The Society for Cardiovascular Angiography and Interventions (SCAI) classification allows risk stratification and guides clinical decision making by capturing the spectrum of shock severity. Percutaneous mechanical circulatory support (pMCS) devices, such as the intra-aortic balloon pump (IABP) and Impella, aim to stabilize hemodynamics by augmenting cardiac output and unloading the left ventricle. However, randomized trials and meta-analyses have not demonstrated a consistent survival advantage of Impella over IABP, while reporting higher rates of bleeding and vascular complications. Landmark trials, including ECLS-SHOCK and DanGer, have provided conflicting results, likely reflecting differences in baseline severity and timing of device implantation. Veno-arterial extracorporeal membrane oxygenator (VA-ECMO) offers full cardiopulmonary support but increases left ventricular afterload, potentially worsening myocardial injury. Combined strategies such as ECPELLA (Impella + VA-ECMO) or ECMO + IABP may mitigate left ventricle (LV) overload and improve bridging to recovery or advanced therapies, although evidence remains largely observational and complication rates are considerable. In right-sided or biventricular failure, tailored options (e.g., Impella RP, Bi-Pella) guided by invasive hemodynamics may be required. Current evidence suggests that pMCS benefits are limited to carefully selected subgroups, underscoring the importance of early diagnosis, prompt referral, and individualized intervention. Robust randomized data are still needed to define the optimal role of pMCS in AMI-related CS. Full article

Background: Arteriovenous fistula (AVF) in patients with end-stage renal disease (ESRD) can lead to high-output heart failure (HOHF). There is limited data on the incidence and outcomes of HOHF in patients with AVF. Objective: The main goal of our study was to determine the incidence and prevalence of HOHF [diagnosed via right heart catheterization (RHC)] in chronic kidney disease (CKD)/ESRD patients with AVF. We also aimed to evaluate the clinical determinants of the development of HOHF in this group. Methods: We conducted a retrospective cohort study at the University of Kansas Medical Center from January 2011 to December 2023. Patients with CKD/ESRD with AVF who underwent RHC after AVF creation were included in the study. HOHF was defined as a cardiac index (CI) ≥ 4.0 L/min/m², measured either with the Fick or the Thermodilution method. Bivariate and multivariable regression analyses were performed to identify independent predictors of HOHF in this population. Results: Out of 84 patients with AVF, 34 patients met established inclusion and exclusion criteria. Ten out of thirty-four patients (29.4%) developed HOHF. Hemoglobin (Hb) was significantly lower in the HOHF group than the non-HOHF group (10.16 vs. 11.52 g/dL; p = 0.02). Patients with HOHF had significantly elevated CI when compared with the non-HOHF group (CI Fick: 4.54 vs. 2.91 L/min/m², p < 0.001). Similar mortality was observed in the HOHF and non-HOHF groups. After multivariant regression analysis, Hb was an independent predictor of HOHF (HR 0.86, 95% CI: 0.76–0.98, p =< 0.01). Conclusions: HOHF is common in patients with AVF; nearly 1/3 (29.4%) of the patients developed HOHF, confirmed with RHC. Low Hb was found to be an independent predictor of HOHF. Further larger studies are needed to confirm these findings and establish an early detection protocol to detect and treat this condition. Full article

Objectives: The purpose of this study was to determine whether concomitant tricuspid valve repair (TVr) at the time of left ventricular assist device (LVAD) implantation improves outcomes in patients with ≥moderate tricuspid regurgitation (TR) and to evaluate the prognostic value of preoperative right ventricular (RV) strain. Methods: In a retrospective analysis of 100 LVAD recipients (44 TVr; 56 No-TVr), preoperative (preop) and postoperative (postop) clinical, echocardiographic, and hemodynamic variables, including pulmonary vascular resistance (PVR) and pulmonary artery pulsatility index (PAPI), were analyzed. RV free wall strain (RV-FWS) and RV fractional area change (RV-FAC) were measured by speckle tracking. Early right heart failure (RHF) was modeled with multivariable logistic regression, and 2-year mortality was assessed with Fine–Gray competing risk regression. Preoperative and three-month measurements were compared within each of the 100 patients. Results: Baseline invasive hemodynamics, RV-FWS, and RV-FAC were similar between the TVr and No-TVr groups. TVr at the time of LVAD implantation reduced postoperative TR grade, but it did not improve RV-FWS or RV-FAC at 3 months. The No-TVr patients were more often discharged home and had lower 30-day readmissions. PVR was comparable preoperatively and at 3 months postoperatively. In adjusted analyses, preop PVR, PAPI, and TVr were not independently associated with early RHF, whereas decreased preoperative RV-FWS and lower preop RV-FAC independently predicted higher 2-year mortality. Conclusions: In LVAD recipients with ≥moderate TR, concomitant TVr lowers postoperative TR severity but does not improve early RHF, RV strain-based remodeling, or 2-year mortality. Preoperative RV deformation metrics, rather than preoperative PVR or PAPI, independently predict survival following LVAD implantation with or without TVr. Full article

Background and Clinical Significance: Idiopathic pulmonary arterial hypertension is a rare disorder, often linked to genetic predisposition. Canonical pulmonary arterial hypertension genes such as BMPR2, KCNK3, and TBX4 are well described, but novel associations continue to emerge. Glomulin (GLMN) encodes a protein essential for vascular smooth-muscle biology, classically implicated in glomuvenous malformations, yet not previously associated with pulmonary arterial hypertension. Case Presentation: We present a 49-year-old woman with progressive dyspnea, edema, and persistent hypercapnic respiratory failure. Right-heart catheterization confirmed precapillary pulmonary hypertension. Comprehensive evaluation, including ventilation/perfusion scanning, autoimmune panel, polysomnography, and high-resolution computed tomography, excluded secondary causes. Respiratory assessment revealed diaphragmatic weakness and reduced respiratory muscle pressures, consistent with primary myopathy and explaining the unusual hypercapnic profile. Whole-genome sequencing identified a heterozygous pathogenic GLMN nonsense variant, while canonical pulmonary arterial hypertension genes were negative. No cutaneous or mucosal glomuvenous malformations were found. The patient was treated with oxygen therapy, diuretics, non-invasive ventilation, and dual oral pulmonary arterial hypertension therapy (ambrisentan and tadalafil), with stabilization but persistent hypercapnia. Conclusions: To our knowledge, this is the first reported co-occurrence of idiopathic pulmonary arterial hypertension and a pathogenic GLMN variant. While causality cannot be inferred, glomulin’s role in vascular smooth-muscle maturation provides a plausible link to pulmonary vascular remodeling. This case underscores the importance of assessing respiratory muscle function in idiopathic pulmonary arterial hypertension patients with hypercapnia and highlights the potential relevance of extended genetic testing in rare pulmonary vascular disease. Full article

Background: Patent ductus arteriosus (PDA) in dogs causes persistent left-to-right shunting, leading to pulmonary overcirculation, left heart volume overload, and potential congestive heart failure. Accurate assessment of fluid imbalance is essential but challenging with conventional echocardiography or biomarkers. Phase angle (PhA), derived from bioelectrical impedance analysis (BIA), may serve as a non-invasive marker of extracellular fluid distribution and cellular integrity. Objectives: This study aimed to evaluate PhA as an indicator of thoracic fluid imbalance in dogs with PDAby analyzing its correlation with pulmonary velocity (PV) and end-diastolic volume (eV), as well as its responsiveness to surgical correction. In addition, we assessed the relationships between PhA and echocardiographic structural indices (LA/Ao, TDI Sep E/Em, TDI Lat E/Em) and examined the influence of the measurement region. Methods: PhA was measured at 5, 50, and 250 kHz in 30 PDA-affected and 15 healthy dogs, with electrode placement across thorax, trunk, and abdomen. Echocardiography evaluated PV, eV, and PDA-specific structural parameters. Results: Thoracic PhA at 5 kHz was significantly reduced in PDAdogs, strongly correlated with PV and moderately with eV. Postoperative measurements showed progressive PhA recovery. Only TDI Lat E/Em correlated with mid-frequency PhA, while other structural indices showed minimal association. Thoracic PhA was lower than trunk or abdominal values, indicating that thoracic measurements may better capture localized extracellular fluid changes in PDAcompared with other regions. Conclusion: Thoracic PhA at 5 kHz effectively reflects extracellular fluid changes in PDA, complements structural echocardiography, and tracks postoperative fluid normalization. Its non-invasive nature supports clinical utility for monitoring hemodynamic burden and therapeutic response. Full article

Background/Objectives: Atrial fibrillation (AF) is the most common sustained arrhythmia, with catheter ablation outcomes differing significantly between paroxysmal and persistent forms. While pulmo-nary vein isolation (PVI) remains the cornerstone of ablation, persistent AF is often associ-ated with atrial remodeling and non-pulmonary vein triggers, reducing procedural success rates and necessitating repeat interventions. However, in selected patients with minimal atrial substrate, a single PVI may achieve durable rhythm control. This case report illus-trates such a scenario in a young patient with persistent AF and tachyarrhythmia-induced cardiomyopathy (TIC). Methods: A 42-year-old previously healthy male presented with newly diagnosed persistent AF complicated by TIC and heart fail-ure (left ventricular ejection fraction [LVEF] 25%). Despite rate control, anticoagulation, guideline-directed heart failure therapy, amiodarone pretreatment, and two failed electrical cardioversions, the patient remained symptomatic. Elec-troanatomic mapping was performed to assess atrial substrate prior to radiofrequency ablation. Results: Mapping revealed no extensive low-voltage zones, indicating absence of significant atrial fibrosis. During ablation, si-nus rhythm was restored spontaneously with a single application targeting the infero-posterior aspect of the right infe-rior pulmonary vein. No additional arrhythmogenic substrate was identified. The patient maintained sinus rhythm throughout 14 months of follow-up, with marked clinical improvement, normalization of LVEF (55%), regression of atrial and ventricular enlargement, and resolution of heart failure symptoms. Quality of life, assessed by the ASTA question-naire, improved from 24 to 0 points. Conclusions: This case highlights that even in therapy-resistant persistent AF with severe structural and functional cardiac impairment, arrhythmia may be driven by discrete pulmonary vein-dependent mechanisms. Careful patient selection, particu-larly in younger individuals without advanced atrial remodeling, can identify those in whom PVI alone achieves durable rhythm control and reverse cardiac remodeling. Full article

Pressure overload in non-treated or resistant hypertension (HTN) increases the risk of heart failure (HF) as well as the occurrence of fatal ventricular arrhythmias and stroke-provoking atrial fibrillation (AF), while perturbed connexin-43 (Cx43) and Cx40 might be involved. In addition, kidney dysfunction may facilitate hemodynamic volume overload and congestive HF. We investigated the impact of volume overload on Cx43 and Cx40 in right and left heart atria of hypertensive pressure overloaded Ren-2 transgenic (TGR) strain and normotensive Hannover Sprague Dawley (HSD) rats, as well as the efficacy of renin–angiotensin blockade with trandolapril and losartan. Key novel findings revealed lower levels of Cx43 and Cx40 proteins in left as well as right heart atria in pressure overloaded hypertensive rats compared to normotensive rats. There was a significant decrease in Cx43 and Cx40 proteins due to volume overload in both atria of normotensive as well as hypertensive rats. Treatment with trandolapril increased Cx43 and Cx40 levels in right and left heart atria of normotensive as well as hypertensive volume overloaded rats. While losartan increased Cx43 and did not affect Cx40 in left and right heart atria of volume overloaded rats. Findings of this study point out that right heart atria of normotensive as well as hypertensive rats are more susceptible to volume overload comparing to the left heart atria. Trandolapril attenuated pro-arrhythmic downregulation of Cx43 and Cx40 in atria of volume overloaded normotensive as well as hypertensive rats. This fact as well as examining AF inducibility requires further investigation. Full article

An atrial septal defect (ASD) is the most common congenital heart defect (CHD) diagnosed in adulthood. It is characterized by significant anatomical heterogeneity and complications that evolve over time. While often asymptomatic in children, the signs of adverse effects of ASD increase with age, including a greater risk of heart failure, stroke, atrial fibrillation (AF), and reduced life expectancy. ASD is traditionally considered a right-heart lesion due to long-term complications such as arrhythmias, right-sided heart failure, thromboembolism, and, in a subset of patients, pulmonary arterial hypertension (PAH). The pathophysiology of atrial shunts also affects the left heart due to volume overload and adverse ventriculo-ventricular interaction. Early diagnosis of interatrial septal anomalies is essential to prevent hemodynamic consequences and/or thromboembolic events. Electrocardiographic (ECG) findings play a crucial role in this early diagnosis. This narrative review aims to update clinicians on the latest evidence regarding the pathophysiological link between ASD and cardiac rhythm disorders, the nuances of optimal diagnostics, treatment options (surgical, interventional, pharmacological), and the need for long-term follow-up for patients with ASD. The review will determine the risk of conduction disorders compared to a healthy population and to compare the prevalences of conduction disorders, mortality, and pacemaker use in patients with closed ASDs versus those with open ASDs. Full article