Search Results (820)

Ventricular tachycardia (VT) remains a major cause of morbidity and mortality in patients with structural heart disease. While catheter ablation has become a cornerstone in VT management, recurrence rates remain substantial due to limitations in electroanatomic mapping (EAM), particularly in cases of deep or heterogeneous arrhythmogenic substrates. Cardiac imaging, especially when multimodal and integrated with mapping systems, has emerged as a critical adjunct to enhance procedural efficacy, safety, and individualized strategy. This comprehensive review explores the evolving role of various imaging modalities, including echocardiography, cardiac magnetic resonance (CMR), computed tomography (CT), positron emission tomography (PET), and intracardiac echocardiography (ICE), in the preprocedural and intraprocedural phases of VT ablation. We highlight their respective strengths in substrate identification, anatomical delineation, and real-time guidance. While limitations persist, including costs, availability, artifacts in device carriers, and lack of standardization, future advances are likely to redefine procedural workflows. Full article

Background: The influence of the initial ablation modality on pulmonary vein (PV) reconnection and substrate characteristics in redo procedures for recurrent atrial fibrillation (AF) remains unclear. We assessed how different thermal strategies—ablation index (AI)-guided radiofrequency (RF) versus cryoballoon (CB) ablation—affect remapping findings during redo pulmonary vein isolation (PVI). Methods: We included patients undergoing redo ablation between 2015 and 2024 with high-density electroanatomic mapping. Initial PVI modalities were retrospectively classified as low-power, long-duration (LPLD) RF; high-power, short-duration (HPSD) RF; or second-/third-generation CB. Reconnection sites were mapped using multielectrode catheters. Redo PVI was performed using AI-guided RF. Segments showing PV reconnection were reisolated; if all PVs remained isolated and AF persisted, posterior wall isolation was performed. Results: Among 195 patients (LPLD: 63; HPSD: 30; CB: 102), complete PVI at redo was observed in 0% (LPLD), 23.3% (HPSD), and 10.1% (CB) (p < 0.01 for LPLD vs. HPSD). Reconnection patterns varied by technique; LPLD primarily affected the right carina, while HPSD and CB showed reconnections at the LSPV ridge. Organized atrial tachycardia was least frequent after CB (12.7%, p < 0.002). Conclusion: Initial ablation strategy significantly influences PV reconnection and post-PVI arrhythmia patterns, with implications for redo procedure planning. Full article

Aims: Sinus tachycardia after heart transplantation (HTX) due to cardiac graft denervation is associated with reduced post-transplant survival and requires adequate treatment. We analyzed the long-term effects of heart rate control with ivabradine or metoprolol succinate in HTX recipients. Methods: This observational retrospective single-center study analyzed the ten-year results of 110 patients receiving ivabradine (n = 54) or metoprolol succinate (n = 56) after HTX. Analysis included comparison of demographics, medications, heart rates, blood pressure values, echocardiographic features, cardiac catheterization data, cardiac biomarkers, and post-transplant survival including causes of death. Results: Both groups showed no significant differences concerning demographics or medications (except for ivabradine and metoprolol succinate). At 10-year follow-up, HTX recipients with ivabradine showed a significantly lower heart rate (72.7 ± 8.5 bpm) compared to baseline (88.8 ± 7.6 bpm; p < 0.001) and to metoprolol succinate (80.1 ± 8.1 bpm; p < 0.001), a significantly lower NT-proBNP level (588.4 ± 461.4 pg/mL) compared to baseline (3849.7 ± 1960.0 pg/mL; p < 0.001) and to metoprolol succinate (1229.0 ± 1098.6 pg/mL; p = 0.005), a significantly lower overall mortality (20.4% versus 46.4%; p = 0.004), and mortality due to graft failure (1.9% versus 21.4%; p = 0.001). Multivariate analysis showed a significantly decreased risk of death within 10 years after HTX in patients with post-transplant use of ivabradine (HR 0.374, CI 0.182–0.770; p = 0.008). Conclusions: In this single-center trial, patients with ivabradine revealed a significantly more pronounced heart rate reduction, a lower NT-proBNP level, and a superior 10-year survival after HTX. Full article

Fetal tachyarrhythmias, particularly supraventricular tachycardia (SVT) and atrial flutter (AFL), pose significant clinical challenges, especially when complicated by hydrops fetalis. This article provides a comprehensive review of the tachyarrhythmia types, the diagnostic modalities applied, and the therapeutic strategies followed in fetal tachyarrhythmias. Diagnostic techniques such as M-mode echocardiography and fetal magnetocardiography (fMCG) are highlighted for their capacity to provide real-time, high-quality assessments of fetal cardiac rhythms. The review, also, focuses on pharmacologic management via transplacental therapy, discussing the safety and efficacy of the key agents including digoxin, flecainide, and sotalol, under different clinical scenarios, such as hydropic fetus and renal impairment. In addition to transplacental administration, alternative approaches such as direct fetal intramuscular or intravascular injections are examined. These direct methods, while potentially more effective in refractory cases, carry risks that necessitate specialized expertise and careful consideration of maternal and fetal safety. The limitations of current evidence, largely based on small case studies and retrospective analyses, underscore the need for larger, prospective multicenter observational studies and randomized control trials to establish standardized protocols for fetal tachyarrhythmia management. Overall, this review advocates for a personalized, multidisciplinary approach, emphasizing early fetal tachyarrhythmias diagnosis, tailored treatment regimens that balances efficacy with safety, and rigorous monitoring to optimize outcomes for both the fetus and the mother. Full article

Cardiac arrhythmias remain a major source of morbidity and mortality, often stemming from molecular and structural abnormalities that are insufficiently addressed by current pharmacologic and interventional therapies. Gene therapy has emerged as a transformative approach, offering precise and durable interventions that directly target the arrhythmogenic substrate. Across the spectrum of inherited and acquired arrhythmias—including long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, atrial fibrillation, and post-infarction ventricular tachycardia—gene-based strategies such as allele-specific silencing, gene replacement, CRISPR-mediated editing, and suppression-and-replacement constructs are showing growing translational potential. Advances in delivery platforms, including cardiotropic viral vectors, lipid nanoparticle-encapsulated mRNA, and non-viral reprogramming tools, have further enhanced the specificity and safety of these approaches. Additionally, innovative applications such as biological pacemaker development and mutation-agnostic therapies underscore the versatility of genetic modulation. Nonetheless, significant challenges remain, including vector tropism, immune responses, payload limitations, and the translational gap between preclinical models and human electrophysiology. Integration of patient-derived cardiomyocytes, computational simulations, and large-animal studies is expected to accelerate clinical translation. This review provides a comprehensive synthesis of the mechanistic rationale, therapeutic strategies, delivery platforms, and translational frontiers of gene therapy for cardiac arrhythmias. Full article

The electrical ventricular storm (VES) is defined as multiple sustained ventricular arrhythmias arising in a short time, often refractory to standard antiarrhythmic treatment. The three pillars of the physiopathogenesis of the VES are autonomic dysfunction, triggers, and an altered ventricular substrate. Incessant or highly recurrent ventricular arrhythmia impacts the hemodynamic status by worsening heart failure and increasing mortality. A stepwise, team-based, and tailored therapeutic approach is required to stop ventricular arrhythmia and regain the hemodynamic and electric stability of the patient. The authors focused on describing all currently available therapeutic approaches for VES, intending to establish the best VES therapeutic approaches. This process involves considering the patient’s specific condition, responses to previous treatments, and the potential risks and benefits of each approach. The options range from adjusting antiarrhythmic therapy to reprogramming of the ICD, sedation, epidural anaesthesia, stellate ganglia anaesthetic block, and the use of ECMO or left ventricular assist devices and radiofrequency catheter ablation. Particular attention is paid to the detailed management of genetic primary arrhythmia syndromes like long-QT syndrome, catecholaminergic polymorphic ventricular tachycardia, Brugada syndrome and Wolff–Parkinson–White syndrome, early repolarisation syndrome, right ventricular arrhythmogenic dysplasia, and idiopathic ventricular fibrillation. After overcoming the acute events of VES and obtaining hemodynamic stability, the treatment should shift toward an optimal balance of heart failure therapy, controlling the substrate by revascularisation procedures and resolving other pathology-generating ventricular arrhythmias. This article provides a comprehensive overview of ESV’s current management options using the most efficient strategies known to date. Full article

Cardiac fibrosis following myocardial infarction plays a critical role in the formation of scar tissue and contributes to ventricular arrhythmias, including ventricular tachycardia and sudden cardiac death. Current clinical diagnostics use electrical and structural markers, but lack precision due to low spatial resolution and absence of molecular information. In this paper, we employed line scan Raman microspectroscopy to classify sheep myocardial tissue into muscle, necrotic, granulated, and fibrotic tissue types, using collagen as a molecular biomarker. Three spectral regions were evaluated: region A (600–2960 cm⁻¹), region B (600–1399 cm⁻¹ and 1751–2960 cm⁻¹), and region C (1400–1750 cm⁻¹), which includes the prominent collagen-associated peaks at 1448 cm⁻¹ and 1652 cm⁻¹. Linear and nonlinear principal component analysis (PCA) and support vector machines (SVMs) were applied for dimensionality reduction and classification, with nonlinear models specifically addressing the nonlinearity of collagen formation during fibrogenesis. Histological validation was performed using Masson’s trichrome staining. Raman bands associated with collagen in region C consistently outperformed regions A and B, achieving the highest explained variance and best class separation in both binary and multiclass PCA models for both linear and nonlinear approaches. The ratio of collagen-related peaks enabled stage-dependent tissue characterization, confirming the nonlinear nature of fibrotic remodeling. Our findings highlight the diagnostic potential of collagen-associated Raman bands for characterizing myocardial fibrosis. The proposed PCA-SVM framework demonstrates robust performance even with limited sample size and has the potential to lay the foundation for real-time intraoperative diagnostics. Full article

Background/Objectives: Pulmonary embolism (PE) remains a major cause of morbidity and mortality. Despite advances in care, its nonspecific symptoms pose diagnostic and therapeutic challenges. Emerging evidence suggests sex-based differences in PE presentation, management, and outcomes, yet real-world data from European settings remain scarce. This study aimed to investigate sex differences in clinical presentation, diagnostic workup, therapeutic interventions, and outcomes among hospitalized PE patients. Methods: We conducted a retrospective cohort study including all adult patients (≥18 years) admitted with a main diagnosis of acute PE at the Cantonal Hospital Baselland between January 2018 and December 2020. Data were extracted from electronic medical records and included demographics, comorbidities, symptoms, diagnostics, treatments, and outcomes. Sex-based comparisons were performed using univariate analyses. Results: Among 197 patients, 54% were women. Compared to men, women were more often admitted by ambulance (42% n = 45 vs. 24% n = 22, p = 0.009), had more frequent tachycardia (38% n = 41 vs. 23% n = 21, p = 0.024), and received lysis therapy more often (10% n = 11 vs. 2% n = 2, p = 0.023). DVT was more frequently diagnosed in women when sonography was performed (82% n = 49 vs. 64% n = 34, p = 0.035). Men had higher rates of B symptoms, smoking, and family history of PE. Women had longer hospital stays and were more frequently discharged to rehabilitation facilities. No sex differences were found in in-hospital mortality, 6-month rehospitalization, or adherence to diagnostic guidelines. Conclusions: This study reveals sex-based differences in PE presentation and management, suggesting potential disparities in care pathways. Further research is needed to promote equitable, personalized treatment strategies. Full article

In acute lymphoblastic leukemia (ALL), neutropenia and fever of unknown origin may occur, indicating the use of antimicrobials to control a probable infection. However, in 60–70% of cases there is no obvious infectious focus so treatment is empirical, increasing the risk of developing systemic inflammatory response syndrome (SIRS). The construction of a prognostic model of fever and development of SIRS based on the identification of endogenous molecules, called alarmins or damage-associated molecular patterns (DAMPs) and inflammatory cytokines, can help identify children with ALL and fever or SIRS and who do not have an infection. A cohort of 30 children with recently diagnosed ALL and absence of infectious microorganisms before starting the remission induction phase was studied. Two groups were identified: (1) a group with SIRS (fever, tachycardia, tachypnea, and leukopenia, without focus of infection) and (2) a group without SIRS. The DAMPs, namely HMGB1 and S100A8 proteins, were quantified by ELISA and inflammatory mediators were determined by multiple protein analysis. The medians of DAMPs and inflammatory mediators in children with SIRS were higher than in children who did not have SIRS, and the delta values of the biomarkers studied in patients with and without SIRS showed important differences, with statistically higher medians in patients with SIRS compared to those without SIRS. HMGB1 together with IL-1β, IL-8, IL-10, and MCP-1 can serve as biomarkers to identify children with ALL and fever or SIRS who should not receive antimicrobial treatment because the origin of their fever is not due to an infectious agent. Full article

Background: The cardiovascular effects of SARS-CoV-2, including autonomic dysregulation, are becoming increasingly recognized, even following mild infections. However, long-term electrocardiographic (ECG) changes remain poorly characterized. Methods: We conducted a prospective study of 151 unvaccinated healthcare workers with RT-PCR-confirmed mild to moderate SARS-CoV-2 infection. Standard 12-lead ECGs were recorded before infection (T0) and at 6–12 months (T1) and >12 months (T2) after infection. Key parameters included heart rate (HR), PR interval, QRS duration, and corrected QT interval (QTc). Results: Heart rate (HR) increased transiently at T1 (p < 0.05) and normalized by T2. Mild but persistent PR interval shortening was observed at both follow-ups (p < 0.01). There were no significant changes in QRS or QTc intervals. No arrhythmias or conduction blocks occurred. ECG alterations were not associated with sex or age, except for greater PR shortening in males. Conclusions: Mild SARS-CoV-2 infection can result in transient sinus tachycardia and subtle PR shortening, which is likely to be a post-viral autonomic effect. Long-term ECG surveillance appears unnecessary in asymptomatic cases. Full article

Background: The onset of cardiomyopathy in Duchenne muscular dystrophy (DMD) is insidious and poorly defined. We proposed integrated wall stress (iWS) as a marker of total left ventricular (LV) workload and tested whether the increased iWS represents early DMD cardiomyopathy. Methods: Peak systolic wall stress (PS-WS) was calculated in M-mode echocardiography with simultaneous blood pressure measurement. iWS was defined as a product of PS-WS and heart rate (HR) divided by 60 (=PS-WS/RR interval). We measured iWS in normal controls (CTRL), DMD with normal LV shortening fraction (%LVSF ≥ 30%) (DMD-A), and DMD with decreased %LVSF (<30%) (DMD-B). Results: 40 CTRL and 79 DMD patients were studied. Despite comparable %LVSF, both HR and iWS were significantly higher in DMD-A (n = 50) than in CTRL (p < 0.0001). iWS was significantly higher in DMD-B (n = 29) than in DMD-A (p < 0.0001) despite comparable HR. PS-WS was significantly higher in DMD-A than in CTRL and higher in DMD-B than in DMD-A, suggesting high HR is not a sole determinant of increased iWS in DMD-A compared with CTRL. In a longitudinal study in 35 DMD patients over 4.0 ± 2.0 years, iWS showed significant increase (p = 0.0062) alongside a significant decline in %LVSF (p < 0.0001). Conclusions: iWS significantly increased in DMD before %LVSF declined. The progressive increase of iWS in DMD is initially associated with increased HR and then with increased PS-WS. iWS may serve as a useful echocardiographic marker in identifying preclinical DMD cardiomyopathy. Full article

Background and Objectives: The perioperative use of beta-blockers remains controversial due to conflicting evidence of their risks and benefits. The aim of this study was to evaluate the association between chronic beta-blocker (bb) therapy and perioperative cardiac events in non-cardiac surgeries using 24 h continuous Holter monitoring. Materials and Methods: A prospective observational study was conducted on patients undergoing elective or emergency non-cardiac surgery at a Romanian tertiary care hospital. The patients were divided into two groups: G1 (not receiving Bb) and G2 (on chronic Bb). The incidences of perioperative cardiac events, such as severe bradycardia (<40 b/min), new-onset atrial fibrillation (AF), extrasystolic arrhythmia (Ex), and sustained ventricular tachycardia (sVT) and arterial hypotension, were compared between the two groups using clinical, electrocardiography (ECG), and Holter ECG data. Beta-blocker indications, complications, and outcomes were analyzed using chi-squared tests and logistic regression. Results: A total of 100 consecutive patients (63% men, mean age of 53.7 years) were enrolled in the study. G2 included 30% (n = 30) of patients on chronic beta-blocker therapy. The indications included atrial fibrillation (46.7%, n = 14), arterial hypertension (36.7%, n = 11), extrasystolic arrhythmias (10%, n = 3), and chronic coronary syndrome (6.6%, n = 2). Beta-blocker use was significantly associated with severe bradycardia (n = 6; p < 0.001) in G2, whereas one patient in G1 had bradycardia, and 15 and 1 patients had hypotension (p < 0.001) in G1 and G2, respectively. The bradycardia and arterial hypotension cases were promptly treated and did not influence the patients’ prognoses. The 14 patients with AF in G2 had a 15-fold higher odds of requiring beta-blockers (p < 0.001, odds ratio (OR) = 15.145). No significant associations were found between beta-blocker use and the surgery duration (p = 0.155) or sustained ventricular tachycardia (p = 0.857). Ten patients developed paroxysmal postoperative atrial fibrillation (AF), which was related to longer surgery durations (165 (150–180) vs. 120 (90–150) minutes; p = 0.002) and postoperative anemia [hemoglobin (Hg): 10.4 (9.37–12.6) vs. 12.1 (11–13.2) g/dL; p = 0.041]. Conclusions: Patients under chronic beta-blocker therapy undergoing non-cardiac surgery have a higher risk of perioperative bradycardia and hypotension. Continuous Holter monitoring proved effective in detecting transient arrhythmic events, emphasizing the need for careful perioperative surveillance of these patients, especially the elderly, in order to prevent cardiovascular complications These findings emphasize the necessity of tailored perioperative beta-blocker strategies and support further large-scale investigations to optimize risk stratification and management protocols. Full article

Background: Left ventricular non-compaction cardiomyopathy (LVNC) is a congenital heart disease characterized by abnormal prenatal development of the left ventricle that has an aberrantly thick trabecular layer and a thinner compacted myocardial layer. However, the underlying molecular mechanisms of LVNC regulated by mitochondrial phosphatase genes remain largely unresolved. Methods: We generated a mouse model with cardiac-specific deletion (CKO) of Ptpmt1, a type of mitochondrial phosphatase gene, using the αMHC-Cre, and investigated the effects of cardiac-specific Ptpmt1 deficiency on cardiac development. Morphological, histological, and immunofluorescent analyses were conducted in Ptpmt1 CKO and littermate controls. A transcriptional atlas was identified by RNA sequencing (RNA-seq) analysis. Results: We found that CKO mice were born at the Mendelian ratio with normal body weights. However, most of the CKO mice died within 24 h after birth, developing spontaneous ventricular tachycardia. Morphological and histological analysis further revealed that newborn CKO mice developed an LVNC phenotype, evidenced by a thicker trabecular layer and a thinner myocardium layer, when compared with the littermate control. We then examined the embryonic hearts and found that such an LVNC phenotype could also be observed in CKO hearts at E15.5 but not at E13.5. We also performed the EdU incorporation assay and demonstrated that cardiac cell proliferation in both myocardium and trabecular layers was significantly reduced in CKO hearts at E15.5, which is also consistent with the dysregulation of genes associated with heart development and cardiomyocyte proliferation in CKO hearts at the same stage, as revealed by both the transcriptome analysis and the quantitative real-time PCR. Deletion of Ptpmt1 in mouse cardiomyocytes also induced an increase in phosphorylated eIF2α and ATF4 levels, indicating a mitochondrial stress response in CKO hearts. Conclusions: Our results demonstrated that Ptpmt1 may play an essential role in regulating left ventricular compaction during mouse heart development. Full article

Background: Histologic chorioamnionitis (HCA) is a placental inflammatory condition characterized by neutrophilic infiltration of the fetal membranes, often occurring without overt clinical signs or symptoms. Risk factors include prolonged labor, premature rupture of membranes (PROM) exceeding 12 h, nulliparity, labor dystocia, and lower socioeconomic status. Although HCA frequently presents as a subclinical condition, its early diagnosis remains challenging. Nevertheless, HCA is associated with an increased risk of maternal and neonatal morbidity, including early-onset neonatal sepsis, cerebral palsy, and long-term neurodevelopmental impairment. We report the case of a 29-year-old primigravida at 40 + 0 weeks of gestation, admitted for decreased fetal movements. Discussion: Cardiotocographic (CTG) monitoring revealed a “zigzag pattern” in the absence of maternal fever, leukocytosis, or tachycardia. Due to the CTG findings suggestive of possible fetal compromise, in addition to reduced fetal movements, an emergency cesarean section was performed. Intraoperative findings included heavily meconium-stained amniotic fluid, then the examination of the placenta confirmed acute HCA with a maternal inflammatory response, without evidence of fetal inflammatory response. Conclusion: This case highlights the crucial role of CTG abnormalities, particularly the “zigzag pattern,” as an early marker of subclinical intrauterine inflammation. Early recognition of such patterns may facilitate timely intervention and improve perinatal outcomes in cases of histologic chorioamnionitis. Full article

The use of temporary mechanical circulatory support in refractory heart failure cardiogenic shock (HFCS) has risen, leading to potential complications. Post-Cardiac Injury Syndrome (PCIS) from Impella insertion is rare but may result from subclavian artery manipulation and aortic irritation. We report the first case of pericarditis (PCIS) caused by Impella 5.5 insertion in an HFCS patient awaiting heart transplantation. The patient developed chest pain, tachycardia, and hypotension post-Impella insertion. Laboratory results and electrocardiograms confirmed PCIS. Treatment with Ibuprofen and Colchicine was successful. He received a heart transplant 14 days later. This case emphasizes recognizing iatrogenic pericarditis after Impella insertion and the need to avoid additional myocardial strain. Full article