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Advanced management of ventricular arrhythmias in chronic Chagas cardiomyopathy.

ABSTRACT: Chagas cardiomyopathy is a parasitic infection caused by Trypanosoma cruzi. Structural and functional abnormalities are the result of direct myocardial damage by the parasite, immunological reactions, dysautonomia, and microvascular alterations. Chronic Chagas cardiomyopathy (CCC) is the most serious and important manifestation of the disease, affecting up to 30% of patients in the chronic phase. It results in heart failure, arrhythmias, thromboembolism, and sudden cardiac death. As in other cardiomyopathies, scar-related reentry frequently results in ventricular tachycardia (VT). The scars typically are located in the inferior and lateral aspects of the left ventricle close to the mitral annulus extending from endocardium to epicardium. The scars may be more prominent in the epicardium than in the endocardium, so epicardial mapping and ablation frequently are required. Identification of late potentials during sinus rhythm and mid-diastolic potentials during hemodynamically tolerated VT are the main targets for ablation. High-density mapping during sinus rhythm can identify late isochronal regions that are then targeted for ablation. Preablation cardiac magnetic resonance imaging with late enhancement can identify potentials areas of arrhythmogenesis. Therapeutic alternatives for VT management include antiarrhythmic drugs and modulation of the cardiac autonomic nervous system.

SUBMITTER: Santacruz D

PROVIDER: S-EPMC8710627 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Left ventricular apical aneurysm in chronic Chagas cardiomyopathy-A case report.

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2018-10-31 | GSE89373 | GEO

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| S-EPMC9392651 | biostudies-literature

A new prediction model for ventricular arrhythmias in arrhythmogenic right ventricular cardiomyopathy.

Project description:AimsArrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVC) is characterized by ventricular arrhythmias (VAs) and sudden cardiac death (SCD). We aimed to develop a model for individualized prediction of incident VA/SCD in ARVC patients.Methods and resultsFive hundred and twenty-eight patients with a definite diagnosis and no history of sustained VAs/SCD at baseline, aged 38.2 ± 15.5 years, 44.7% male, were enrolled from five registries in North America and Europe. Over 4.83 (interquartile range 2.44-9.33) years of follow-up, 146 (27.7%) experienced sustained VA, defined as SCD, aborted SCD, sustained ventricular tachycardia, or appropriate implantable cardioverter-defibrillator (ICD) therapy. A prediction model estimating annual VA risk was developed using Cox regression with internal validation. Eight potential predictors were pre-specified: age, sex, cardiac syncope in the prior 6 months, non-sustained ventricular tachycardia, number of premature ventricular complexes in 24 h, number of leads with T-wave inversion, and right and left ventricular ejection fractions (LVEFs). All except LVEF were retained in the final model. The model accurately distinguished patients with and without events, with an optimism-corrected C-index of 0.77 [95% confidence interval (CI) 0.73-0.81] and minimal over-optimism [calibration slope of 0.93 (95% CI 0.92-0.95)]. By decision curve analysis, the clinical benefit of the model was superior to a current consensus-based ICD placement algorithm with a 20.6% reduction of ICD placements with the same proportion of protected patients (P < 0.001).ConclusionUsing the largest cohort of patients with ARVC and no prior VA, a prediction model using readily available clinical parameters was devised to estimate VA risk and guide decisions regarding primary prevention ICDs (www.arvcrisk.com).

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Project description:Previous reports indicate that IL18 is a novel candidate gene for diastolic dysfunction in sickle cell disease (SCD)-related cardiomyopathy. We hypothesize that interleukin-18 (IL-18) mediates the development of cardiomyopathy and ventricular tachycardia (VT) in SCD. Compared with control mice, a humanized mouse model of SCD exhibited increased cardiac fibrosis, prolonged duration of action potential, higher VT inducibility in vivo, higher cardiac NF-κB phosphorylation, and higher circulating IL-18 levels, as well as reduced voltage-gated potassium channel expression, which translates to reduced transient outward potassium current (Ito) in isolated cardiomyocytes. Administering IL-18 to isolated mouse hearts resulted in VT originating from the right ventricle and further reduced Ito in SCD mouse cardiomyocytes. Sustained IL-18 inhibition via IL-18-binding protein resulted in decreased cardiac fibrosis and NF-κB phosphorylation, improved diastolic function, normalized electrical remodeling, and attenuated IL-18-mediated VT in SCD mice. Patients with SCD and either myocardial fibrosis or increased QTc displayed greater IL18 gene expression in peripheral blood mononuclear cells (PBMCs), and QTc was strongly correlated with plasma IL-18 levels. PBMC-derived IL18 gene expression was increased in patients who did not survive compared with those who did. IL-18 is a mediator of sickle cell cardiomyopathy and VT in mice and a novel therapeutic target in patients at risk for sudden death.

| S-EPMC7933768 | biostudies-literature

Developments in the management of Chagas cardiomyopathy.

Project description:Over 100 years have elapsed since the discovery of Chagas disease and there is still much to learn regarding pathogenesis and treatment. Although there are antiparasitic drugs available, such as benznidazole and nifurtimox, they are not totally reliable and often toxic. A recently released negative clinical trial with benznidazole in patients with chronic Chagas cardiomyopathy further reinforces the concerns regarding its effectiveness. New drugs and new delivery systems, including those based on nanotechnology, are being sought. Although vaccine development is still in its infancy, the reality of a therapeutic vaccine remains a challenge. New ECG methods may help to recognize patients prone to developing malignant ventricular arrhythmias. The management of heart failure, stroke and arrhythmias also remains a challenge. Although animal experiments have suggested that stem cell based therapy may be therapeutic in the management of heart failure in Chagas cardiomyopathy, clinical trials have not been promising.

| S-EPMC4810774 | biostudies-literature

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