210 resultados para ablation
Resumo:
Ventricular tachycardia (VT) late after myocardial infarction is an important contributor to morbidity and mortality. This prospective multicenter study assessed the efficacy and safety of electroanatomical mapping in combination with open-saline irrigated ablation technology for ablation of chronic recurrent mappable and unmappable VT in remote myocardial infarction.
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In patients with ventricular tachycardia (VT) and a history of myocardial infarction, intervention with an implantable cardioverter defibrillator (ICD) can prevent sudden cardiac death and thereby reduce total mortality. However, ICD shocks are painful and do not provide complete protection against sudden cardiac death. We assessed the potential benefit of catheter ablation before implantation of a cardioverter defibrillator.
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VT Ablation in Apical Hypertrophic Cardiomyopathy.
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The aim of this study was to perform a systematic evaluation of safety and midterm complications after epicardial ventricular tachycardia (VT) ablation.
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Mapping and ablation of atrial tachycardias (ATs) secondary to catheter ablation of atrial fibrillation (AF) is often challenging due to the complex atrial substrate, different AT mechanisms, and potential origin not only in the left atrium (LA) but also from the right atrium (RA) and the adjacent thoracic veins.
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Catheter ablation procedures for atrial fibrillation (AF) often involve circumferential antral isolation of pulmonary veins (PV). Inability to reliably identify conduction gaps on the ablation line necessitates placing additional lesions within the intended lesion set.
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As the population ages, recurrent ventricular tachycardia (VT) is increasingly encountered in elderly patients with ischemic heart disease. Radiofrequency catheter ablation is useful for reducing VT therapy in patients with an implantable defibrillator. The utility of radiofrequency catheter ablation in the elderly is not well defined.
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What's known on the subject? And what does the study add? We have previously shown that percutaneous radiofrequency ablation guided by image-fusion technology allows for precise needle placement with real time ultrasound superimposed with pre-loaded imaging, removing the need for real-time CT or MR guidance. Emerging technology also allows real-time tracking of a treatment needle within an organ in a virtually created 3D format. To our knowledge, this is the first study utilising a sophisticated ultrasound-based navigation system that uses both image-fusion and real-time probe-tracking technologies for in-vivo renal ablative intervention.
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Rationale: Myofibroblasts typically appear in the myocardium after insults to the heart like mechanical overload and infarction. Apart from contributing to fibrotic remodeling, myofibroblasts induce arrhythmogenic slow conduction and ectopic activity in cardiomyocytes after establishment of heterocellular electrotonic coupling in vitro. So far, it is not known whether α-smooth muscle actin (α-SMA) containing stress fibers, the cytoskeletal components that set myofibroblasts apart from resident fibroblasts, are essential for myofibroblasts to develop arrhythmogenic interactions with cardiomyocytes. Objective: We investigated whether pharmacological ablation of α-SMA containing stress fibers by actin-targeting drugs affects arrhythmogenic myofibroblast–cardiomyocyte cross-talk. Methods and Results: Experiments were performed with patterned growth cell cultures of neonatal rat ventricular cardiomyocytes coated with cardiac myofibroblasts. The preparations exhibited slow conduction and ectopic activity under control conditions. Exposure to actin-targeting drugs (Cytochalasin D, Latrunculin B, Jasplakinolide) for 24 hours led to disruption of α-SMA containing stress fibers. In parallel, conduction velocities increased dose-dependently to values indistinguishable from cardiomyocyte-only preparations and ectopic activity measured continuously over 24 hours was completely suppressed. Mechanistically, antiarrhythmic effects were due to myofibroblast hyperpolarization (Cytochalasin D, Latrunculin B) and disruption of heterocellular gap junctional coupling (Jasplakinolide), which caused normalization of membrane polarization of adjacent cardiomyocytes. Conclusions: The results suggest that α-SMA containing stress fibers importantly contribute to myofibroblast arrhythmogeneicity. After ablation of this cytoskeletal component, cells lose their arrhythmic effects on cardiomyocytes, even if heterocellular electrotonic coupling is sustained. The findings identify α-SMA containing stress fibers as a potential future target of antiarrhythmic therapy in hearts undergoing structural remodeling.
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The aims of the study were (i) to assess the characteristics of patients selected for atrial fibrillation (AF) ablation as first-line therapy, (ii) to identify current clinical criteria for such a strategy, and (iii) to analyse the outcome compared with patients who had failure of antiarrhythmic drug (AAD) therapy prior to ablation.
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In patients with Ebstein's anomaly (EA) arrhythmias are frequently encountered. Although most arrhythmias can be targeted with catheter ablation, specific issues render the procedure more challenging in EA. This study examines the mechanisms of the different arrhythmias related to EA and the outcome after catheter ablation.
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Background—Pulmonary vein stenosis (PVST) is a well-known complication of pulmonary vein isolation (PVI). Specific anatomically designed ablation catheters for antral PVI have not been evaluated with regard to the incidence of PVST. We investigated the incidence, severity, and characteristics of PVST after PVI with the Pulmonary Vein Ablation Catheter (PVAC) and phased radiofrequency technology. Methods and Results A total of 100 patients (55 men) underwent PVI for atrial fibrillation using the PVAC. PVI was guided by selective angiography of each pulmonary vein (PV) in 70 (70%) patients and by reconstructed 3D atriography (ATG) in 30 (30%) patients. Gadolinium-enhanced MRI or multidetector CT was performed in all patients before treatment and 93±78 days after PVI. PVST was classified as follows: insignificant (<25%), mild (25%–50%), moderate (50%–75%), or severe (>75%). A total of 410 PVs were analyzed. Cardiac imaging demonstrated a detectable narrowing of the PV diameter in 23 (23%) patients and in 28 (7%) PVs. In detail, insignificant PVST was observed in 12 (2.9%) PVs, mild PVST in 15 (3.7%), and moderate PVST in 1 (0.2%). No instances of severe PVST were observed. The use of 3D-ATG was associated with a lower incidence of PVST (0.8% [95% CI, 0.0%–2.2%] versus 5.4% [95% CI, 2.7%–8.1%], P=0.027). Conclusions To our knowledge, this study is the first to report the incidence of PVST using the PVAC. In this regard, the PVAC seems to be safe if used in an experienced center. In addition, the use of 3D-ATG may decrease the risk of PVST.
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The identification of cellular pathways capable of limiting ischemia/reperfusion (I/R) injury remains a frontier in medicine, and its clinical relevance is urgent. Histidine triad nucleotide binding protein 1 (HINT1) is a tumor suppressor that influences apoptosis. Because apoptotic pathways are a feature of I/R injury, we asked whether Hint1 influences hepatic I/R injury. Hint1(-/-) and C57BL/6 mice were subjected to 70% liver ischemia followed by reperfusion for 3 or 24 hours or to a sham operation. The serum aminotransferase levels, histological lesions, apoptosis, reactive oxygen species, and expression of B cell lymphoma 2-associated X protein (Bax), heme oxygenase 1 (HO-1), interleukin-6 (IL-6), IL-10, tumor necrosis factor-a, Src, nuclear factor kappa B (p65/RelA), and c-Jun were quantified. The responses to toll-like receptor ligands and nicotinamide adenine dinucleotide phosphate oxidase activity in Kupffer cells were compared in Hint1(-/-) mice and C57BL/6 mice. After I/R, the levels of serum aminotransferases, parenchymal necrosis, and hepatocellular apoptosis were significantly lower in Hint1(-/-) mice versus control mice. Furthermore, Bax expression decreased more than 2-fold in Hint1(-/-) mice, and the increases in reactive oxygen species and HO-1 expression that were evident in wild-type mice after I/R were absent in Hint1(-/-) mice. The phosphorylation of Src and the nuclear translocation of p65 were increased in Hint1(-/-) mice, whereas the nuclear expression of phosphorylated c-Jun was decreased. The levels of the protective cytokines IL-6 and IL-10 were increased in Hint1(-/-) mice. These effects increased survival after I/R in mice lacking Hint1. Hint1(-/-) Kupffer cells were less activated than control cells after stimulation with lipopolysaccharides. CONCLUSION: The Hint1 protein influences the course of I/R injury, and its ablation in Kupffer cells may limit the extent of the injury.