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Cardiovascular AND Tachycardia, ventricular, [keywords]
- Reperfusion-induced sustained ventricular tachycardia, leading to ventricular fibrillation, in chronically instrumented, intact, conscious mice. [Journal Article]
- Physiol Rep 2014 Jun 1; 2(6)
Reperfusion-induced lethal ventricular arrhythmias are observed during relief of coronary artery spasm, with unstable angina, exercise-induced ischemia, and silent ischemia. Accordingly, significant efforts are underway to understand the mechanisms responsible for reperfusion-induced lethal arrhythmias and mice have become increasingly important in these efforts. However, although reperfusion-induced sustained ventricular tachycardia leading to ventricular fibrillation (VF) has been recorded in many models, reports in mice are sparse and of limited success. Importantly, none of these studies were conducted in intact, conscious mice. Accordingly, a chronically instrumented, intact, conscious murine model of reperfusion-induced lethal arrhythmias has the potential to be of major importance for advancing the concepts and methods that drive cardiovascular therapies. Therefore, we describe, for the first time, the use of an intact, conscious, murine model of reperfusion-induced lethal arrhythmias. Male mice (n = 9) were instrumented to record cardiac output and the electrocardiogram. In addition, a snare was placed around the left main coronary artery. Following recovery, the susceptibility to sustained ventricular tachycardia produced by 3 min of occlusion and reperfusion of the left main coronary artery was determined in conscious mice by pulling on the snare. Reperfusion culminated in sustained ventricular tachycardia, leading to VF, in all nine conscious mice. The procedures conducted in conscious C57BL/6J mice, a strain commonly used in transgenic studies, can be utilized in genetically modified models to enhance our understanding of single gene defects on reperfusion-induced lethal ventricular arrhythmias in intact, conscious, and complex animals.
- Left ventricular four-dimensional rotational angiography with low radiation dose through interphase registration. [JOURNAL ARTICLE]
- Europace 2014 Jun 27.
Ventricular tachycardia ablations could benefit from four-dimensional (4D) (dynamic 3D) visualization of the left ventricle (LV) as roadmap for anatomy-guided procedures. Our aim was to develop an algorithm that combines information of several cardiac phases to improve signal-to-noise ratio in low-dose, noisy rotational angiography [three-dimensional rotational angiography (3DRA)] image datasets, enabling semi-automatic segmentation and generation of 4D rotational angiography (4DRA) LV surface models.We developed a novel slow pacing protocol for low-dose 4DRA imaging and applied interphase registration (IPR) to improve contrast-to-noise ratio (CNR) such that 4D LV segmentation could be achieved using a single iso-intensity value (ISO). The method was applied to construct four-phase dynamic LV models from five porcine experiments. Optimal choice of IPR and ISO parameters and resulting LV model accuracy were assessed by comparison with 'groundtruth' manual LV delineations using surface distance measures [root mean square distance (RMSD), Hausdorff distance (HD), fraction of surface distances ≤3 mm (d3 mm)]. Using IPR with optimized parameters, CNR improved by 88% (P < 0.0001) and increased segmentation accuracy was proven irrespective of ISO. Significant improvement was achieved in RMSD [mean at optimal ISO: -28.3% (95% confidence interval (CI) -21.7 to -35.0, P < 0.0001)], HD [-21.4% (95% CI -18.6 to -24.1, P < 0.0001)], and d3 mm [+7.8% (95% CI +4.6 to +10.9, P < 0.0001)]. An average d3 mm of 95.6 ± 2.8% was reached at optimal ISO. Time to generate a 4D model was ±11.5 min with IPR vs. ±22 min without.Interphase registration significantly improves 4DRA image quality and facilitates semi-automatic segmentation, resulting in clinically useful accuracy despite low-dose image acquisition protocols, while shortening 4D model generation time. This opens the prospect of 4D imaging in clinical settings.
- From wide QRS tachycardia to a diagnostic surprise. [JOURNAL ARTICLE]
- Anadolu Kardiyol Derg 2014 Jun 9.
A 29-year old male patient presented with a hemodynamically significant ventricular tachycardia. Despite a comprehensive examination, the correct diagnosis was unfortunately established after two years. We discuss why the correct diagnosis was initially overlooked in physical examination, electrocardiogram, echocardiography and cardiac magnetic resonance imaging, and which findings led the cardiologists to misdiagnose the patient. We have organized this report in a format that the information is presented to a consultant physician by a resident physician to simulate the way such information emerges in the real life as we have encountered. The consultant physician responds as new information is presented, expressing his reasoning with the reader.
- Role of late gadolinium enhancement cardiovascular magnetic resonance in the risk stratification of hypertrophic cardiomyopathy. [JOURNAL ARTICLE]
- Heart 2014 Jun 24.
Myocardial fibrosis identified by late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) in patients with hypertrophic cardiomyopathy (HCM) is associated with adverse cardiovascular events, but its value as an independent risk factor for sudden cardiac death (SCD) is unknown. We investigated the role of LGE-CMR in the risk stratification of HCM.We conducted a prospective cohort study in a tertiary referral centre. Consecutive patients with HCM (n=711, median age 56.3 years, IQR 46.7-66.6; 70.0% male) underwent LGE-CMR and were followed for a median 3.5 years. The primary end point was SCD or aborted SCD.Overall, 471 patients (66.2%) had myocardial fibrosis (median 5.9% of left ventricular mass, IQR: 2.2-13.3). Twenty-two (3.1%) reached the primary end point. The extent but not the presence of fibrosis was a significant univariable predictor of the primary end point (HR per 5% LGE: 1.24, 95% CI 1.06 to 1.45; p=0.007 and HR for LGE: 2.69, 95% CI 0.91 to 7.97; p=0.073, respectively). However, on multivariable analysis, only LV-EF remained statistically significant (HR: 0.92, 95% CI 0.89 to 0.95; p<0.001). For the secondary outcome of cardiovascular mortality/aborted SCD, the presence and the amount of fibrosis were significant predictors on univariable but not multivariable analysis after adjusting for LV-EF and non-sustained ventricular tachycardia.The amount of myocardial fibrosis was a strong univariable predictor of SCD risk. However, this effect was not maintained after adjusting for LV-EF. Further work is required to elucidate the interrelationship between fibrosis and traditional predictors of outcome in HCM.
- Arrhythmogenic calmodulin mutations disrupt intracellular cardiomyocyte Ca2+ regulation by distinct mechanisms. [Journal Article, Research Support, N.I.H., Extramural]
- J Am Heart Assoc 2014 Jun; 3(3):e000996.
Calmodulin (CaM) mutations have been identified recently in subjects with congenital long QT syndrome (LQTS) or catecholaminergic polymorphic ventricular tachycardia (CPVT), but the mechanisms responsible for these divergent arrhythmia-susceptibility syndromes in this context are unknown. We tested the hypothesis that LQTS-associated CaM mutants disrupt Ca(2+) homeostasis in developing cardiomyocytes possibly by affecting either late Na current or Ca(2+)-dependent inactivation of L-type Ca(2+) current.We coexpressed CaM mutants with the human cardiac Na channel (NaV1.5) in tsA201 cells, and we used mammalian fetal ventricular cardiomyocytes to investigate LQTS- and CPVT-associated CaM mutations (LQTS- and CPVT-CaM). LQTS-CaM mutants do not consistently affect L-type Na current in heterologous cells or native cardiomyocytes, suggesting that the Na channel does not contribute to LQTS pathogenesis in the context of CaM mutations. LQTS-CaM mutants (D96V, D130G, F142L) impaired Ca(2+)-dependent inactivation, whereas the CPVT-CaM mutant N54I had no effect on Ca(2+)-dependent inactivation. LQTS-CaM mutants led to loss of Ca(2+)-transient entrainment with the rank order from greatest to least effect: CaM-D130G~CaM-D96V>CaM-F142L. This rank order follows measured Ca(2+)-CaM affinities for wild-type and mutant CaM. Acute isoproterenol restored entrainment for CaM-130G and CaM-D96V but caused irreversible cytosolic Ca(2+) overload for cells expressing a CPVT-CaM mutant.CaM mutations associated with LQTS may not affect L-type Na(+) current but may evoke defective Ca(2+)-dependent inactivation of L-type Ca(2+) current.
- Gene therapy for the treatment of catecholaminergic polymorphic ventricular tachycardia. [Editorial]
- Circulation 2014 Jun 24; 129(25):2633-5.
- Complete Recovery From Severe Tachycardia-Induced Cardiomyopathy in a Patient With Ebstein's Anomaly. [JOURNAL ARTICLE]
- World J Pediatr Congenit Heart Surg 2014 Jun 23; 5(3):484-487.
We report the case of a young patient with repaired Ebstein's anomaly who developed severe tachycardia-induced cardiomyopathy and a large apical thrombus as a consequence of sustained atrial flutter with a 2:1 conduction. In spite of a dramatic course in hospital with prolonged mechanical resuscitation and extracorporeal membrane oxygenation, she survived and made a rapid and full recovery. This remarkable case underlines that atrial arrhythmias, the most common complication in adults with congenital heart disease, may have devastating outcomes when timely recognition is missed and treatment delayed-thus, emphasizing the importance of good patient education.
- Multivalvular Replacement and Ventricular Arrhythmias in a Female Child With Congenital Polyvalvular Disease. [JOURNAL ARTICLE]
- World J Pediatr Congenit Heart Surg 2014 Jun 23; 5(3):463-466.
We report the clinical course of a female child with a normal karyotype and chromosomal microarray who presented as an infant with clinical findings consistent with congenital polyvalvular disease (CPVD). This clinical entity describes patients with multiple congenitally dysplastic valves, often showing nodular or cystic malformation in at least two cardiac valves. This patient then developed medically refractory multifocal ventricular arrhythmia and required radiofrequency ablation at seven months of age. She had good tachycardia control but became symptomatic with right heart failure related to progressive tricuspid, pulmonary, and mitral valve dysfunction necessitating multivalvular replacement at 21 months of age.
- Cardiac ablation of Rheb1 reduces sodium currents in infant mice. [Journal Article]
- Int J Clin Exp Med 2014; 7(4):947-54.
The Ras homolog enriched in brain gene (Rheb) is a center player within the insulin/Rheb/Mammalian Target of Rapamycin (mTOR) pathway, and plays a critical role in regulating cellular growth. Rheb-/- embryos have been reported to die around midgestation, due to the defects of the development of the cardiovascular system. Recent studies from ours and another group consistently showed that Rheb1 was indispensable for the cardiac hypertrophic growth after early postnatal period. Besides that, we also found that Rheb1 a-MHC-Cre (cKO) mice exhibited ventricular tachycardia. However, the precise mechanism by which Rheb1 knockout causes ventricular arrhythmia in these mice is still unclear.Mouse cardiomyocytes were isolated using 10 days suckling Rheb1 cKO and wide type mice using Collagenase Type II. Sodium currents and L-type calcium currents were recorded using the whole-cell patch clamping technique.The sodium current density of ventricular cardiomyocytes from Rheb1 cKO mice was decreased by about 60%. Significant left shift but no slope altered was observed in activation curve with V1/2 values of -35.35 ± 1.12 mV for Rheb1 cKO group and -40.72 ± 1.18 mV for the controls. In addition, the area of window current, which refers the overlap of normalized activation and inactivation, was larger in Rheb1 cKO mice. Moreover, the sodium current, in general, was recovered much slower in Rheb1 cKO mice than that of the controls. However, L-type calcium currents were preserved in Rheb1 cKO mice.Sodium currents are decreased in Rheb1 cKO mice, which might be responsible for the phenotype of arrhythima in Rheb1 cKO mice. Understanding the molecular composition of sodium ion channel complexes in the heart of these Rheb1 cKO mice will be critical to develop innovative and effective therapies for the treatment of cardiac arrhythmia.
- Cardioverter-defibrillator implantation to treat cardiac fibroma-induced ventricular tachycardia in a 70-year-old woman. [Journal Article]
- Tex Heart Inst J 2014 Jun; 41(3):329-31.
Benign cardiac fibroma is rarely reported in adults. Its clinical symptoms are related to outflow obstruction or dysrhythmias. We present the case of a 70-year-old woman who had a syncopal episode from ventricular tachycardia caused by cardiac fibroma. Because of unfavorable tumor anatomy, the patient was not a candidate for surgical excision, and she declined orthotopic heart transplantation. To prevent sudden cardiac death, we placed an implantable cardioverter-defibrillator, and the patient remained well throughout the 2-year follow-up period. To our knowledge, this is the first report of implantable cardioverter-defibrillator therapy to treat an adult patient's unresectable cardiac fibroma.