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Cardiovascular AND Tachycardia, ventricular, [keywords]
- Deep sedation in patients undergoing atrioventricular nodal reentry tachycardia ablation. [Journal Article]
- Res Cardiovasc Med 2013 Nov; 2(4):176-9.
General anesthesia and deep sedation can be used during cardiac EPS to relief pain and provide comfort and immobility, but many electrophysiologists avoid sedation for better arrhythmia induction.To determine anesthesia effects in ablation procedures in adults, we used intravenous anesthetic agents in patients who underwent slow pathway ablation.One hundred patients who were to undergo radiofrequency catheter ablation were randomly assigned to with and without intravenous anesthesia groups. All patients had palpitation with a documented electrocardiography (ECG) compatible with atrio-ventricular nodal reentrant tachycardia (AVNRT). We used propofol, fentanyl and midazolam for intravenous sedation. Electrophysiological parameters were checked for the two groups and compared before and after the ablation.Electrophysiological parameters were not significantly different in the two groups. In the anesthetic group, patients were more satisfied with the procedure (P value < 0. 001).Intravenous anesthesia could be done safely in patients who underwent electrophysiological procedures. It had no effect on arrhythmia induction or slow pathway ablation in patients with documented AVNRT.
- Status of Primary Prevention of Sudden Cardiac Death With Implantable Cardioverter Defibrillator in Patients With Chronic Heart Failure. [JOURNAL ARTICLE]
- Circ J 2014 Dec 3.
Background:The current status of primary prevention of sudden cardiac death (SCD) with implantable cardioverter defibrillator (ICD) in patients with heart failure with reduced ejection fraction remains to be fully elucidated in Japan.Methods and
Results:In the chronic heart failure (CHF) cohort study, the CHART-2 Study, we enrolled 2,778 consecutive patients with NYHA class II-III. According to the Japanese Circulation Society guideline of prophylactic ICD, we divided them into 3 groups: group A, class I indication; B, class IIa; and C, no indication. During the (median) 3.2-year follow-up, 79 fatal arrhythmic events (FAE), defined as composite of sudden cardiac/arrhythmic death, ventricular tachycardia/fibrillation and appropriate ICD therapy, occurred. In the groups A, B and C, the prevalence of FAE was 16.1%, 8.9% and 1.9%, respectively; the use of prophylactic ICD among those with FAE, however, was only 44%, 9% and 6%, respectively. In the groups A and B combined, chronic atrial fibrillation (cAF) and left ventricular end-diastolic dimension (LVDd) ≥65 mm were independent predictors of FAE, and, when combined, their prognostic impact was highly significant (hazard ratio, 7.01; P<0.001).
Conclusions:Primary prevention of SCD with ICD in CHF patients is validated but is still underused in Japan, and the combination of cAF and LVDd ≥65 mm may be a useful indication of prophylactic ICD implantation.
- Variable Clinical Features and Ablation of Manifest Nodofascicular/ Ventricular Pathways. [JOURNAL ARTICLE]
- Circ Arrhythm Electrophysiol 2014 Dec 3.
-Manifest nodofascicular/ventricular (NFV) pathways are rare.-From 2008 to 2013, four cases were identified with manifest NFV pathways from three centers. The clinical findings and ablation sites are reported. All four cases presented with a wide complex tachycardia but with different QRS morphologies. Case one showed a LBBB/superior axis, case two a RBBB/inferior axis, case three a LBBB/inferior axis, and case four showed a narrow QRS tachycardia as well as a wide complex tachycardia with a LBBB/inferior axis. Three of the four tachycardias had AV dissociation ruling out extranodal accessory pathways, including atriofascicular pathways. Programmed extrastimuli showed evidence of a decremental accessory pathway in three of the four cases. Coexisting tachycardia mechanisms were seen in three of the four cases (AVNRT (2) and AVRT (1)). Ablation in the slow pathway region eliminated the NFV pathway in three (transient in one) with the other responding to surgical closure of a large ASD. The NFV pathway was a critical part of the tachycardia circuit in one and proved to be a bystander in the other three cases.-Manifest NFV pathways presented with variable QRS expression dependent on ventricular insertion site, and often coexisted with other tachycardia mechanisms (AVNRT and AVRT). In most cases, the atrial insertion of the pathway was in or near the slow pathway region. The NFV pathways were either critical to the tachycardia circuit or served as bystanders.
- Adverse Structural Remodeling of the Left Ventricle and Ventricular Arrhythmias in Patients With Depressed Ejection Fraction. [JOURNAL ARTICLE]
- J Card Fail 2014 Nov 6.
The relationship of life-threatening ventricular arrhythmias to specific patterns of adverse LV remodeling has not been reported. We examined the relationship of ventricular tachycardia and/or fibrillation (VT/VF) to the pattern of left ventricular (LV) structural remodeling and to the degree of LV dysfunction in patients with a low ejection fraction (EF).Data from 127 patients with a low EF (≤0.45) and an implantable cardioverter-defibrillator (ICD) were examined and VT/VF identified by means of ICD device interrogation. Echocardiographic data were used to define LV structural remodeling (eccentric hypertrophy, concentric remodeling/hypertrophy, and normal geometry). VT/VF occurred in 26% of the 127 patients. VT/VF was more common in the 60 patients with LV hypertrophy versus the 67 with normal LV mass (40% vs 13%; P = .001) and in the 61 patients with LV enlargement versus the 66 with a normal chamber size (34% vs 18%; P = .04). When LV chamber size, wall mass, and geometry were assessed in a combinatorial fashion, a Kaplan-Meier analysis indicated that the occurrence of VT/VF was highest in the patients with eccentric hypertrophy (43%), intermediate in those with concentric remodeling/hypertrophy (30%), and lowest (12%) in those with normal geometry (all P < .02). The EFs were similar (P = ns) in these 3 groups of distinctly different patterns of remodeling.Life-threatening ventricular arrhythmias in patients with a low EF are related to the pattern of LV remodeling, not the degree of LV dysfunction. Risk stratification of such patients might be improved by a consideration of the pattern of LV remodeling.
- Increased extent of myocardial fibrosis in genotyped hypertrophic cardiomyopathy with ventricular tachyarrhythmias. [JOURNAL ARTICLE]
- J Cardiol 2014 Nov 14.
Occurrence of malignant ventricular tachyarrhythmias such as ventricular tachycardia and fibrillation (VT/VF) in hypertrophic cardiomyopathy (HCM) can be related to the extent of myocardial fibrosis. Although late gadolinium enhancement (LGE) on cardiovascular magnetic resonance (CMR) imaging has been used to detect myocardial fibrosis, few data exist regarding relationships between CMR-determined myocardial fibrosis and VT/VF in genotyped HCM populations.We retrospectively investigated whether the extent of LGE can be increased in HCM patients with VT/VF compared to those without VT/VF in the genotyped HCM population.We studied 35 HCM patients harboring sarcomere gene mutations (TNNI3=22, MYBPC3=12, MYH7=1) who underwent both CMR imaging and 24-h ambulatory electrocardiographic monitoring. VT/VF were identified in 6 patients (2 men, mean age 55.0 years). The extent of LGE was significantly increased in patients with VT/VF (n=6) compared with those without VT/VF (n=29) (18.6±14.4% vs. 8.3±11.4%, p=0.04), although the LGE extent was not an independent predictor for the occurrence of VT/VF. Applying a cut-off point ≥3.25%, episodes of VT/VF were identified with a sensitivity of 100%, specificity of 51.7%, positive predictive value of 30%, negative predictive value of 100%, and the area under the curve of 0.767 (95% confidence interval: 0.590-0.944).These results demonstrate that myocardial fibrosis determined by CMR imaging may be increased in genotyped HCM patients with episodes of VT/VF. A further prospective study will be needed to clarify the association between the LGE extent and arrhythmic events in HCM patients harboring sarcomere gene mutations.
- Recessive cardiac phenotypes in induced pluripotent stem cell models of Jervell and Lange-Nielsen syndrome: Disease mechanisms and pharmacological rescue. [Journal Article]
- Proc Natl Acad Sci U S A 2014 Dec 16; 111(50):E5383-92.
Jervell and Lange-Nielsen syndrome (JLNS) is one of the most severe life-threatening cardiac arrhythmias. Patients display delayed cardiac repolarization, associated high risk of sudden death due to ventricular tachycardia, and congenital bilateral deafness. In contrast to the autosomal dominant forms of long QT syndrome, JLNS is a recessive trait, resulting from homozygous (or compound heterozygous) mutations in KCNQ1 or KCNE1. These genes encode the α and β subunits, respectively, of the ion channel conducting the slow component of the delayed rectifier K(+) current, IKs. We used complementary approaches, reprogramming patient cells and genetic engineering, to generate human induced pluripotent stem cell (hiPSC) models of JLNS, covering splice site (c.478-2A>T) and missense (c.1781G>A) mutations, the two major classes of JLNS-causing defects in KCNQ1. Electrophysiological comparison of hiPSC-derived cardiomyocytes (CMs) from homozygous JLNS, heterozygous, and wild-type lines recapitulated the typical and severe features of JLNS, including pronounced action and field potential prolongation and severe reduction or absence of IKs. We show that this phenotype had distinct underlying molecular mechanisms in the two sets of cell lines: the previously unidentified c.478-2A>T mutation was amorphic and gave rise to a strictly recessive phenotype in JLNS-CMs, whereas the missense c.1781G>A lesion caused a gene dosage-dependent channel reduction at the cell membrane. Moreover, adrenergic stimulation caused action potential prolongation specifically in JLNS-CMs. Furthermore, sensitivity to proarrhythmic drugs was strongly enhanced in JLNS-CMs but could be pharmacologically corrected. Our data provide mechanistic insight into distinct classes of JLNS-causing mutations and demonstrate the potential of hiPSC-CMs in drug evaluation.
- Characterization of an anesthetized dog model of transient cardiac ischemia and rapid pacing: A pilot study for preclinical assessment of the potential for proarrhythmic risk of novel drug candidates. [JOURNAL ARTICLE]
- J Pharmacol Toxicol Methods 2014 Oct 23.
Preclinical proarrhythmic risk assessment of drug candidates is focused predominantly on arrhythmias arising from repolarization abnormalities. However, drug-induced cardiac conduction slowing is associated with significant risk of life-threatening ventricular arrhythmias, particularly in a setting of cardiac ischemia. Therefore, we optimized and characterized an anesthetized dog model to evaluate the potential proarrhythmic risk of drug candidates in ischemic heart disease patients.Anesthetized dogs were instrumented with atrial and ventricular epicardial electrodes for pacing and measurement of conduction times, and a balloon occluder and flow probe placed around the left anterior descending coronary artery (LAD) distal to the first branch. Conduction times, ECG intervals and incidence of arrhythmias were assessed serially at the end of each dose infusion (flecainide: 0.32, 0.63, 1.25, 2.5 and 5mg/kg, i.v.; dofetilide:1.25, 2.5, 5, 10 and 20μg/kg, i.v.; or vehicle; n=6/group) both during normal flow (with and without rapid pacing) and during 5-min LAD occlusion (with and without rapid pacing). Compound X, a development candidate with mild conduction slowing activity, was also evaluated.Flecainide produced pronounced, dose-dependent slowing of conduction that was exacerbated during ischemia and rapid pacing. In addition, ventricular tachycardia (VT) and fibrillation (VF) occurred in 4 of 6 dogs (3 VF @ 0.63mg/kg; 1VT @ 2.5mg/kg). In contrast, no animals in the vehicle group developed arrhythmias. Dofetilide, a potent IKr blocker that does not slow conduction, prolonged QT interval but did not cause further conduction slowing during ischemia with or without pacing and there were no arrhythmias. Compound X, like flecainide, produced marked conduction slowing and arrhythmias (VT, VF) during ischemia and pacing.This model may be useful to more accurately define shifts in safety margins in a setting of ischemia and increased cardiac demand for drugs that slow conduction.
- First Case of Left Posterior Fascicle in a Bystander Circuit of Idiopathic Left Ventricular Tachycardia. [Journal Article]
- Can J Cardiol 2014 Nov; 30(11):1460.e11-3.
We describe a case of idiopathic left ventricular tachycardia in which the left posterior fascicle was clearly delineated to be a bystander in a re-entry circuit, with participation of the left interventricular myocardium as the retrograde limb instead. To the best of our knowledge, this is the first case report that has directly proven the left posterior fascicle to be a bystander during idiopathic left ventricular tachycardia.
- Scar Characteristics for Prediction of Ventricular Arrhythmia in Ischemic Cardiomyopathy. [JOURNAL ARTICLE]
- Pacing Clin Electrophysiol 2014 Nov 27.
Better risk-stratification tools are needed to identify the best candidates for implantable cardioverter defibrillator implantation. Infarct characterization by cardiac magnetic resonance (CMR) has become an evolving potential tool for risk stratification.We assessed the ability of scar characteristics by CMR in patients with postinfarction left ventricular (LV) dysfunction to predict sustained monomorphic ventricular tachycardia (SMVT).Forty-eight patients with postinfarction LV dysfunction underwent CMR study. Twenty-four patients had history of SMVT and the other 24 were control group and underwent electrophysiological study to assess SMVT inducibilty. Various scar characteristics were assessed in the spontaneous SMVT group and were compared with the inducible and noninducible SMVT groups.Only six patients in the control group had inducible SMVT. In univariable analysis, total scar (absolute and as percent of LV), scar core (absolute and as percent of LV), peri-infarct zone (absolute and as percent of LV), mean infarct transmurality, and number of segments with late gadolinium enhancement (LGE) were statistically significant predictors of spontaneous SMVT experience and SMVT inducibility. In multivariable analysis, total infarct as percent of LV mass was the only significant independent predictor of spontaneous SMVT experience (odds ratio [OR] 1.33 per% change, 95% confidence interval [CI] 1.12-1.6, P = 0.001) and SMVT inducibility (OR 1.3 per% change, 95% CI 1.1-1.6, P = 0.004).Characterization of myocardial infarct by LGE-CMR, specifically total infarct size, is better predictor of spontaneous SMVT experience and SMVT inducibility than LV ejection fraction.
- Ventricular Arrhythmia Risk Stratification in Patients with Tetralogy of Fallot at the Time of Pulmonary Valve Replacement. [JOURNAL ARTICLE]
- Circ Arrhythm Electrophysiol 2014 Nov 21.
-Most patients with repaired tetralogy of Fallot (TOF) require pulmonary valve replacement (PVR), but the evaluation for and management of ventricular arrhythmia remains unclear. This study is aimed at clarifying the optimal approach to this potentially life-threatening issue at the time of PVR.-A retrospective analysis was performed on 205 patients with repaired TOF undergoing PVR at our institution between 1988 and 2010. Median age was 32.9 (range 25.6 years). Previous ventricular tachycardia (VT) occurred in 16 patients (8%) and 37 (16%) had left ventricular (LV) dysfunction, defined as LV ejection fraction <50%. Surgical right ventricular outflow tract cryoablation was performed in 22 patients (10.7%). The primary outcome was a combined event including VT, out-of-hospital cardiac arrest, appropriate implantable cardioverter-defibrillator therapy and sudden cardiac death. Freedom from the combined event at 5, 10, and 15 years was 95, 90, and 79%, respectively. In the first year following PVR, 2 events occurred. Conversely, in the 22 patients who underwent surgical cryoablation, a single event occurred 7 years after PVR. A history of VT and LV dysfunction were associated with higher risk for the combined event (HR 4.7, p=0.004 and HR 0.8, p=0.02 respectively).-Patients with repaired TOF undergoing PVR with history of VT and/or LV dysfunction appear to be associated with a higher risk of arrhythmic events after operation. Events in the first year after PVR are rare, and in select high risk patients, surgical cryoablation does not appear to increase arrhythmic events and may be protective.