Premature Ventricular Complexes (premature + ventricular_complex)

Distribution by Scientific Domains


Selected Abstracts


Calcium Channel Antagonism Reduces Exercise-Induced Ventricular Arrhythmias in Catecholaminergic Polymorphic Ventricular Tachycardia Patients with RyR2 Mutations

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2005
HEIKKI SWAN M.D.
Introduction: Recently, gain-of-function mutations of cardiac ryanodine receptor RyR2 gene have been identified as a cause of familial or catecholaminergic polymorphic ventricular tachycardia. We examined the influence of the calcium channel blockers, verapamil and magnesium, on exercise-induced ventricular arrhythmias in patients with RyR2 mutations. Methods and Results: Six molecularly defined catecholaminergic polymorphic ventricular tachycardia patients, all carrying a RyR2 mutation and on ,-adrenergic blocker therapy, underwent exercise stress test four times: at baseline, after verapamil and magnesium sulphate infusions, and finally, without interventions. The number of isolated and successive premature ventricular complexes during exercise ranged from 40 to 374 beats (mean 165 beats) at baseline, and was reduced during verapamil by 76 ± 17% (P < 0.05). Premature ventricular complexes appeared later and at higher heart rate during verapamil than at baseline (119 ± 21 vs. 127 ± 27 min,1, P < 0.05). Magnesium did not inhibit the arrhythmias. Results in the fourth exercise stress test without interventions were similar to those in the first baseline study. Conclusions: This study provides the first in vivo demonstration that a calcium channel antagonist, verapamil, can suppress premature ventricular complexes and nonsustained ventricular salvoes in catecholaminergic polymorphic ventricular tachycardia caused by RyR2 mutations. Modifying the abnormal calcium handling by calcium antagonists might have therapeutic value. [source]


Clinical Usefulness of a Multielectrode Basket Catheter for Idiopathic Ventricular Tachycardia Originating from Right Ventricular Outflow Tract

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2001
TAKESHI AIBA M.D.
Basket Catheter in Idiopathic VT.Introduction: It often is difficult to determine the optimal ablation site for idiopathic ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT) when the VT or premature ventricular complex (PVC) does not occur frequently. The aim of our study was to evaluate the usefulness of a multielectrode basket catheter for ablation of idiopathic VT originating from the RVOT. Methods and Results: Radiofrequency (RF) catheter ablation was performed using a 4-mm tip, quadripolar catheter in 50 consecutive patients with 81 VTs originating from the RVOT with (basket group = 25 patients with 45 VTs) or without (control group = 25 patients with 36 VTs) predeployment of a multielectrode basket catheter composed of 64 electrodes. Deployment of the multielectrode basket catheter was possible and safe in all 25 patients in the basket group. Ablation was successful in 25 (100%) of 25 patients in the basket group and in 22 (88%) of 25 patients in the control group. The total number of RF applications and the number of RF applications per PVC morphology did not differ between the two groups. However, both the fluoroscopic and ablation procedure times per PVC morphology were shorter in the basket group than in the control group (36.8 ± 14.1 min vs 52.0 ± 32.5 min, P = 0.04; 60.0 ± 14.6 vs 81.5 ± 51.2 min, P = 0.05). This difference was more pronounced in the 29 patients in whom VT or PVC was not frequently observed. Conclusion: The multielectrode basket catheter is safe and useful for determining the optimal ablation site in patients with idiopathic VT originating from the RVOT, especially in those without frequent VT or PVC. [source]


Calcium Channel Antagonism Reduces Exercise-Induced Ventricular Arrhythmias in Catecholaminergic Polymorphic Ventricular Tachycardia Patients with RyR2 Mutations

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2005
HEIKKI SWAN M.D.
Introduction: Recently, gain-of-function mutations of cardiac ryanodine receptor RyR2 gene have been identified as a cause of familial or catecholaminergic polymorphic ventricular tachycardia. We examined the influence of the calcium channel blockers, verapamil and magnesium, on exercise-induced ventricular arrhythmias in patients with RyR2 mutations. Methods and Results: Six molecularly defined catecholaminergic polymorphic ventricular tachycardia patients, all carrying a RyR2 mutation and on ,-adrenergic blocker therapy, underwent exercise stress test four times: at baseline, after verapamil and magnesium sulphate infusions, and finally, without interventions. The number of isolated and successive premature ventricular complexes during exercise ranged from 40 to 374 beats (mean 165 beats) at baseline, and was reduced during verapamil by 76 ± 17% (P < 0.05). Premature ventricular complexes appeared later and at higher heart rate during verapamil than at baseline (119 ± 21 vs. 127 ± 27 min,1, P < 0.05). Magnesium did not inhibit the arrhythmias. Results in the fourth exercise stress test without interventions were similar to those in the first baseline study. Conclusions: This study provides the first in vivo demonstration that a calcium channel antagonist, verapamil, can suppress premature ventricular complexes and nonsustained ventricular salvoes in catecholaminergic polymorphic ventricular tachycardia caused by RyR2 mutations. Modifying the abnormal calcium handling by calcium antagonists might have therapeutic value. [source]


Clinical Characteristics of Patients With Spontaneous or Inducible Ventricular Fibrillation Without Apparent Heart Disease Presenting with J Wave and ST Segment Elevation in Inferior Leads

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2000
MASAHTKO TAKAGI M.D., Ph.D.
Ventricular Fibrillation with J Wave in Inferior Leads. Introduction: The clinical characteristics of three patients with spontaneous or inducible ventricular fibrillation (VF) without apparent heart disease, who presented with J wave and ST segment elevation in inferior leads, are described. Methods and Results: All patients were male and experienced syncope. Their symptoms occurred at night or early in the morning. Holter ECG revealed infrequent premature ventricular complexes. Injection with disopyramide 2 mg/kg augmented ST segment elevation. Conclusion: These characteristics were very similar to those of patients with Brugada syndrome. These three patients with these specific features might have a variant of Brugada syndrome. [source]


First Evidence of Premature Ventricular Complex-Induced Cardiomyopathy: A Potentially Reversible Cause of Heart Failure

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 3 2000
SUMEET S. CHUGH M.D.
PVC-Induced Cardiomyopathy. Tachycardia-induced cardiomyopathy is a well-recognized and reversible condition, but left ventricular dysfunction due to frequent isolated premature ventricular complexes (PVCs) has not been reported. We observed resolution of dilated cardiomyopathy in a patient after a focal source of PVCs was eliminated by radiofrequency ablation. In a subset of patients with heart failure, PVC-induced cardiomyopathy may be a potentially reversible cause of left ventricular dysfunction. [source]


Temporal Variability of Ventricular Arrhythmias in Boxer Dogs with Arrhythmogenic Right Ventricular Cardiomyopathy

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2009
B.A. Scansen
Background: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is prevalent in the Boxer. There is little information on the temporal variability of ventricular arrhythmias within affected dogs. Objective: To evaluate ambulatory electrocardiograms (AECG) from Boxers with ARVC for hourly variation in premature ventricular complexes (PVC) and heart rate (HR). Animals: One hundred and sixty-two Boxer dogs with ARVC. Methods: Retrospective, observational study of 1,181 AECGs collected from Boxer dogs at The Ohio State University from 1997 to 2004 was evaluated. The proportion of depolarizations that were PVCs was compared across each hour of the day, during six 4-hour periods of day, to the time after AECG application, and to the maximum and minimum HR. Results: A lower proportion of PVCs was noted during early morning (midnight to 0400 hours) as compared with the morning (0800,1200 hours) and late (1600,2000 hours) afternoon (P= .012). There was no increase in PVC proportion in the 1st hour after AECG application as compared with all other hours of the day (P= .06). There was poor correlation between maximum (,= 0.19) and minimum (,= 0.12) HR and PVC proportion. Conclusions and Clinical Importance: The likelihood of PVC occurrence in Boxer dogs with ARVC was relatively constant throughout the day, although slightly greater during the hours of 0800,1200 and 1600,2000. A biologically important correlation with HR was not apparent. The role of autonomic activity in the modulation of electrical instability in the Boxer with ARVC requires further study. [source]


Altered Autonomic Cardiac Control Predicts Restenosis After Percutaneous Coronary Intervention

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2006
MATTHIAS GOERNIG
Background: Early and late restenosis in up to 30% remains a major problem for long-term success after percutaneous coronary intervention (PCI). Compared to bare metal stents, the use of drug-eluting stents reduces restenosis below 10%, but implant coasts have to be considered. In restenosis noninvasive testing lacks diagnostic power. We applied a new approach to identify patients with a high risk for restenosis after PCI by combining heart rate (HR) and blood pressure variability (BPV) analyses. Methods: In 52 patients with clinical suspicion of restenosis and history of PCI, we investigated patterns of cardiovagal autonomic regulation prior to cardiac catheterization. The patients were separated in (i) patients with restenosis (CAD+R) and (ii) patients without restenosis (CAD,R), where restenosis is defined as a stenosis greater than 75% of luminal diameter in at least one main vessel. The following parameters/methods were evaluated: Canadian Cardiovascular Society grade (CCS-grade), vessel disease score (CAD-level), left ventricular ejection fraction (LVEF), heart rate variability (HRV), BPV, baroreflex sensitivity (BRS), as well as HR turbulence and blood pressure (BP) potentiation caused by premature ventricular complexes. Results: Whereas age, LVEF, CAD-level, CCS-grade, and mean BP did not differ between CAD+R and CAD,R, significant differences were found in (i) BPV: diastolic LF/P, systolic, and diastolic UVLF, (ii) in BRS: slope of tachycardic sequences, and (iii) in extrasystolic parameters: heart rate turbulence onset (HRTO) and potentiation of systolic BP (SBPP). Standard HRV parameters did not show significant differences between the groups. Using the two parameters diastolic LF/P (threshold >0.2) and HRTO (threshold >0) restenosis were predicted in 83.4%. Conclusions: These results demonstrate that indicators of sympathetic activation or vagal depression identify restenosis in patients after PCI, thus opening a perspective for a new noninvasive monitoring. [source]


Frequent Premature Ventricular Complexes Originating from the Right Ventricular Outflow Tract Are Associated with Left Ventricular Dysfunction

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2008
Yumiko Kanei M.D.
Background: Recent case series have shown reversal of left ventricular (LV) dysfunction after catheter ablation of frequent premature ventricular complexes (PVCs) originating from the right ventricular outflow tract (RVOT). We conducted a retrospective study to evaluate the prevalence of patients with frequent RVOT PVCs (,10 per hour) and LV dysfunction. Methods: RVOT PVC was defined as PVC with left bundle branch block morphology and inferior axis on a 12-lead ECG. We included patients with frequent RVOT PVCs on 24-hours Holter monitor who had a recent evaluation of LV function. Patients with structural heart disease, including obstructive coronary artery disease, were excluded. Patients were divided into three groups based on the number of PVCs (<1000/24 hour, 1000,10,000/24 hour, ,10,000/24 hour), and the prevalence of LV dysfunction was evaluated in each group. Results: Our analysis included 108 patients: 24 patients had <1000PVCs/24 hour, 55 patients had 1000,10,000PVCs/24 hour, and 29 patients had ,10,000PVCs/24 hour. The prevalence of LV dysfunction was 4%, 12%, and 34%, respectively (P = 0.02). With logistic regression analysis, non-sustained ventricular tachycardia was an independent predictor of LV dysfunction with odds ratio of 3.6 (1.3,10.1). Conclusion: We demonstrated a significant association between frequent RVOT PVCs and LV dysfunction in patients without structural heart disease. [source]