Premature Ventricular Contraction Publications (6148)
Premature Ventricular Contraction Publications
Thirty-four patients receive both endocardial and epicardial mapping. Abnormal endocardial substrates and epicardial substrates were characterized. Three groups were defined according to the epicardial and endocardial scar gradient (<10%: transmural, 10-20%: intermediate, >20%: horizontal, as groups 1, 2, and 3, respectively). Sinus rhythm electrograms underwent a Hilbert-Huang spectral analysis and were displayed as 3D Simultaneous Amplitude Frequency Electrogram Transformation (SAFE-T) maps, which represented the arrhythmogenic potentials. The baseline characteristics were similar between the three groups. Group 3 patients had a higher incidence of fatal ventricular arrhythmias requiring defibrillation and cardiac arrest during the initial presentation despite having fewer premature ventricular complexes. A larger area of arrhythmogenic potentials in the epicardium was observed in patients with horizontal scar. The epicardial-endocardial scar gradient was independently associated with the occurrence of fatal ventricular arrhythmias after a multivariate adjustment. The total, ventricular tachycardia, and VF recurrent rates were higher in Group 3 during 38 ± 21 months of follow-up.
For ARVC, the epicardial substrate that extended in the horizontal plane rather than transmurally provided the arrhythmogenic substrate for a fatal ventricular arrhythmia circuit.
Clinical event data were retrieved from the Bureau of National Health Insurance of Taiwan. Multivariate Cox hazards regression models and propensity-score matching were applied to assess the association between PVCs and adverse clinical outcome.Average follow-up time was 10[REPLACEMENT CHARACTER]± 1 year. In all, 1403 subjects expired, 1301 subjects were hospitalized in the cardiovascular (CV) ward, 3384 were hospitalized for any reason, and 631 subjects developed new-onset heart failure (HF). The optimal cut-off PVC frequency (12 beats per day) was obtained through receiver operator characteristic curves, with a sensitivity of 58.4% and specificity of 59.8%. Upon multivariate analysis, a PVC frequency >12 beats per day was an independent predictor for all mortality (hazard ratio [HR]: 1.429, 95% confidence interval [CI]: 1.284-1.590), CV hospitalization (HR: 1.127, 95% CI: 1.008-1.260), all-cause hospitalization (HR 1.094, 95% CI: 1.021-1.173), and new-onset HF (HR: 1.411, 95% CI: 1.203-1.655). Subjects with a PVC frequency >12 beats per day had an increased risk of cardiac death attributable to HF and sudden cardiac death. The incidence rates for mortality and HF were significantly increased in cases of raised PVC frequency. Propensity-score matching analysis also echoed the main findings.Increased PVC burden was associated with a higher incidence of all-cause mortality, CV hospitalization, all-cause hospitalization, and new-onset HF which was independent of other clinical risk factors.
Variations in the ECG signal and its features may indicate heart condition of patients. The first step to extract features of ECG in time domain is finding R peaks. In this paper, a combination of two algorithms of Pan-Tompkins and state logic machine has been used to find R peaks in heart signals for normal sinus signals and ventricular abnormalities. Then, a healthy or sick beat may be realized by comparing the difference between R peaks obtained from two algorithms in each beat. The morphological features of the ECG signal in the range of QRS complex are evaluated. Ventricular tachycardia (VT), ventricular flutter (VFL), ventricular fibrillation (VFI), ventricular escape beat (VEB), and premature ventricular contractions (PVCs) are abnormalities studied in this paper. In the classification step, the support vector machine (SVM) classifier with Gaussian kernel (one in front of everyone) is used. Accuracy percentages of ventricular abnormalities mentioned above and normal sinus rhythm are respectively obtained as 95.8%, 92.8%, 94.5, 98.9%, 91.5%, and 100%. The database of this paper has been taken from normal sinus rhythm and MIT-SCD banks available on Physionet.org.
Although no spontaneous VPCs were seen after the elimination of Type 1 and 2 VPCs, pacing resulting in capture at the APM induced type 3 VPC (RBBB configuration and superior axis) reproducibly. The electrophysiological findings observed in our representative case have important implications both for understanding the pathophysiology of CPVT and for considering therapeutic strategies. This article is protected by copyright. All rights reserved.
Clinical available electrocardiographic imaging (ECGi) techniques that incorporate patient-specific anatomy may improve the localization of these PVCs, but require body surface maps with greater specificity for the epicardium. The purpose of this report is to demonstrate that a novel cardiac isochrone positioning system (CIPS) program can accurately detect the specific location of the PVC on the papillary muscle using only a 12-lead ECG.
Cardiac isochrone positioning system uses three components: (i) endocardial and epicardial cardiac anatomy and torso geometry derived from MRI, (ii) the patient-specific electrode positions derived from an MRI model registered 3D image, and (iii) the 12-lead ECG. CIPS localizes the PVC origin by matching the anatomical isochrone vector with the ECG vector. The predicted PVC origin was compared with the site of successful ablation or stimulation. Three patients who underwent electrophysiological mapping and ablation of PVCs originating from the papillary muscles were studied. CIPS localized the PVC origin for all three patients to the correct papillary muscle and specifically to the base, mid, or apical region.
A simplified form of ECGi utilizing only 12 standard electrocardiographic leads may facilitate accurate localization of the origin of papillary muscle PVCs.
We observed reduced sodium and potassium current densities in ventricular myocytes, as well as conduction slowing in the right ventricular outflow tract region. Functional reentry, resulting from the interplay between slowed conduction, prolonged repolarization, and increased incidence of premature ventricular complexes, was found to underlie the mechanism of spontaneous polymorphic ventricular tachycardia. Scn5a transcript levels were similar in Scn2b null and wild-type ventricles, as were levels of Nav1.5 protein, suggesting that similar to the previous work in neurons, the major function of β2-subunits in the ventricle is to chaperone voltage-gated sodium channel α-subunits to the plasma membrane. Interestingly, Scn2b deletion resulted in region-specific effects in the heart. Scn2b null atria had normal levels of sodium current density compared with wild type. Scn2b null hearts were more susceptible to atrial fibrillation, had increased levels of fibrosis, and higher repolarization dispersion than wild-type littermates.
Genetic deletion of Scn2b in mice results in ventricular and atrial arrhythmias, consistent with reported SCN2B mutations in human patients.
Classically the outflow tract (right or left), with the typical inferior axis with left (eventually right) bundle brunch block like ECG morphology, is considered the most frequent site of origin for idiopathic VPC, but with the widespread of EP procedures and advancement of technology making possible to map and ablate difficult locations, it is possible to see a growing and changing population referred for idiopathic VPC ablation, displaying that, almost any region of the heart may be source of this kind of arrhythmia that can be successfully treated. A well-planned procedure, with the presumed region of origin settled and employing the current technology and knowledge (tips), will have a high chance of cure.