Premature Ventricular Contraction Publications (6148)

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Premature Ventricular Contraction Publications

Whether the distribution of scar in arrhythmogenic right ventricular cardiomyopathy (ARVC) plays a role in predicting different types of ventricular arrhythmias is unknown. This study aimed to investigate the prognostic value of scar distribution in patients with ARVC.
We studied 80 consecutive ARVC patients (46 men, mean age 47 ± 15 years) who underwent an electrophysiological study with ablation. Read More

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.

2017Jan
Medicine (Baltimore)
Medicine (Baltimore) 2017 Jan;96(1):e5476
aDivision of Cardiology, Department of Medicine, Taipei Veterans General Hospital bDepartment of Medicine, Division of Cardiology, National Yang-Ming University School of Medicine, Taipei cDepartment of Medicine, Taipei Veterans General Hospital, Yuanshan Branch, Yilan dInstitute of Epidemiology and Preventive Medicine College of Public Health, National Taiwan University, Taipei eDivision of Cardiology, National Yang-Ming University Hospital, Yi-Lan, Taiwan.

The long-term clinical impact of premature ventricular complexes (PVCs) on mortality and morbidity has not been fully studied. This study aimed to investigate the association between the burden of PVCs and adverse clinical outcome.A total of 5778 subjects, who were pacemaker-free and ventricular tachycardia-free at baseline, received 24-hour electrocardiography monitoring between January 1, 2002 and December 31, 2004. Read More

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.

2016Dec
J. Cardiovasc. Electrophysiol.
J Cardiovasc Electrophysiol 2016 Dec 29. Epub 2016 Dec 29.
Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, AL, USA.
2016Dec
J Med Signals Sens
J Med Signals Sens 2016 Oct-Dec;6(4):218-223
Department of Engineering, Shahed University, Tehran, Iran.

Ventricular arrhythmias are one of the most important causes of annual deaths in the world, which may lead to sudden cardiac deaths. Accurate and early diagnosis of ventricular arrhythmias in heart diseases is essential for preventing mortality in cardiac patients. Ventricular activity on the electrocardiogram (ECG) signal is in the interval from the beginning of QRS complex to T wave end. Read More

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.

2016Dec
Europace
Europace 2016 Dec;18(suppl 4):iv16-iv22
UCLA Cardiac Arrhythmia Center, UCLA Heath System, David Geffen School of Medicine at UCLA, Suite 660 Los Angeles, CA 90095, USA.

The precise localization of the site of origin of a premature ventricular contraction (PVC) prior to ablation can facilitate the planning and execution of the electrophysiological procedure. In clinical practice, the targeted ablation site is estimated from the standard 12-lead ECG. The accuracy of this qualitative estimation has limitations, particularly in the localization of PVCs originating from the papillary muscles. Read More

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.

2016Dec
Clin Case Rep
Clin Case Rep 2016 Dec 13;4(12):1195-1200. Epub 2016 Nov 13.
Department of Arrhythmia and ElectrophysiologyDivision of CardiologyZentralklinik Bad BerkaBad BerkaGermany; Otto-von-Guericke University School of MedicineMagdeburgGermany.

Catheter ablation of para-Hisian premature ventricular contractions (PVCs) still represents a challenge and is a compromise between success and inadvertent AV block. We describe a possible strategy to address PVCs from this location with high-amplitude His-bundle potentials at the site of earliest activation. Read More

2016Dec
Circ Arrhythm Electrophysiol
Circ Arrhythm Electrophysiol 2016 Dec;9(12)
From the Department of Pharmacology, University of Michigan Medical School, Ann Arbor (Y.B., C.R.F., L.F.L.-S., C.C., L.L.I.); Center for Arrhythmia Research and Department of Medicine/Cardiovascular Medicine, University of Michigan, Ann Arbor (B.C.W., R.R.-M., J.A., H.H.V., J.J.); Leon H. Charney Division of Cardiology, New York University School of Medicine, NY (X.L., M.D.); Department of Pharmacology and Physiology, University of Rochester Medical Center, NY (D.S.A.); and Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis (Z.W.).

Mutations in SCN2B, encoding voltage-gated sodium channel β2-subunits, are associated with human cardiac arrhythmias, including atrial fibrillation and Brugada syndrome. Because of this, we propose that β2-subunits play critical roles in the establishment or maintenance of normal cardiac electric activity in vivo.
To understand the pathophysiological roles of β2 in the heart, we investigated the cardiac phenotype of Scn2b null mice. Read More

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.