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Ventricular Premature Beats (ventricular + premature_beat)

Distribution by Scientific Domains

Medical Sciences	91%

Selected Abstracts

Relationship Between Heart Rate Turbulence and Heart Rate, Heart Rate Variability, and Number of Ventricular Premature Beats in Coronary Patients

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2004
IWONA CYGANKIEWICZ M.D., Ph.D.
Introduction: Heart rate variability (HRV) illustrates regulation of the heart by the autonomic nervous system whereas heart rate turbulence (HRT) is believed to reflect baroreflex sensitivity. The aim of this study was to determine the association between HRT and HRV parameters and the relationship between HRT parameters and heart rate and number of ventricular premature beats (VPBs) used to calculate HRT parameters. Methods and Results: In 146 patients (117 males and 29 females; mean age 62 years) with coronary artery disease, a 24-hour ECG Holter monitoring was performed to calculate mean heart rate (RR interval), number of VPBs, time- and frequency-domain HRV parameters and two HRT parameters: turbulence onset (TO) and turbulence slope (TS). Univariate and multivariate regression analyses were performed to evaluate the association between tested parameters. Significant correlation between TS and mean RR interval was observed (r = 0.42; p < 0.001), while no association for TO vs. RR interval was found. TS values were significantly higher in patients with less than 10 VPBs/24 hours than in patients with more frequent VPBs. Significant associations between HRT and HRV parameters were found with TS showing stronger correlation with HRV parameters than TO (r value ranging from 0.35 to 0.62 for TS vs. ,0.16 to ,0.38 for TO). Conclusion: HRT parameters correlate strongly with HRV parameters indicating that HRT should be considered as a reflection of both baroreceptors response and overall autonomic tone. Heart rate dependence of turbulence slope indicates the need to adjust this parameter for heart rate. (J Cardiovasc Electrophysiol, Vol. 15, pp. 731-737, July 2004) [source]

Stepwise Transition of 2:1 Atrio-Ventricular Block to 1:1 Conduction Induced by Ventricular Premature Beats in a Patient with Atypical AVNRT

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2010
ANTONIO SORGENTE M.D.
A 55-year-old man with a 2-year history of recurrent paroxysmal palpitations and with an electrocardiogram documentation of atypical atrioventricular nodal re-entrant tachycardia (AVNRT) was referred to us for catheter ablation. After an initial ablation attempt, several episodes of atypical AVNRT were induced. During one of these episodes, we documented a stepwise transition of 2:1 atrioventricular block to 1:1 conduction, following two single ventricular premature beats. This phenomenon confirmed the functional nature of the AV block during AVNRT and indirectly its infra-nodal location. (PACE 2010; 33:e20,e23) [source]

Impact of Preceding Ventricular Premature Beats on Heart Rate Turbulence

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 4 2009
Hung Yi Chen M.D.
Background: Heart rate turbulence (HRT) has recently been introduced as a noninvasive tool for studying autonomic dysfunction. It presented short time fluctuation of sinus cycle length following single ventricular premature contraction (VPC). However, HRT parameters may be influenced by different factors. This study aimed to evaluate the possible influence of VPC frequency on HRT. Methods: 24-h Holter recording was performed in patients with VPCs initially detected by 12-lead electrocardiography (ECG) in the outpatient department. The numbers of VPCs in 2- and 5-minute durations preceding each VPC tachogram were calculated. The HRT parameters and the numbers of the VPCs preceding VPC tachograms were analyzed. Results: There were 23,122 available VPC tachograms from 107 healthy subjects included in the study. The turbulence onset (TO) value increased and the turbulence slope (TS) value decreased as VPC's frequency increased. The TO values rapidly increased when the number of VPCs was >15 beats in the 2-minute and >35 beats in the 5-minute durations. There was also a prominent decrease in TS values when the VPCs reached 14 and 30 beats in the 2- and 5-minute durations, respectively. Conclusion: Physiologic baroreflex may be attenuated under intensive stimulation, which is evidenced by blunted HRT parameters by frequent VPCs. Physiologic response to VPC's frequency may be related to baroreflex fatigue and is demonstrated as a sigmoid curve. [source]

Remodelling of action potential and intracellular calcium cycling dynamics during subacute myocardial infarction promotes ventricular arrhythmias in Langendorff-perfused rabbit hearts

THE JOURNAL OF PHYSIOLOGY, Issue 3 2007
Chung-Chuan Chou
We hypothesize that remodelling of action potential and intracellular calcium (Cai) dynamics in the peri-infarct zone contributes to ventricular arrhythmogenesis in the postmyocardial infarction setting. To test this hypothesis, we performed simultaneous optical mapping of Cai and membrane potential (Vm) in the left ventricle in 15 rabbit hearts with myocardial infarction for 1 week. Ventricular premature beats frequently originated from the peri-infarct zone, and 37% showed elevation of Cai prior to Vm depolarization, suggesting reverse excitation,contraction coupling as their aetiology. During electrically induced ventricular fibrillation, the highest dominant frequency was in the peri-infarct zone in 61 of 70 episodes. The site of highest dominant frequency had steeper action potential duration restitution and was more susceptible to pacing-induced Cai alternans than sites remote from infarct. Wavebreaks during ventricular fibrillation tended to occur at sites of persistently elevated Cai. Infusion of propranolol flattened action potential duration restitution, reduced wavebreaks and converted ventricular fibrillation to ventricular tachycardia. We conclude that in the subacute phase of myocardial infarction, the peri-infarct zone exhibits regions with steep action potential duration restitution slope and unstable Cai dynamics. These changes may promote ventricular extrasystoles and increase the incidence of wavebreaks during ventricular fibrillation. Whereas increased tissue heterogeneity after subacute myocardial infarction creates a highly arrhythmogenic substrate, dynamic action potential and Cai cycling remodelling also contribute to the initiation and maintenance of ventricular fibrillation in this setting. [source]

Relationship Between Heart Rate Turbulence and Heart Rate, Heart Rate Variability, and Number of Ventricular Premature Beats in Coronary Patients

Stepwise Transition of 2:1 Atrio-Ventricular Block to 1:1 Conduction Induced by Ventricular Premature Beats in a Patient with Atypical AVNRT

Unmasking Effect of Propafenone on the Concealed Form of the Brugada Phenomenon

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2000
ANTE MATANA
A case report of a patient with frequent ventricular premature beats but with an otherwise normal ECG and no structural heart disease. Propafenone in therapeutical doses unmasked the ECG picture of the Brugada phenomenon [source]

Microvolt T-Wave Alternans during Holter Monitoring in Children and Adolescents

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2010
Leonid Makarov M.D.
Background: Time-domain microvolt T-wave alternans (TWA) has been described as a noninvasive marker of sudden cardiac death in adults. The incidence of TWA in pediatric populations has not been defined well. The aim of the study was to determine peculiarities of TWA in children. Methods: We examined 68 healthy patients,newborns (20) and children in age group of 7,17 years (48),and 85 pediatric patients: ventricular premature beats,65; dilated cardiomyopathy (DCMP),2; long QT syndrome (LQTS),10; Brugada syndrome (BrS),5, catecholaminergic ventricular tachycardia (CVT),3. All underwent Holter monitoring (HM) with definition of the peak value of TWA by modified moving average method. Results: In healthy newborns, TWA was 32 ± 8 (12,55) ,V (HR 123,156 bmp). In healthy children (7,17 years) it was 30 ± 11 (10,l 55) ,V, (HR 64,132 bmp) without any differences between boys and girls. In all group of patients, TWA were significantly higher (P < 0.05) than in healthy. Circadian peak of TWA was found (90%) in a second part of day and at sleep (8%). Among them 60% (LQTS, BrS, and DCPM) had TWA > 55 ,V. Conclusion: Time-domain TWA during HM in children was independent of age, gender, and heart rate. In 94% healthy children, values of TWA do not exceed 55 ,V but 20,50% children with cardiac pathology had TWA more than 55 ,V. Night circadian type of TWA in diseases with risk of life-threatening arrhythmias associated with TWA was more than 55 ,V. Ann Noninvasive Electrocardiol 2010;15(2):138,144 [source]

Electrocardiographic Differentiation between Acute Pulmonary Embolism and Non-ST Elevation Acute Coronary Syndromes at the Bedside

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2010
Krzysztof Jankowski M.D., Ph.D.
Background: Clinical picture of acute pulmonary embolism (APE), with wide range of electrocardiographic (ECG) abnormalities can mimic acute coronary syndromes. Objectives: Assessment of standard 12-lead ECG usefulness in differentiation at the bedside between APE and non-ST elevation acute coronary syndrome (NSTE-ACS). Methods: Retrospective analysis of 143 patients: 98 consecutive patients (mean age 63.4 ± 19.4 year, 45 M) with APE and 45 consecutive patients (mean age 72.8 ± 10.8 year, 44 M) with NSTE-ACS. Standard ECGs recorded on admission were compared in separated groups. Results: Right bundle branch block (RBBB) and S1S2S3 or S1Q3T3 pattern were found in similar frequency in both groups (10 [11%] APE patients vs 6 [14%] NSTE-ACS patients, 27 [28%] patients vs 7 [16%] patients, respectively, NS). Negative T waves in leads V1-3 together with negative T waves in inferior wall leads II, III, aVF (OR 1.3 [1.14,1.68]) significantly indicated APE with a positive predictive value of 85% and specificity of 87%. However, counterclockwise axis rotation (OR 4.57 [2.74,7.61]), ventricular premature beats (OR 2.60 [1.60,4.19]), ST depression in leads V1-3 (OR 2.25 [1.43,3.56]), and negative T waves in leads V5-6 (OR 2.08 [1.31,3.29]) significantly predicted NSTE-ACS. Conclusions: RBBB, S1S2S3, or S1Q3T3 pattern described as characteristic for APE were not helpful in the differentiation between APE and NSTE-ACS in studied group. Coexistence of negative T waves in precordial leads V1-3 and inferior wall leads may suggest APE diagnosis. Ann Noninvasive Electrocardiol 2010;15(2):145,150 [source]

Modulation of gap junctions by nitric oxide contributes to the anti-arrhythmic effect of sodium nitroprusside?

BRITISH JOURNAL OF PHARMACOLOGY, Issue 5 2009
Márton Gönczi
Background and purpose:, Nitric oxide (NO) donors provide a preconditioning-like anti-arrhythmic protection in the anaesthetized dog. As NO may modulate gap junction (GJ) function, the present study investigated whether this anti-arrhythmic effect is due to a modification of GJs by NO, derived from the NO donor sodium nitroprusside (SNP). Experimental approach:, In chloralose-urethane-anaesthetized, open-chest dogs, either saline (controls; n= 11) or SNP (0.2 µg·kg,1·min,1; n= 10) was infused at a rate of 0.5 mL·min,1 by the intracoronary route. The infusions were started 20 min prior to and maintained throughout the entire 60 min occlusion period of the left anterior descending coronary artery. The severity of ischaemia and of arrhythmias, tissue electrical impedance and permeability, as well as the phosphorylation of connexin43, were assessed. Key results:, Compared with the controls, SNP infusion markedly suppressed the total number of ventricular premature beats (666 ± 202 vs. 49 ± 18; P < 0.05), and the number of ventricular tachycardiac episodes (8.1 ± 2.3 vs. 0.2 ± 0.1; P < 0.05) without significantly modifying the incidence of ventricular tachycardia or ventricular fibrillation. The severity of ischaemia (epicardial ST-segment changes, inhomogeneity of electrical activation) and tissue electrical impedance changes were significantly less in the SNP-treated dogs. SNP improved GJ permeability and preserved the phosphorylated form of connexin43. Conclusion and implications:, The anti-arrhythmic protection resulting from SNP infusion in the anaesthethized dog may, in part, be associated with the modulation of gap junctional function by NO. [source]

Sildenafil (Viagra) reduces arrhythmia severity during ischaemia 24 h after oral administration in dogs

BRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2004
Orsolya Nagy
Sildenafil (Viagra) prolongs repolarisation in cardiac muscle, an effect that could lead to ventricular fibrillation (VF). Sildenafil (2 mg kg,1) was given by mouth to 12 mongrel dogs and, 24 h later, these dogs were anaesthetised, thoracotomised and subjected to a 25 min occlusion of the anterior descending coronary artery. Haemodynamic parameters were similar in this and the control group, but there were fewer and less serious ventricular arrhythmias during occlusion in the sildenafil group (VF 17 vs 60%; ventricular premature beats 140±52 vs 437±127% and episodes of ventricular tachycardia 4.0±3.2 vs 19.3±7.7%, all P<0.05). However, reperfusion VF and indices of ischaemia severity (epicardial ST-segment mapping, inhomogeneity) were not modified by the drug. Sildenafil increased the QT interval, especially during ischaemia. Our conclusion is that ischaemia-induced ventricular arrhythmias are reduced by sildenafil, but this protection is less pronounced than that following cardiac pacing or exercise. British Journal of Pharmacology (2004) 141, 549,551. doi:10.1038/sj.bjp.0705658 [source]

Proarrhythmic potential of halofantrine, terfenadine and clofilium in a modified in vivo model of torsade de pointes

BRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2002
Andrew J Batey
This study was designed to compare the proarrhythmic activity of the antimalarial drug, halofantrine and the antihistamine, terfenadine, with that of clofilium a K+ channel blocking drug that can induce torsade de pointes. Experiments were performed in pentobarbitone-anaesthetized, open-chest rabbits. Each rabbit received intermittent, rising dose i.v. infusions of the ,-adrenoceptor agonist phenylephrine. During these infusions rabbits also received increasing i.v. doses of clofilium (20, 60 and 200 nmol kg,1 min,1), terfenadine (75, 250 and 750 nmol kg,1 min,1), halofantrine (6, 20 and 60 ,mol kg,1) or vehicle. Clofilium and halofantrine caused dose-dependent increases in the rate-corrected QT interval (QTc), whereas terfenadine prolonged PR and QRS intervals rather than prolonging cardiac repolarization. Progressive bradycardia occurred in all groups. After administration of the highest dose of each drug halofantrine caused a modest decrease in blood pressure, but terfenadine had profound hypotensive effects resulting in death of most rabbits. The total number of ventricular premature beats was highest in the clofilium group. Torsade de pointes occurred in 6 out of 8 clofilium-treated rabbits and 4 out of 6 of those which received halofantrine, but was not seen in any of the seven terfenadine-treated rabbits. These results show that, like clofilium, halofantrine can cause torsade de pointes in a modified anaesthetized rabbit model whereas the primary adverse effect of terfenadine was cardiac contractile failure. British Journal of Pharmacology (2002) 135, 1003,1012; doi:10.1038/sj.bjp.0704550 [source]