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At least 235 records · Page 13Linked to original sources
PubMed1984

[Lorcainide in stable ventricular extrasystole. A double-blind study with 48-hour continuous ECG recording].

In a randomized double-blind cross-over trial, the effectiveness of lorcainide at a dosage of three times 100 mg/d by mouth was compared with that of a placebo for the treatment of subjectively disturbing stable ventricular extrasystoles (VES), using 48-hour continuous ECG monitoring. In 11 of 20 patients there was a regression in the VES rate to under 5%, in other 3 patients to under 50% of the initial values. Continuing the treatment, good therapeutic effect was still demonstrable 14 and 28 days later. However, only three patients had no side-effects. The others had sleep disturbances, hot flushes, sweating, restlessness, anxiety, dizziness, hallucinations and gastrointestinal symptoms. Lorcainide thus has a good anti-arrhythmic effect but, because of its side-effects, it should be used only in special circumstances.

Adult↗
PubMed1978

Effect of ventricular extrasystoles on idioventricular rhythm in patients with complete heart block.

Idioventricular rate, QRS width, site of block and responses to premature ventricular stimulation were studied in 23 patients with chronic complete heart block in an attempt to distinguish patients liable to syncopal attacks. Seven patients were asymptomatic, five gave a history of presyncope and 11 of syncope. Although the mean idioventricular rate of the nine patients in the narrow QRS group (39.7 per min) was significantly faster than that of the 14 patients in the wide QRS group (35.3 per min; P less than 0.05), the rate did not distinguish symptomatic patients within either the narrow or the wide QRS groups. His bundle studies of the site of block and the effect of single and paired right ventricular stimulation upon idioventricular rhythm were also unhelpful. The response of the return cycle to increasingly premature ventricular extrasystoles, however, proved more complex than was anticipated.

Adams-Stokes Syndrome↗
PubMed1993

Effects of positive inotropic stimulation (post-extrasystolic potentiation) on non-uniformity of left ventricular contraction in patients with coronary artery disease.

In patients with chronic coronary artery disease, post-extrasystolic potentiation (PESP) slightly worsens relaxation, increasing the constant tau of ventricular pressure decay. However, it does not negatively influence left ventricular (LV) diastolic filling. To our knowledge, no data are available on the effects of PESP on segmental relaxation in chronic coronary artery disease. The effects of PESP on the LV pressure-volume (P/V) relationship and on segmental pressure-length loops (P/L) were studied in eight patients with coronary artery disease submitted to LV angiography. P/V loops were constructed by means of frame-to-frame analysis of ventriculograms and simultaneous high-fidelity LV pressure tracings; P/L loops were calculated by the endocardial movement of 45 chords intersecting the LV outline (centreline method). PESP was produced by programmed stimulation during ventriculography. P/V and P/L loops were studied in basal conditions and after PESP.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Ventricular extrasystolic arrhythmias in exercise testing. II. Haemodynamic correlations.

Exercise testing (ET) has been used for assessing the arrhythmogenic tendency of myocardium in patients (pts) with coronary heart disease. It has been suggested that coronary patients with left ventricular (LV) dyssynergy are prone to present ventricular extrasystolic arrhythmia (VA) during ET. We studied the functional status of the LV in a group of 25 coronary patients who presented VA during ET (Group A), and compared the results with a group of 87 patients without VA during ET (Group B). No statistically significant difference was found between the two groups in end-diastolic pressure, ejection fraction, and extent of dyssynergy of the LV. Furthermore, no significant difference was noted in the extent of development of the collateral circulation.

Blood Pressure↗
PubMed1998

The Endothelin-A antagonist LU 135 252 supresses ischemic ventricular extrasystoles and fibrillation in pigs and prevents hypoxic cellular decoupling.

The endothelin-A (ETA) antagonist LU 135 252 (1 mg/kg, n = 10) or saline (control, n = 10) was injected i.v. into anesthetized pigs 15 min before occlusion of the last third of the left anterior descending coronary artery (LAD) for up to 90 min. Then, or when ventricular fibrillation occurred, the ischemic mass was determined and amounted to about 13% of ventricular mass in all groups. Heart rate, QT interval, blood pressure, and the left ventricular contractility parameter LV dp/dtmax were not altered by LU in the 15 min pretreatment period. The lower dose of the ETA antagonist had only marginal antiarrhythmic effects. At the 3 mg/kg dose, LU prolonged the time of regular sinus rhythm within the first 20 min of ischemia by 50% (mean +/- SEM: 12 +/- 2 min in control vs. 18 +/- 1 after LU; p < 0.05) and reduced the number of ventricular extrasystoles by 87% (54 +/- 18 vs. 7 +/- 3; p < 0.05). The total incidence of ventricular fibrillation (VF) (80% vs. 50%; p = 0.17) and also the incidence of late VF (ischemia > 20 min) was reduced by 3 mg/kg LU (78% vs. 38%; p = 0.12). In vitro, LU (10(-6) mol/L) prevented the hypoxia-induced (N2 gassing) impairment of intercellular coupling, measured as the delay between a direct stimulus and a distal action potential in guinea pig papillary muscles.

Animals↗
PubMed1990

Clinical assessment of the right ventricle anterior papillary muscle extrasystoles with Holter recordings.

To assess the short-term behavior of the right ventricle anterior papillary muscle extrasystoles (APME) based on Holter recording and exercise data, 20 subjects (age 31.5 +/- 13.7 years) with otherwise normal electrocardiogram were studied. APME was diagnosed when it resembled LBBB morphology, with downward oriented AQRS in the frontal plane, slurred r wave in lead V1, and an R/S ratio less than 1 in this same lead. Except for palpitations in ten patients, there were no other symptoms related to the arrhythmia. Two Holter recordings, 30 to 330 days apart, were performed and their results compared. In the first Holter recording, the average rate of VPB/minute was 9.9 +/- 2.5 (xg +/- SD). Half of the patients had couplets and five had ventricular tachycardia. In the second Holter recording, the average rate of VPB/minute was 8.7 +/- 3. In eight cases, couplets were recorded, in half of which one or more episodes of ventricular tachycardia were also noted. Six patients showed another VPB morphology distinct from APME. Stress test suppressed VPB in 10/13 patients, couplets in 2/3 and ventricular tachycardia in the only one with this arrhythmia at the start of the test. Repetitive forms vs APME frequency and vs heart rate exhibited an inverse relationship. We conclude that APME is a clinical condition with both high and stable VPB levels, which can be found in subjects with otherwise normal hearts and in the short-term has a spontaneous uncomplicated outcome.

Adolescent↗
PubMed1997

Pacemaker induced repetitive nonreentrant ventriculoatrial synchrony: initiation and termination by ventricular extrasystole.

During dual chamber pacing, repetitive ventriculoatrial (VA) synchrony secondary to retrograde conduction can occur whenever otherwise effectual atrial stimuli fall continually within the atrial myocardial refractory period generated by preceding unsensed retrograde atrial depolarization. The latter falls within the pacemaker atrial refractory period and cannot initiate endless loop tachycardia, another form of repetitive VA synchrony secondary to a reentrant process through the pacemaker and the heart. This report describes the usefulness of Holter recordings in the diagnosis of repetitive nonreentrant VA synchrony and documents initiation and termination of this process by a ventricular extrasystole.

Aged↗
PubMed1999

The heart extrasystole: an energetic approach.

The consequences of an extrasystole (ES) on cardiac muscle's energetics and Ca2+ homeostasis were investigated in the beating heart. The fraction of heat release related to pressure development (pressure dependent) and pressure-independent heat release were measured during isovolumic contractions in arterially perfused rat ventricle. The heat release by a contraction showed two pressure-independent components (H1 and H2) of short evolution and a pressure-dependent component (H3). The additional heat released by ES was decomposed into one pressure-independent (H'2) and one pressure-dependent (H'3) component with time courses similar to those of control components H2 and H3. ES also induced the potentiation of pressure development (P) and heat release during the postextrasystolic (PES) beat. The slope of the linear relationship between pressure-dependent heat and pressure maintenance was similar in control, ES, and PES contractions (0.08 +/- 0.01, 0.10 +/- 0.02, and 0.08 +/- 0.01 mJ. g-1. mmHg-1. s-1, respectively). The potentiation of H2 (heat component related with Ca2+ removal processes) in PES was equal to H'2 at 0.3, 0.5, 1, and 2 mM Ca2+, suggesting that the extra amount of Ca2+ mobilized during ES was recycled in PES. Pretreatment with 1 mM caffeine to deplete sarcoplasmic reticulum Ca2+ content inhibited both the mechanical and energetic potentiation of PES. However, the heat released and the pressure developed during ES were not changed by sarcoplasmic reticulum depletion. The results suggest that 1) the source of Ca2+ for ES would be entirely extracellular, 2) the Ca2+ entered during ES is accumulated in the sarcoplasmic reticulum, and 3) the Ca2+ stored by the sarcoplasmic reticulum during ES induces an increased contribution of this organelle during PES compared with the normal contraction.

Animals↗
PubMed1976

Repetitive extrasystole as an index of vulnerability to ventricular fibrillation.

The assessment of ventricular vulnerability by inducing ventricular fibrillation (VF) presents limitations when neural activity is being investigated, especially in the unanesthetized animal. As repetitive extrasystoles (RE) have been observed to precede the occurrence of VF, it was relevant to determine whether the RE threshold provides a reliable index of cardiac susceptivility to fibrillation. The RE and VF threshold relationships were studied in 32 chloralose-anesthetized dogs during left stellate ganglion stimulation, vagus nerve stimulation, and beta-adrenergic blockage with practolol. The vulnerable period was scanned at 1-ms intervals and at 2-mA increments with a single, 2-ms, constant-current cathodal stimulus; RE and multiple RE were induced reproducibly when 66% and 82%, respectively, of the fibrillatory current was administered. The nadirs for RE and multiple RE were coincident in the cardiac cycle with the vulnerable-period threshold for VF. Stellate and vagal stimulation and beta-adrenergic blockade resulted in comparable changes in RE and VF thresholds and produced equivalent shifts in the cardiac cycle of the RE and VF vulnerable-period nadirs. These observations suggest that RE and VF phenomena share a common electrophysiologic basis and that the RE threshold can be used as an end point for measuring ventricular vulnerability to VF.

Animals↗
PubMed1976

Influence of ventricular conduction defects on ventricular repolarisation and coupling intervals of ventricular extrasystoles.

In all conduction disorders of the left ventricle the Q-T interval is prolonged in relation to the prolongation of the QRS duration, but the S-T interval (measured from the end of the S wave) is within normal limits. Right ventricular conduction defects are associated with prolongation of the Q-T interval, but the S-T interval in incomplete and complete right bundle branch block is subnormal. In the absence of a broad QRS, the Q-T and S-T intervals are not prolonged in left anterior hemiblock. However, an associated non-specific left intraventricular conduction defect or right bundle branch block does prolong the QRS and thus the Q-T interval. The S-T interval is normal or subnormal in the presence of right bundle branch block and left anterior hemiblock confirming that left anterior hemiblock does not effect the Q-T interval and repolarisation. In the presence of any conduction defect which prolongs the QRS duration, extrasystoles have longer coupling intervals. The coupling intervals are longer in the presence of left bundle branch block than right bundle branch block. It is postulated that this is due to the differences in the time of depolarisation and thus repolarisation of the left ventricle.

Bundle-Branch Block↗
PubMed1989

Effects of antiarrhythmic drugs on the repetitive extrasystole threshold and the ventricular fibrillation threshold.

The effects of class 1 antiarrhythmic drugs on the repetitive extrasystole threshold (RET) and the ventricular fibrillation threshold (VFT) were studied in 32 anesthetized dogs with localized transmural necrosis. All four drugs significantly increased VFT. Although lidocaine and mexiletine increased RET, procainamide and disopyramide did not. We conclude that class 1b antiarrhythmic agents prevent ventricular fibrillation by suppressing the initiation of reentry, and that class 1a drugs decrease the vulnerability by preventing the reentrant repetitive excitation from degenerating into chaotic multiple reentries.

Animals↗
PubMed1993

Prognostic significance of ventricular extrasystoles in healthy professional athletes: results of a 5-year follow-up.

To assess the natural history of ventricular extrasystoles (VE), a 5-year follow-up of 52 professional endurance athletes was made. All remained well during this period. Forty-four accepted to undergo repeat extensive noninvasive cardiologic examination. In the 23 athletes still in activity at the second study the prevalence of total and complex VE at 24-hour Holter monitoring was substantially unchanged, while in the 21 subjects who had stopped training, complex VE were no longer present (p = 0.01 vs. baseline). Echocardiographic dimensional parameters were significantly higher in the still active athletes than in the no longer active subjects; however, in the latter, left ventricular mass index was still greater than in a group of 40 sedentary subjects previously studied (107 vs. 81 g/m2; p = 0.001). High-intensity physical training does not seem to be harmful in athletes with complex VE, without evidence of underlying cardiac disease.

Adult↗
PubMed2000

Predictive power of increased QT dispersion in ventricular extrasystoles and in sinus beats for risk stratification after myocardial infarction.

BACKGROUND: QT dispersion, commonly measured in sinus beats (QTd-S), can also be calculated in premature ventricular beats (QTd-V). To date, no studies have addressed the relation between these 2 variables. METHODS AND RESULTS: In 148 patients with remote myocardial infarction and premature ventricular beats on a routine ECG, QT dispersion, defined as the difference between the maximum and the minimum QT interval across the 12-lead ECG, was calculated separately for the ventricular extrasystole and the preceding sinus beat. In the total group of patients, QTd-V was greater than QTd-S (83+/-33 versus 74+/-34 ms, respectively; P=0.001). During a follow-up period of 35+/-17 months, arrhythmic events (sustained ventricular tachycardia, ventricular fibrillation, or sudden death) were noted in 30 patients. A QTd-V of >/=100 ms was a stronger univariate marker of arrhythmic events than was a QTd-S of >/=100 ms, and multivariate analysis selected only prolonged QTd-V (hazard ratio 3.81, 95% CI 2.2 to 11.2) and low ejection fraction (hazard ratio 3.05, 95% CI 1.6 to 7.6) as independent predictors of arrhythmic events. CONCLUSIONS: The magnitude of QTd-V was greater than that of QTd-S in the total group of patients. Prolonged QTd-V is associated with a significantly increased risk for arrhythmic events in postinfarction patients, and the prognostic significance of QTd-V exceeds that of QTd-S.

Aged↗
PubMed1976

Muscarinic effects of vagosympathetic trunk stimulation on the repetitive extrasystole (RE) threshold.

The precise mechanism of the vagus in opposing adrenergic influences on cardiac vulnerability has not been defined. In the present investigation, cholinergic stimulation was produced by administering the selective muscarinic agent methacholine (MCh) and ventricular vulnerability was assessed by measuring the repetitive extrasystole (RE) threshold. MCh produced a sustained 98 +/- 12% (P less than 0.0001) increase in the RE threshold; the increase was abolished by concurrent infusion of atropine (0.2 mg/kg). When MCh was administered during beta-adrenergic blockade with propranolol, however, no further increase in RE threshold occurred beyond that resulting from propranolol alone. Infusion of norepinephrine (NE), in a dose insufficient to provoke systemic hypertension, significantly lowered the vulnerable period threshold. This decrease was completely abolished by concurrent vagosympathetic stimulation (VS). It is concluded that VS affects ventricular vulnerability through its muscarinic action and that the protection against VF is in part due to modulation of neural and humoral beta-adrenergic inputs.

Animals↗