Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “EXTRASYSTOLE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed1991

Signal averaging of pre- and post-extrasystolic beats in patients with ventricular arrhythmias.

To evaluate the effects of premature ventricular beats on the impulse conduction of adjacent sinus cycles, we compared the high amplification signal-averaged electrocardiogram parameters of the pre- and post-extrasystolic beats with those of the remaining sinus cycle. According to the duration of filtered QRS (fQRS), to the voltage of root mean square of the terminal 40 ms (RMS 40) and to the duration of low amplitude terminal components of the sinus cycles, ventricular late potentials were detected in nine out of 29 subjects. Patients with an abnormal signal-averaged electrocardiogram exhibited a longer fQRS (146 +/- 6 versus 116 +/- 2 ms), a reduced RMS40 voltage (18 +/- 2 versus 80 +/- 10 microV) and a prolonged duration of less than 40 microV components (42 +/- 4 versus 17 +/- 2 ms). Analysis of the pre-extrasystolic beats did not reveal any significant variation in the above parameters, showing a mean difference of 0.44 +/- 2.4 ms; 0.02 +/- 1.14 microV; 1 +/- 1.9 ms and of -1.45 +/- 1.02 ms; 3.5 +/- 8.6 microV; -0.7 +/- 0.84 ms respectively, for patients with and without ventricular late potentials. In addition, no significant variation was observed when the post-extrasystolic beats were considered. These results indicate that the sinus cycles adjacent to premature ventricular discharges do not present variations of signal-averaged electrocardiogram parameters that may suggest an influence of the ectopic beats on their intramyocardial impulse propagation.

Adult↗
PubMedDate not supplied

Effects of lidocaine on conduction of extrasystoles in the normal canine heart.

The effect of lidocaine on the conduction of extrasystoles was studied in 8 open-chest dogs after atrioventricular nodal block. Simultaneous recording of endocardial and epicardial activation provided separate measures of endocardial (Purkinje) conduction as well as myocardial (muscle) conduction. Lidocaine (1.25--10.0 mg/kg) caused a dose-dependent slowing of conduction of midrange extrasystoles (250--400 ms) in both the Purkinje system and the myocardium, which became statistically significant at doses larger than 1.25 mg/kg. On the other hand, low doses of lidocaine caused speeding of early extrasystoles, i.e., coupling intervals (less than 250 ms) in the Purkinje system but not in the myocardium. Measurement of transmural conduction time as a function of coupling interval revealed a period of "apparent" supernormal conduction through ventricular muscle that was eliminated at high doses of lidocaine.

Animals↗
PubMed1988

Effect of SUN 1165, a new potent antiarrhythmic agent, on the kinetics of rate-dependent block of Na channels and ventricular conduction of extrasystoles.

Effects of SUN 1165, disopyramide, lorcainide, and mexiletine were studied either on the kinetics of onset of and recovery from rate-dependent depression of maximum rate of rise of phase 0 action potential (Vmax) in isolated guinea pig papillary muscles using standard microelectrode techniques or on intraventricular conduction time of extrasystoles evoked at varied coupling intervals in anesthetized dogs. SUN 1165 and lorcainide produced a slow-developing rate-dependent block of Vmax with the rate constant of 0.12 AP-1 and 0.09 AP-1, respectively. Mexiletine also produced a rate-dependent block of Vmax, but with very rapid onset so as not to be fitted by a single exponential curve. Disopyramide produced an intermediate rate-dependent block of Vmax with the rate constant of 0.46 AP-1. The time constants for recovery from the rate-dependent block for SUN 1165, lorcainide and disopyramide were 27.3-28.2, 23.2, and 17.0 s, respectively, while that for mexiletine was 0.118 s. SUN 1165, lorcainide, and disopyramide slowed ventricular conduction time of extrasystoles at all coupling intervals of 800-250 ms. On the other hand, mexiletine slowed conduction time at short coupling intervals of 500-250 ms. These findings suggest that, like lorcainide, SUN 1165 belongs to class Ic antiarrhythmic agents, and that SUN 1165 and lorcainide as well as disopyramide with slow and intermediate kinetics and mexiletine with fast kinetics may inhibit ventricular extrasystoles conducted at long and short range of coupling intervals, respectively.

Animals↗
PubMed1987

Intermittent fascicular extrasystoles producing pseudo AV block: electrophysiologic effects of beta agonists and antagonists.

This report describes a patient with pseudo-type II second-degree AV block due to an intermittent parasystolic focus located in the left bundle branch. A paradoxical increase in the fascicular rate was seen following intravenous propranolol, and fascicular extrasystoles were suppressed after intravenous isoproterenol treatment. All propagated fascicular extrasystoles were conducted to the ventricle with incomplete or complete right bundle branch block and a decrease in the H'-V interval compared to the H-V interval during sinus rhythm. Treatment with oral quinidine abolished fascicular extrasystoles without worsening of AV conduction.

Bundle-Branch Block↗
PubMed1962

Conditioning of extrasystoles in humans with respiratory maneuvers as conditional stimulus.

Extrasystoles are known to occur in some healthy individuals during common respiratory maneuvers such as holding the breath. Evidence is presented which shows that under controlled laboratory conditions this kind of extrasystole can be conditioned. Conditional stimuli signaling inspiration and expiration acquired the properties of the respiratory maneuvers by inducing extrasystoles during normal breathing.

Biological Phenomena↗
PubMed2002

Increasing plasma potassium with amiloride shortens the QT interval and reduces ventricular extrasystoles but does not change endothelial function or heart rate variability in chronic heart failure.

OBJECTIVES: To test whether simply increasing plasma potassium with amiloride would exert any of the same beneficial effects on "surrogate outcome measures" that are seen with spironolactone. The latter has been shown to improve mortality in chronic heart failure, possibly as a result of improvements in endothelial dysfunction, vascular angiotensin converting enzyme (ACE), autonomic function, myocardial fibrosis, ventricular arrhythmias, and QT interval indices. DESIGN: Randomised, placebo controlled trial. SETTING: Teaching hospital. PATIENTS AND INTERVENTIONS: Double blind crossover study involving 10 patients with New York Heart Association functional class II-III chronic heart failure comparing 5 mg/day amiloride (one month) with placebo. MAIN OUTCOME MEASURES: Endothelial function, vascular ACE, collagen markers, 24 hour ECG, and QT interval results. RESULTS: The amiloride induced increase in serum potassium (0.4 mmol/l) did not significantly change endothelial dysfunction, vascular ACE, collagen markers, or heart rate variability. However, amiloride significantly improved QT interval indices, reducing both QT dispersion (from 65.7 ms to 50.9 ms, p = 0.001) and mean maximal corrected QT (from 445 ms to 435 ms, p = 0.008). Amiloride also reduced ventricular extrasystoles (p < 0.05). CONCLUSIONS: Amiloride shortens QT interval length and reduces ventricular extrasystoles in chronic heart failure, implying that this effect is caused by potassium retention per se. However, unlike spironolactone, amiloride did not improve endothelial dysfunction, vascular ACE, heart rate variability, or myocardial fibrosis, implying that spironolactone improves these latter effects by aldosterone blockade rather than by simply increasing serum potassium. Therefore, amiloride has fewer beneficial mechanistic effects than spironolactone, but it does share with spironolactone the ability to shorten the QT interval and reduce ventricular extrasystoles.

Aged↗
PubMed1992

Influence of age on the relation between heart rate variability, left ventricular ejection fraction, frequency of ventricular extrasystoles, and sudden death after myocardial infarction.

AIMS: To examine the influence of age on the prediction of sudden death after acute myocardial infarction based on heart rate variability (HRv), left ventricular ejection fraction (LVEF), and the frequency of ventricular extrasystoles. BACKGROUND: Autonomic and left ventricular function and the frequency of ventricular extrasystoles change with age but the influence of age on the prediction of sudden death from these variables has not been examined. METHODS: The 477 patients who had been through an early postinfarction risk stratification protocol and followed up for a mean of 790 days were dichotomised at 60 years of age. RESULTS: Sudden deaths occurred with similar frequency in both age groups (12 (4.7%) of the 256 patients aged < 60 years and seven (3.2%) of the 221 older patients). Sudden death, however, accounted for 52% of all deaths in the young group but only 18.4% of all deaths in the older group (p < 0.01). An HRv index of < 20 units combined with an average of more than 10 ventricular extrasystoles an hour on Holter monitoring (VE10) had a sensitivity of 50%, a positive predictive accuracy of 33%, and a risk ratio of 18 in the young group (p < 0.001) but was not significantly predictive in older patients. The situation was similar when the combination of an LVEF < 40% with VE10 was considered. This combination had a sensitivity of 44%, positive predictive accuracy of 36.4%, and a risk ratio of 16.1 in young patients (p < 0.001), but was not significantly predictive in older patients. The combination of VE10 with either LVEF < 40% or HRv < 20 units gave a sensitivity of 75%, positive predictive accuracy of 30%, and a risk ratio of 30 in young patients (p < 0.001), but the relation between this combination and sudden death in older patients was not statistically significant. CONCLUSION: In postinfarction patients aged < 60 sudden death was a more predominant mode of death and was more reliably predicted from a depressed HRv index, an LVEF < 40%, and VE10 than in older postinfarction patients. These findings may have important implications for post-infarction risk stratification and management.

Age Factors↗
PubMed1977

Re-entrant ventricular arrhythmias in the late myocardial infarction period. 3. Manifest and concealed extrasystolic grouping.

Re-entrant beats with regular extrasystolic grouping were seen in 44- of dogs 3--7 days following ligation of the anterior descending coronary artery. Utilizing direct recording of the re-entrant pathway (RP) from the epicardial surface of the infarction zone, we found extrasystolic grouping to be based on the infarction tachycardia-dependent conduction disorders in a potentially RP. Trigeminy and quadrigeminy were related, respectively, to a 3:2 and 4:3 Wenckebach-like conduction cycle in a RP. However, quadrigeminy could also be due to an underlying bigeminal rhythm with concealment of alternate re-entrant beats, i.e., concealed bigeminy. A bigeminal rhythm was the result of a 2:1 conduction pattern in a re-entrant pathway with a sufficient degree of conduction delay during the conducted beat of the 2:1 cycle to result in re-entry. A trigeminal or quadrigeminal rhythm could change to a bigeminal rhythm on critical shortening of the cardiac cycle. Fixed and variable coupling were related, respectively, to stable and changing conduction pattern in a re-entrant pathway. On the other hand, extrasystolic grouping could be concealed due to either block in the re-entrant pathway or entrapment in a small area of the closely bordering normal zone.

Animals↗
PubMedDate not supplied

[Early arterial reflexion and ventricular extrasystole. A novel mechanism detected with sphygmokinetocardiography].

UNLABELLED: ANTECEDENT: Through sphygmokynetocardiography (SKCG) an exploratory method that records an electrocardiographic signal, a carotid pulse (CP), and two vibriograms (kinetocardiograms) of the left ventricle (LV) recorded in the left hemithorax (anterior kinetocardiogram, AKC) and the subcostal region of left abdomen (posterior kinetocardiogram of PKC, vibrations transmitted through the hemidiaphragm) we observed a systolic precocious reflection wave (Rw) in the CP and prolongation of LV ejection time (LVET) measured in AKC or in PKC of the previous sinusal pre-extrasystolic beat (PEB) vs control beats (CB) in cases with ventricular extrasystoles (VEs). OBJECTIVE: To demonstrate whether the intervals just mentioned are associated with ventricular extrasystoles. METHOD: Sixty cases: 30 with VEs, group A, and 30 without arrhythmia, group B, were studied through SKCG. The LVET and the arterial reflection index or ARI = Ta-rw/LEVT, Ta-rw = time between initial ventricular impulse to reflexive wave, were measured. RESULTS: Demography was similar in both groups. PEB had a longer LVET than the CB (291 +/- 41 vs 279 +/- 39, p < 0.01) and ARI was shorter (0.36 +/- 0.17 vs 0.58 +/- 0.21, p < 0.001). CONCLUSIONS: 1) Distention of the LV due to Rw, possibly through the well-known experimental mechanism of electromechanic feedback, is believed to underlie the arrhythmia. 2) The observation has important clinical implications.

Aged↗
PubMed1992

Mechanical restitution and post extrasystolic potentiation of perfused rat heart: quantitative comparison of normal right and left ventricular responses.

Interval-force relationship of right and left ventricles of the isolated perfused rat heart was quantified by fitting polynomial, linear and mixed linear-exponential functions to the mechanical restitution (MRC) and post extrasystolic potentiation (PESPC) curves. Ventricular maximum developed pressure (Pmax) and its first derivative (dP/dtmax) were used as indices of contractility. MRCs and PESPCs could be separated into two distinct phases: phase A and phase B of MRCs; phase I and phase II of PESPCs. These phases for the right and left ventricle of the rat heart could be explained on the same model of cellular kinetics of the activator calcium, but showed distinct differences from other species. Right and left ventricle inotropic reserve (CRmax), as quantified from the centre of mass of the phase B of MRCs (from normalized Pmax), was (mean +/- SE): 132.4 +/- 2.05% and 132.1 +/- 1.7% at 1 Hz, which increased significantly (P less than 0.001) to 181.0 +/- 5.8% and 182.3 +/- 5.2% at 3.3 Hz, respectively. Linear regression of normalized right ventricle extrasystolic responses on the left ventricle responses gave a high correlation coefficient (typically r2 = 0.97). Time constants of the fitted mechanical restitution (TMRC) and post extrasystolic potentiation (TPESPC) curves were at 1 Hz, TMRC and TPESPC (from normalized dP/dtmax) were (mean +/- SE): 161.6 +/- 10.8 and 159.0 +/- 13.2 ms for right ventricle, and 196.1 +/- 14.5 and 188.3 +/- 10.7 ms for left ventricle, respectively. The results of this study indicate that interval-force relationship of the rat heart, as exemplified by CRmax and time constants of the fitted curves, could provide a useful index for quantifying and comparing right and left ventricular functions.

Action Potentials↗
PubMed1991

[Comparison of the efficacy of moricizine and disopyramide in the treatment of ventricular extrasystoles].

Moricizine chlorhydrate (Ethmozine), a relatively unknown antiarrhythmic agent in France, is a derivative of Phenothiazine, related to the Vaughan-Williams Class IB drugs. A randomised, double-blind, crossover trial with Disopyramide 600 mg/day after a placebo period in 10 patients with ventricular extrasystoles, half of whom had underlying cardiac disease, showed that moricizine 750 mg/day significantly reduced (p less than 0.05) the overall number of ventricular extrasystoles by 81 +/- 46% (disopyramide 72 +/- 69%; NS) and that this drug is effective in 2/3 of patients by suppressing 70 to 100% of ventricular extrasystoles, whereas disopyramide was effective in only 40% of the same patients and never gave better results than Moricizine. Cardiac and extracardiac tolerance of Moricizine was good in this study, confirming previously reported results and its superiority when compared with disopyramide (20% of unwanted effects in this series).

Adolescent↗
PubMed1986

[Effect of hyperbaric oxygenation on the extrasystole in ischemic heart disease patients].

A study of the effect of hyperbaric oxygenation (HBO), applied as single sessions or a treatment course, on cardiac rhythm in 82 coronary patients with chronic extrasystole demonstrated positive therapeutic effect to be achieved after the first 5 or 6 HBO sessions in all patients. Further treatment may provoke an aggravation of arrhythmia in some patients. Positive antiarrhythmic effect of a complete HBO course is doubtful, where ectopic activity is increased following the 7th session. There is a correlation between the results of ECG monitoring from the hyperbaric chamber, from session 7 onwards, and 24-hour ECG recording before and after a HBO course. As shown by 24-hour ECG monitoring, positive effect was obtained in 67% of patients with ventricular extrasystole, the number of ventricular extrasystoles remained basically unchanged after a HBO course in 17%, and ectopic activity increased in 15.4%.

Aged↗
PubMed1986

[Effectiveness and characteristics of the action of etmozin in treating extrasystole in middle-aged and elderly patients].

Antiarrhythmic efficiency and specific effects of ethmozine, taken alone in increasing oral doses from 300 to 450 mg daily, were evaluated in 48 elderly and old coronary patients with stable supraventricular and ventricular extrasystoles (SVES, VES). It was demonstrated clinically and instrumentally (ECG, rhythmography, bicycle ergometry with standard exercise, cardiac rhythm monitoring and computer analysis, polycardiography, tetrapolar chest rheography) that ethmozine's antiarrhythmic effect was marked (a more than 75% post-treatment decline in the frequency of extrasystoles at rest and during exercise, provided that paired polytopic extrasystoles and paroxysms of tachycardia are suppressed completely) in 52.1% of SVES patients and 60% of VES patients. Antiarrhythmic action of a 300 mg ethmozine load dose was particularly apparent within 2-7 hours after administration. Ethmozine treatment, as described above, delayed atrioventricular conduction, causing however no significant decrease in heart rate, nor depressing cardiac output and myocardial function; arterial blood pressure and myocardial oxygen requirement remained basically unchanged either. Unlike propranolol effect on cardiac rhythm undulating pattern, there is evidence that ethmozine mechanism of action involves sympathetic activation. Ethmozine had to be discontinued in 10.4% of the 35.4% of patients with side effects.

Aged↗
PubMed1986

[Variability and stability of ventricular extrasystole in patients with a history of myocardial infarction].

Changes in ventricular extrasystole were examined using 3 sessions of 24-hour Holter ECG monitoring in 304 myocardial infarction survivors. The highest reproducibility was shown by the maximum ventricular extrasystole gradations 1, 3, 4b, according to the Lown-Wolff classification. Evidence of possible transformation of the maximum ventricular extrasystole gradations at repeated prolonged ECG monitoring sessions is presented.

Cardiac Complexes, Premature↗
PubMed1989

[Anti-arrhythmia effect of prolecophen in patients with extrasystole in comparison with other anti-arrhythmia drugs].

Oral prolecohen (LEK, Yugoslavia) was given in a single dose of 300 mg to 15 patients with extrasystole of various genesis. The drug produced an antiarrhythmic effect in 50% of patients with ventricular extrasystole, but in those with supraventricular extrasystole. Prolecophenum showed a good tolerance. In 20% of the patients the adverse reactions appeared as mild headache, dizziness, dry mouth, malaise in the epigastric region. There is also evidence for efficacy of other antiarrhythmic agents used in this group of patients.

Administration, Oral↗
PubMedDate not supplied

[Effects of caffeine on post-extrasystolic potentiation and mechanical restitution in mammalian papillary muscle].

The excitation-contraction coupling theory postulates that the main source of activator calcium is the sarcoplasmic reticulum that releases calcium in response to an electrical stimulus. This happens to be true in skeletal muscle, but recently several discrepancies have been raised about the validity of this hypothesis in cardiac muscle. These discrepancies are related to morphological as well as physiological data. The new information postulates that sarcoplasmic reticulum in cardiac muscle does not supply calcium as a main source in physiological conditions. The aim of the present paper was to evaluate the sarcoplasmic reticulum role in the supply of activator calcium in excitation-contraction coupling. A series of experiments were performed using the mechanical restitution and the post-extrasystolic potentiation models in the presence of caffeine, which is known to provoke functional elimination of the sarcoplasmic reticulum. It was observed that caffeine diminished the post-extrasystolic potentiation when 1 mM was used. At higher dose (4mM) the post-extrasystolic potentiation was completely abolished. On the other hand the late part of mechanical restitution is also abolished by caffeine. The amount of calcium that recirculates seems to increase in the presence of caffeine. The results obtained seem to support the idea that the sarcoplasmic reticulum has only a minor role in the supply of activator calcium, when physiological stimulation rates are used.

Animals↗