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At least 19 recordsLinked to original sources
PubMed1977

Evaluation of children with ventricular arrhythmias.

Ventricular arrhythmias are rare in childhood but may be associated with syncope and sudden death. This report describes 8 children with ventricular arrhythmias, 6 of whom suffered syncopal episodes. Ventricular tachycardia was documented in 5. One boy died suddenly. Complete cardiac investigation was carried out with exercise testing, Holter monitoring, echocardiography, cardiac catheterization, angiography, and electrophysiological studies. The spectrum of abnormalities related to the arrhythmias included prolapsing mitral valve, prolonged QT syndrome, sick sinus syndrome, congenital heart disease, cardiomyopathy, and idiopathic ventricular tachycardia. Exercise testing and Holter monitoring were particularly useful in documenting the arrhythmias and monitoring response to therapy.

Adolescent↗
PubMed1979

Fetal and neonatal ventricular arrhythmia.

Ventricular arrhythmia in the perinatal period is observed with greater frequency than reported in the literature. Four cases from the authors' experience and an analysis of the literature are presented. Of the total of 45 cases, nine were detected in utero, three persisted beyond the neonatal period, and two resulted in death with associated disorders. Twenty-four percent of the entire group had serious medical disorders associated with arrhythmia; however, 43% of the group with ventricular tachycardia had major associated disease.

Arrhythmias, Cardiac↗
PubMed1977

Ventricular arrhythmias in acute myocardial infarction. A comparative study on some tests for ventricular arrhythmias.

A continuous ECG recording has been made in 31 myocardial infarction patients during the first 24 hours after admission to hospital. The number and severity of ventricular arrhythmias were recorded in great detail. Before discharge from hospital the patients were submitted to 20 hours of ECG tape recording, an exercise test on a bicycle ergometer and a static work test (handgrip). Another exercise test was performed one month after discharge. During the first day in the Coronary Care Unit (CCU) all 31 patients had ventricular arrhythmias and in 27 of them the arrhythmia was classified as major (calling for treatment according to Lown's criteria). At the exercise tests 23 patients showed ventricular arrhythmias, 12 of them considered as major. No antiarrhythmic therapy was given during the investigation. No correlation was found between the degree of arrhythmia during the first day in the CCU and during the exercise tests. Tape-recorded ECG's appeared to be inferior to dynamic exercise tests in the ability to disclose a latent tendency to ventricular arrhythmia. Static work did not provoke any ventricular arrhythmias. At a 2-year follow-up 5 patients had died, 4 of them suddenly. Examination of additional material on 11 patients with ventricular tachycardia or ventricular fibrillation during the CCU stay, showed that 2 had died, but only one suddenly. Frequency and severity of arrhythmias during the first day after the infarction seemed to correlate poorly to a persistent tendency to arrhythmias during the first day after the infarction seemed to correlate poorly to a persistent tendency to arrhythmias or to the risk of sudden death during the following 2 years. A dynamic exercise test performed before discharge would appear to be more effective in selecting patients in need of long-term prophylaxis. However, very few patients seem to need such a specific antiarrhythmic prophylaxis.

Acute Disease↗
PubMed1979

[Quantitative evaluation of the efficacy of anti-arrhythmia agents in chronic ventricular arrhythmia].

The authors describe a computer system for the analysis of ventricular arrhythmias and its use in the evaluation of anti-arrhythmic drugs. Provided the arrhythmia is stable, this method allows an estimation of the onset and duration of action of the drug and gives guidelines for the choice of an appropriate drug regimen. Using this system, a comparison can be made between different drugs based on quantification of their efficacy.

Amiodarone↗
PubMed1977

Management of patients with malignant ventricular arrhythmias.

The patient with recurrent malignant ventricular arrhythmias (ventricular fibrillation or ventricular tachycardia with syncope) presents a complex therapeutic problem. To examine this problem, a study was made of 43 consecutive patients with such arrhythmias (mean age 54 years for the 33 men and 43 years for the 10 women). Arrhythmias were not precipitated by either remediable clinical conditions or acute myocardial infarction. The population was divided into two nonrandomized groups based on the type of therapeutic intervention employed. The 26 patients in Group 1 (20 with ventricular fibrillation, 6 with ventricular tachycardia) were subjected to a systematic attempt to select two independently effective antiarrhythmic drugs. Acute drug testing was followed by drug usage over 48 to 72 hours with drug efficacy determined with use of ambulatory monitoring and exercise stress. The 17 patients in Group 2 (10 with ventricular fibrillation, 7 with ventricular tachycardia) received standard antiarrhythmic therapy based on clinical factors and "therapeutic" blood drug concentrations. Twenty-four of 26 patients in Group 1 (92 percent) demonstrated control of arrhythmias and are alive at a mean follow-up period of 17 months. Of 121 drug tests, 47 (39 percent) were effective, 58 (48 percent) were ineffective and 16 (13 percent) provoked major adverse effects. The most effective combination of drugs involved a beta adrenergic blocking agent, a cardiac glycoside and quinidine. Ten of 17 patients in Group 2 (59 percent) have died after a mean follow-up period of 14.8 months. Elements of a successful management program are outlined.

Adult↗
PubMedDate not supplied

Treatment of chronic ventricular arrhythmias [proceedings].

Treatment of ventricular arrhythmias at the present time is difficult and requires a strong commitment on the part of the physician and the patient. Adequate documentation of the arrhythmia with continuous ECG recordings (Holter recordings), preferably for 24 hours, should be performed in each case. Exercise testing can be utilized in selected patients, but is generally inferior to the Holter technique. Underlying cardiac pathology should be searched for, utilizing echocardiography in all patients and coronary angiography and left ventriculography in patients with more severe ventricular tachycardias. Estimation of the prognostic significance of the VPBs must be made in the context of the underlying disease, and goals for treatment must be set. Treatment in all cases first requires measures to avoid known precipitating factors. If antiarrhythmic therapy is utilized, a systematic empirical trial of available agents should be undertaken, utilizing repeated Holter monitoring to document effectiveness. Serum levels of the antiarrhythmic medications should be measured in most cases. Combinations of antiarrhythmic agents can be employed if the need is great, but the agents singly are ineffective. If treatment is determined to be ineffective, it should be discontinued. Surgical techniques may be useful in cases of refractory ventricular tachycardia, and they include overdrive pacing, surgical sympathectomy, or ventricular aneurysmectomy with or without coronary bypass. Coronary bypass alone or resection of a hypokinetic but not aneurysmal area of myocardium may be successful in some cases, but the results are less predictable than when a true aneurysm is resected. Electrophysiologic studies, performed as part of the preoperative evaluation and provoking a self-perpetuating ventricular tachycardia, may permit selection of patients suitable for ventriculotomy to interrupt the re-entry pathway. At present, this must be considered experimental and is performed in only a few centers equipped for the required complex epicardial mapping. Surgery has not been shown to affect complex VPBs outside the setting of acute ischemia. Control of ventricular arrhythmias requires a highly individualistic approach with documentation of effectiveness.

Adrenergic beta-Antagonists↗
PubMed1979

Patterns of activation in ventricular arrhythmias of late myocardial infarction in dogs.

Ventricular arrhythmias were produced in 12 dogs 4 to 6 days after coronary artery ligation by programmed ventricular stimulation. The electrocardiogram and 7 composite electrograms from endocardial and epicardial surfaces of the ischemic, border and normal zones, as well as from the right ventricle, were recorded during and after programmed ventricular stimulation. The ventricular arrhythmias were preceded and sustained by delayed, fragmented activity in the ischemic epicardial zone bridging diastole. Efferent pathways from the ischemic epicardium led to direct epicardial spread to adjacent normal epicardium in most instances. Efferent pathways into the endocardial regions were also observed, but to a lesser extent. The efferent reentry pathways led to both ventricles, and produced right and left ventricular arrhythmias in 8 of the 12 dogs; they were exclusively of left ventricular origin in the remaining 5. Classification of right and left ventricular arrhythmias may only be related to the exit points and not necessarily to their origin.

Animals↗
PubMed1977

Clinical evaluation of the enhancement of vagal tone in acute myocardial infarction by edrophonium hydrochloride: effects on ventricular arrhythmias, His bundle electrography, and left ventricular function.

Enhanced electrical stability of acutely ischemic myocardium with vagal stimulation and acetylcholinesterase inhibition has been demonstrated experimentally. To extend these findings clinically, within 24 hours of acute myocardial infarction, 11 patients underwent continuous 10 hour Holter monitoring: 2.5 hour control before and after 5 hour constant edrophonium infusion (0.25 to 2.00 mg./minute). Continuous infusion of the agent lowered heart rate 92 to 78 b.p.m. (p less than 0.01). Although mean total ventricular extrasystoles (PVC's) per 5 hours per patient (131) and PVC's per 1,000 beats (4.7) were unchanged (p greater than 0.05), potentially lethal tachyarrhythmias (malignant PVC's: multifocal, R on T, paried, greater than 5 per minute or ventricular tachycardia) were terminated in six of 10 patients by edrophonium. However, serious ventricular arrhythmias continued in three patients and appeared in four despite the agent. Ventricular fibrillation did not occur during the 10 hour period of study. In addition, the patients were evaluated hemodynamically and by His bundle electrograms before and after a 10 mg. bolus of edrophonium prior to the 10 hour constant infusion: heart rate declined (88 to 72 b.p.m., p less than 0.01), while mean arterial pressure (98 mm. Hg), left ventricular filling pressure (14 mm. Hg), cardiac index (2.4 L. per minute per square meter), and stroke work index (36 Gm.m./M.2) were unchanged (p greater than 0.05). The edrophonium bolus prolonged the A-H interval (117 to 135 msec., p less than 0.01) while the H-Q interval was unaltered (48 msec; p greater than 0.05). It is concluded that increased vagal tone with edrophonium did not reduce the over-all presence of premature ventricular contractions in the entire study group; however, the malignant nature of PVCs and ventricular tachycardia appeared to be lessened by the parasympathomimetic agent in certain patients. In addition, no adverse hemodynamic or intraventricular conduction effects were produced by edrophonium administration.

Acetylcholinesterase↗
PubMed1978

Origin of so-called right and left ventricular arrhythmias in acute myocardial ischemia.

The anatomic origin of ventricular arrhythmias occurring immediately after coronary arterial ligation was studied in 32 dogs. The electrocardiogram and seven single or composite bipolar electrograms were recorded from various sites within and surrounding the ischemic area in the left and right ventricles. Delay and fragmentation in the activation of the epicardial ischemic zone of the left ventricle, bridging diastole, preceded the appearance of ventricular arrhythmias and were continuous during the rhythm disorders. So-called left and right ventricular arrhythmias were associated with similar delay and fragmentation in left ventricular ischemic epicardial activity. Multiple and simultaneous activation of both the right and left ventricles produced ventricular fusion premature complexes. Multiple exit points increased before ventricular fibrillation occurred. The ultimate origin of premature ectopic impulse formation in the ventricles is not necessarily related to one or more exit points in either ventricle. Ischemic damage to the heart produces ventricular arrhythmias that appear to originate from both ventricles. The site of origin of ventricular arrhythmias should not be the sole factor in assessing the benign or malignant properties of the arrhythmia.

Animals↗
PubMed1977

Phasic aortocoronary bypass graft blood velocity during ventricular arrhythmias in man.

With use of the Doppler ultrasonic flowmeter catheter, phasic aortocoronary bypass graft blood velocity was measured in 16 conscious subjects during ventricular arrhythmias. Ventricular extrasystoles reduced peak systolic and diastolic graft blood velocities by 20 to 80 percent, generally in relation to their respective coupling intervals. When extrasystoles appeared in closely coupled salvos diastolic bypass blood velocity virtually ceased. Nineteen episodes of ventricular tachycardia produced an average 50 percent decrease in peak graft blood velocity (control mean +/- 1 standard deviation blood velocity 28 +/- 11 cm/sec; value during ventricular tachycardia 14 +/- 8 cm/sec, P less than 0.001). An "overshoot" of peak blood velocity was observed after ventricular extrasystoles and tachycardia. All such changes in aortocoronary bypass blood velocity related to tachyarrhythmia were more prominent during the systolic fraction of flow. It is concluded that (1) ventricular arrhythmias adversely influence aortocoronary bypass graft function, and (2) this finding supports an aggressive approach to the treatment of these arrhythmias in subjects with bypass grafts.

Adult↗
PubMed1975

Relation between infarct size and ventricular arrhythmia.

In order to determine whether ventricular arrhythmia is quantitatively related to infarct size estimated enzymatically we studied 31 patients with acute myocardial infarction without cargiogenic shock. Infarct size index was estimated from hourly serum creatine kinase (CK) changes during periods of 48 to 72 hours. Ventricular arrhythmia was quantified by automated analysis of continuous electrocardiographic recordings over a period of 20 hours with the use of the Argus/H computer system. Patients were classified into three groups according to infarct size index. Patients in all groups had similar average heart rate, blood pressure, serum potassium, and arterial pH and PCO2 values during the first 10 hours after admission. The total number of ventricular ectopic beats (VEB), frequency of couplets, and ventricular tachycardia, and peak rate of ventricular ectopic beats during the first 10 hours after admission were all related to infarct size index. For example, patients with small, medium, and large estimated infarct size averaged 26, 104, and 405 ventricular ectopic beats, respectively. These results suggest that the severity of ventricular arrhythmia early after myocardial infarction is related to the extent of myocardial injury as estimated enzymatically. Thus the apparent efficacy and therefore the evaluation of antiarrhythmic agents early after myocardial infarction may be influenced by the magnitude of injury sustained by the heart.

Arrhythmias, Cardiac↗
PubMed1976

Automaticity and time-dependent conduction disturbance produced in canine ventricular myocardium. New aspects for initiation of ventricular arrhythmias.

1) In isolated canine ventricular myocardium, automaticity could be induced by a passage of small depolarizing DC-currents. The mechanism was attributed to inflowing Ca++ and Na+ currents and time-dependent deactivation of outward K+ current under a condition of high membrane resistance due to an anomalous rectification. Significance of the automaticity was discussed in relation to the ventricular arrhythmias encountered in very early stage of myocardial infarction. 2) In in situ canine hearts, chloropromazine induced time (preceding cycle length)-dependent decrease in conduction velocity within the ventricle. Thus QRS-duration of non-premature beats was lenghtened at rapid pacing rates while QRS-duration of atrial premature beats was lengthened also at short coupling intervals in the drug-treated dogs. These slow conductions were not due to reduced take-off potential of action potentials bue due to drug-induced slow recovery of rapid Na+ system. The phenomenon may be responsible for reported QRS-prolongation and fatal ventricular arrhythmias encountered in the patients receiving phenothiazines.

Action Potentials↗
PubMed1979

Stress-induced ventricular arrhythmias.

Restraint stress produced ventricular arrhythmias in seven of seven guinea pigs monitored by a Holter ECG recorder. Couplets and ventricular tachycardia, never seen in unrestrained guinea pigs, were noted in three. The arrhythmias were associated with high heart rates which showed no tendency to decrease during the restraint period.

Animals↗
PubMed1978

Long-term tocainide therapy for ventricular arrhythmias.

Long-term tocainide therapy has been evaluated in 17 patients with ventricular arrhythmias. Ventricular tachycardia and/or fibrillation was recurrent and sustained in nine patients, and symptomatic but unsustained in three others. Five patients had frequent but only mildly symptomatic ventricular irritability. In all patients, arrhythmias could not be managed with quinidine, procainamide or propranolol. Tocainide doses ranged from 300 to 700 mg every 8 hours (mean steady-state plasma concentrations ranged from 5.75 to 12.18 microgram/ml). Tocainide therapy was unsuccessful in eight patients; three died during therapy and five had no antiarrhythmic response. The data suggest that evaluation of long-term drug efficacy, using the criterion of reduction of asymptomatic arrhythmias, is best documented by multiple sequential ambulatory electrocardiographic recordings, both on and off the drug. Tocainide controlled arrhythmias in nine patients (53%), with criteria of success being continued reduction of ectopic beats and/or control of symptomatic recurrences. Seven patients remain on therapy. Side effects generally have been minor and well-tolerated.

Adult↗
PubMed1979

Two periods of early ventricular arrhythmia in the canine acute myocardial infarction model.

The time course of ventricular arrhythmias in the early period (0--30 minutes) after ligation of the left anterior descending coronary artery was studied in 41 open-chest mongrel dogs anesthetized with pentobarbital sodium (Nembutal). ECGs and seven single and composite electrograms from various regions in and around the ischemic zone were recorded throughout the experiments. Two periods of ventricular arrhythmias were clearly seen. The first occurred 2--10 minutes after coronary ligation, peaking at 5--6 minutes, and was designated as immediate ventricular arrhythmias (IVAs). There was a distinct correlation between incidence, severity, onset and termination of IVA and the degree of local delay and fragmentation of the normal sinus activation spread in the ischemic subepicardial zone. The second wave of ventricular arrhythmias occurred 12--30 minutes after ligation independently of the previous increased delay and fragmentation of activation in the ischemic subepicardium. Delayed ventricular arrhythmias (DVAs) were as severe as IVAs--there were nine instances of ventricular fibrillation during DVA and seven during IVA. While the mechanism of IVA is most probably related to reentry accompanied by delay and fragmentation of ischemic subepicardial activation, the mechanism of DVA remains unclear. Our evidence suggests that DVAs are also reentrant, with the reentry pathways located in deep myocardial structures or involving microscopic pathways at the Purkinje muscle junction.

Acute Disease↗
PubMed1975

Ventricular arrhythmias during unstable angina pectoris.

In order to study the occurrence and frequency of ischemia-induced ventricular arrhythmias, we analyzed 105 episodes of spontaneous angina pectoris occurring at rest in 28 hospitalized patients with unstable angina pectoris and proved coronary artery disease. Of 24 patients with serious ventricular arrhythmias during pain, 17 (57%) were arrhythmia-free during monitoring. In the other four patients, 17 of 29 (59%) pain episodes were associated with serious ventricular arrhythmias, and three of these four had serious ventricular arrhythmias during pain-free periods. Each patient tended to manifest the same type of arrhythmia during repeat episodes of pain. It appears that continuous electrocardiogram (ECG) monitoring is important during the initial hospitalization of the patient with unstable angina. The presence of ventricular arrhythmias during pain-free periods indicates a high risk for serious ventricular arrhythmias during episodes of spontaneous pain. These patients should be considered for continued ECG monitoring and antiarrhythmic therapy.

Adult↗