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Biomedical subjects

J J Heger

Publications and source records attributed to J J Heger.

At least 55 records · Page 3Linked to original sources
PubMed1984

Preexcitation syndromes. Mechanisms and management.

Ventricular preexcitation occurs when, in relation to atrial events, some or all of the ventricular muscle is activated earlier by the atrial impulse than would be expected if conduction of the impulse activated the ventricles by way of the normal atrioventricular conduction system. The purpose of this article is to review the pathophysiology of the variants of preexcitation and to discuss the therapeutic approach to patients who have tachyarrhythmias.

Anti-Arrhythmia Agents↗
PubMed1984

Clinical efficacy and electrophysiologic effects of cibenzoline therapy in patients with ventricular arrhythmias.

Cibenzoline, a new antiarrhythmic agent, was tested in 26 patients who had symptomatic ventricular tachycardia (24 patients) or premature ventricular complexes (2 patients) unresponsive to conventional drugs. Cibenzoline was given orally every 8 hours to maximal doses of 65 mg in 2 patients, 81.25 mg in 22 patients and 97.5 mg in 2 patients. Cibenzoline abolished spontaneous episodes of ventricular tachycardia in 8 of 16 patients with ventricular tachycardia during a 72 hour control electrocardiographic recording, and 7 of 22 patients had greater than 83% decrease in premature ventricular complexes compared with control. The PR interval increased 14% (p less than 0.001), QRS duration increased 17% (p less than 0.001), QT interval did not change and mean ejection fraction in 10 patients did not change. Electrophysiologic studies were performed on 10 patients in the control period and during maximal cibenzoline dosage. Cibenzoline did not affect electrophysiologic properties of the atrium or atrioventricular (AV) node. It prolonged the ventricular effective (223 +/- 16 to 241 +/- 22 ms, p less than 0.02) and functional (247 +/- 18 to 264 +/- 25 ms, p less than 0.02) refractory periods. At control electrophysiologic studies, ventricular tachycardia was induced in 9 of 10 patients (mean cycle length 210 +/- 31 ms). Cibenzoline therapy prevented ventricular tachycardia induction in two patients, and in the other seven patients the mean ventricular tachycardia cycle length increased from 210 to 260 ms. The one patient with no ventricular arrhythmia induced during the control study still had no arrhythmia induced while receiving cibenzoline.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Amiodarone: electrophysiologic actions, pharmacokinetics and clinical effects.

Interest in amiodarone has increased because of its remarkable efficacy as an antiarrhythmic agent. The purpose of this report is to review what is known about the electrophysiologic actions, hemodynamic effects, pharmacokinetics, alterations of thyroid function, response to treatment of supraventricular and ventricular tachyarrhythmias and adverse effects of amiodarone. Understanding the actions of amiodarone and its metabolism will provide more intelligent use of the drug and minimize the development of side effects. The mechanism by which amiodarone suppresses cardiac arrhythmias is not known and may relate to prolongation of refractoriness in all cardiac tissues, suppression of automaticity in some fibers, minimal slowing of conduction in fast channel-dependent tissue, or to interactions with the autonomic nervous system, alterations in thyroid metabolism or other factors. Amiodarone exerts definite but fairly minor negative inotropic effects that may be offset by its vasodilator actions. Amiodarone has a reduced clearance rate, large volume of distribution, low bioavailability and a long half-life that may last 2 months in patients receiving short-term therapy. Therapeutic serum concentrations range between 1.0 and 3.5 micrograms/ml. The drug suppresses recurrences of cardiac tachyarrhythmias in a high percent of patients, in the range of 80% or more for most supraventricular tachycardias and in about 66% of patients with ventricular tachyarrhythmias, sometimes requiring addition of a second antiarrhythmic agent. Side effects, particularly when high doses are used, may limit amiodarone's usefulness and include skin, corneal, thyroid, pulmonary, neurologic, gastrointestinal and hepatic dysfunction. Aggravation of cardiac arrhythmias occurs but serious arrhythmias are caused in less than 5% of patients. Amiodarone affects the metabolism of many other drugs and care must be used to reduce doses of agents combined with amiodarone.

Administration, Oral↗
PubMed1984

Cibenzoline plasma concentration and antiarrhythmic effect.

The relationship between plasma concentrations of cibenzoline and its antiarrhythmic effect was evaluated in patients receiving the drug orally as part of an ascending multiple dose efficacy and tolerance study. Twenty-five patients participated in a 3-day placebo period, 3 days of 32.5 mg cibenzoline every 6 hr, 3 days of 65 mg cibenzoline every 6 hr, 3 days of 81.25 mg cibenzoline every 6 hr, and 3 final placebo days. Arrhythmia frequency was monitored by 24-hr Holter monitoring and blood samples were drawn during and after dosing. Percent reduction in baseline premature ventricular complex (PVC) frequency for the 25 subjects demonstrated considerable interpatient variability in antiarrhythmic response. Cibenzoline plasma concentrations over 300 ng/ml were associated with some decrease in PVC frequency in virtually all cases. The relationship between plasma concentration and PVC frequency was studied more rigorously in eight of the 25 patients and that for ventricular couplet (VC) frequency was studied in six. For these analyses, PVC and VC frequency data were averaged over 6-hr intervals and plotted against trough cibenzoline concentrations. The data from each patient were fitted with a concentration-effect function (Hill equation) by means of least squares regression. With the exception of two extreme values, the concentration corresponding to 90% reduction in PVC frequency (C90) ranged from 215 to 405 ng/ml. In five of the six patients with arrhythmia in whom VC data were also evaluated, the individual C90 for VCs were considerably less than those for PVCs. The agreement between the observed concentration-response relationships and those predicted by curve-fitting the data suggests that the antiarrhythmic effect of cibenzoline is proportional to its plasma concentration, and that the Hill equation provides an accurate mathematic description of the concentration-response relationship.

Administration, Oral↗
PubMed1984

Synchronous intracardiac cardioversion.

The concept of synchronous transvenous cardioversion of sustained ventricular tachycardia is discussed. This article reviews the animal experience, initial and collective studies in patients, and results of permanent implantation in two patients.

Aged↗
PubMed1984

Future directions: electrical therapy for cardiac tachyarrhythmias.

Directions and research opportunities in basic animal and clinical investigations and in industry that relate to the application and development of electrical devices which control tachyarrhythmias are presented. In basic research, a better understanding of mechanisms responsible for tachyarrhythmias , their onset and methods of termination, would provide increased rationale for selecting a particular therapeutic approach. Knowing the distribution in the heart of applied electrical current when delivered by different types of electrodes placed at different myocardial sites would be helpful. Clinically, we must develop appropriate algorithms to accurately differentiate sinus tachycardia, the various forms of supraventricular tachycardias and ventricular tachycardia. These must be incorporated into future cardioverters and defibrillators . In industry, new sensors, electrodes, expanded telemetry capabilities and implanted microprocessors will aid in creation of a universally applicable generic form of electrical therapy that can be programmed to treat any form of tachycardia.

Animals↗
PubMed1984

Initial experience with Symbios Model 7008 pacemaker.

The Symbios 7008 pacemaker is capable of treating both bradycardias and tachycardias. In this report, we summarize operation of the pacemaker and the initial experience in 21 patients who have received implants. All patients have supraventricular tachyarrhythmias that have been terminated successfully with automatic atrial burst pacing (19 patients) or AV sequential pacing. More than half of the patients also have bradyarrhythmias requiring pacing and thus benefit from both functions of the device. Experience to date has been favorable.

Adult↗
PubMed1984

Preliminary experience with the implantable transvenous cardioverter.

A synchronized shock of less than or equal to 2.0 joules delivered over a specially designed catheter electrode passed to the apex of the right ventricle effectively terminates sustained ventricular tachycardia in dogs and in patients. The capability has been engineered into a 95 gram device implanted using lidocaine anesthesia, which is also capable of VVI pacing and of performing programmed electrophysiologic studies. Seven patients have received the implant and the initial experience is described.

Aged↗
PubMed1984

Clinical efficacy and electrophysiologic effects of encainide in patients with Wolff-Parkinson-White syndrome.

We performed electrophysiologic studies in 19 patients with accessory pathways before and during encainide therapy with a mean daily dose of 197 mg. Fourteen patients had manifest accessory atrioventricular connections, and five patients had concealed accessory atrioventricular connections. The patients had recurrent atrioventricular reentrant tachycardia for a mean of 15.8 years and had received a mean of 3.6 drug trials without successful suppression of recurrent arrhythmias. Encainide caused complete antegrade conduction block in the accessory pathway in eight of 14 patients with manifest accessory atrioventricular connections. The shortest atrial pacing cycle length maintaining 1:1 conduction over the accessory pathway at control study w3as 328 +/- 66 msec in patients in whom antegrade conduction block occurred, and it was 247 +/- 21 msec (p less than .01) in patients in whom conduction remained during encainide therapy. Retrograde conduction over accessory atrioventricular connections could be evaluated in 14 patients, and complete block occurred in seven patients during encainide therapy. There was no correlation between control retrograde effective refractory period or conduction of the accessory pathway and subsequent development of conduction block with encainide therapy. It should be noted that five patients who developed drug-related retrograde block over the accessory pathway had initial retrograde effective refractory periods for the accessory pathway less than 270 msec. Nineteen patients had atrioventricular reentrant tachycardia initiated at control electrophysiologic study. Encainide prevented induction of tachycardia in 10 patients, and in the other nine patients, cycle length of tachycardia increased during drug treatment from 313.9 +/- 53.1 to 418.3 +/- 80.9 msec (p less than .001), primarily due to an increase in ventriculoatrial conduction time from 162.2 +/- 43.8 to 238.3 +/- 87.9 msec (p less than .01). Fifteen patients continued encainide treatment for a mean of 18 months (range 7 to 38), and all but one patient remain asymptomatic. Encainide is well tolerated and prevents recurrence of reentrant tachycardia in patients with Wolff-Parkinson-White syndrome very effectively.

Adolescent↗
PubMed1983

Enhanced parasympathetic tone shortens atrial refractoriness in man.

The purpose of this study was to determine the effects of enhanced vagal tone on human right atrial refractoriness in 12 patients. A specially built neck collar connected to a vacuum source was placed around the patient's neck and enhanced vagal tone was produced during neck suction using intracollar negative pressures of 50 to 60 mm Hg. Refractory periods were determined with a catheter electrode positioned in the high right atrium near the sinus node. Induced neck suction increased the spontaneous sinus cycle length from 837 +/- 96 to 1.136 +/- 273 ms (p less than 0.001) and shortened the atrial effective refractory period from 241 +/- 24 to 230 +/- 20 ms (p less than 0.01) and the atrial functional refractory period from 272 +/- 32 to 262 +/- 29 ms (p less than 0.01). In 2 of 2 patients, collar-induced decreases in atrial refractoriness and increases in spontaneous cycle length were prevented after atropine (0.03 mg/kg) was given intravenously. It is concluded that enhanced vagal tone mediated through muscarinic receptors shortens atrial refractory periods in man.

Adolescent↗
PubMed1983

Cellular electrophysiologic abnormalities of diseased human ventricular myocardium.

Using standard microelectrode techniques, the cellular electrophysiologic features of ventricular myocardium resected from 8 patients with refractory arrhythmias were studied in vitro. Action potentials from damaged myocardium compared with normal myocardium had reduced resting membrane potential, amplitude, and maximal upstroke velocity. Tetrodotoxin, but not verapamil, suppressed 3 action potentials with resting potentials of -60 to -64 mV and Vmax less than 70 V/s. Verapamil, but not tetrodotoxin, suppressed 4 action potentials with resting potentials of -44 to -57 mV and Vmax less than 20 V/s. Unidirectional block, Wenckebach block, and summation occurred in damaged zones. Exit block from and frequency-dependent entrance block into an ectopic focus were noted. Subthreshold responses in the focal area induced by action potentials in the surrounding myocardium and by subthreshold current pulses injected through the recording microelectrode altered the spontaneous discharge rate of the focus, as previously described for modulated parasystole. Pulses early in the spontaneous cycle delayed the next expected discharge, and later pulses accelerated the subsequent discharge. Pulses injected at the singular point completely suppressed automaticity (annihilation). Tetrodotoxin and verapamil suppressed automaticity in some fibers. Single action potentials induced in quiescent fibers triggered and terminated sustained rhythmic activity. These data suggest that depressed fast responses, slow responses, and subthreshold potentials can generate and modulate ectopic activity in damaged human ventricle and that fast- and slow-channel blocking agents and single premature stimuli can terminate such activity.

Action Potentials↗
PubMed1983

Pathophysiology of arrhythmias: clinical electrophysiology.

We have endeavored to relate known electrophysiologic mechanisms of arrhythmia development to clinically occurring arrhythmias, realizing that definitive conclusions can only be surmised at present. Arrhythmias that may be due to disorders of impulse formation include slow atrial, junctional, and ventricular escape rhythms, certain types of atrial tachycardias (such as those produced by digitalis), accelerated junctional (nonparoxysmal junctional tachycardia) and idioventricular rhythms, and parasystole. Arrhythmias that may be due to disorders of impulse conduction include flutter and fibrillation, atrioventricular nodal reentrant tachycardia, reciprocating tachycardias associated with an accessory pathway, sinus nodal reentry, some atrial tachycardias, and many ventricular tachycardias. Understanding the mechanism of the tachycardia, in some instances, helps direct rational therapeutic approaches.

Animals↗
PubMed1983

Clinical efficacy of amiodarone in treatment of recurrent ventricular tachycardia and ventricular fibrillation.

The clinical antiarrhythmic efficacy of amiodarone treatment was examined in 196 patients with recurrent ventricular tachycardia (VT) or ventricular fibrillation (VF) resistant to other antiarrhythmic drugs. Patients had received a mean of 4.4 +/- 1.9 unsuccessful drug trials over a mean of 15.2 months prior to amiodarone treatment of recurrent VF in 57 patients; recurrent, sustained VT in 95 patients; and recurrent, nonsustained VT in 44 patients. Amiodarone dosage during the first 2 to 4 weeks of treatment was 800 to 1600 mg/day. During long-term follow-up, amiodarone dosage was reduced to 200 to 600 mg/day, based on the control of arrhythmia and patient tolerance. Electrophysiologic studies were performed prior to and after 2 or more weeks of amiodarone treatment. After a mean follow-up of 16.2 +/- 13.0 months, 126 (64%) of 196 patients continued successful treatment with amiodarone. At electrophysiologic study, amiodarone prevented VT induction in 13 patients, and although VT was induced in 101 patients, 80 patients continued treatment for 14.2 months without recurrence of spontaneous VT. Amiodarone treatment was discontinued because of recurrent VT in 22 patients, sudden cardiac death in 15 patients, adverse effects in 12 patients, and noncardiac death in 21 patients. In nine patients, recurrent VT/VF appeared related to amiodarone-induced exacerbation of arrhythmia. Pulmonary toxicity occurred in seven patients, and 19 patients developed blue skin discoloration. Other adverse effects were usually dosage related. In summary, amiodarone was a highly effective antiarrhythmic drug, but at the dosages employed, the risk of significant adverse effects warrants careful surveillance during treatment.

Adolescent↗
PubMed1983

Relationships between amiodarone dosage, drug concentrations, and adverse side effects.

The relationships between size of loading dose and drug concentration, size of maintenance dose and drug concentration, and pulmonary and cutaneous adverse side effects and drug dosage were examined in patients given amiodarone. Amiodarone and metabolite concentrations in plasma and red cell samples were measured by specific high-pressure liquid chromatography. During drug loading, a daily dose schedule of 1600 mg/day produced significantly higher drug concentrations than did a loading dose schedule of 800 mg/day. During maintenance therapy, amiodarone dosage correlated with drug concentrations but with a wide interpatient variability for any given dosage level. The ratio of desethylamiodarone to amiodarone remained relatively constant over different dosage or drug concentration ranges, but increased with duration of treatment, suggesting a time-dependent metabolic function that may be analogous to the time-dependent attainment of maximal antiarrhythmic effect. The occurrence of pulmonary toxicity from amiodarone was not related to duration of treatment or cumulative dose of drug, buy may relate to the magnitude of the maintenance dose of amiodarone. Blue skin discoloration occurred in 19 (36%) of 53 patients receiving amiodarone for longer than 17 months, and may relate to the cumulative dose.

Amiodarone↗
PubMed1983

Influence of tachycardia cycle length and antiarrhythmic drugs on pacing termination and acceleration of ventricular tachycardia.

We examined the influence of ventricular tachycardia (VT) cycle length and antiarrhythmic drugs on the frequency of VT termination and acceleration by single and double extrastimuli and right ventricular burst pacing. In 57 patients, 89 episodes of sustained VT (32 control, 57 drug) were induced by programmed electrical stimulation. Overall, 60 of 89 (67%) episodes of ventricular tachycardia were terminated by means of programmed electrical stimulation. In patients with relatively slow ventricular tachycardia (VT cycle length greater than or equal to 350 msec) pacing terminated 37 of 44 (84%) episodes but terminated only 24 of 45 (51%) episodes of more rapid VT (VT cycle length less than or equal to 349 msec, p less than 0.005). Pacing successfully terminated VT in nine of 49 (18%) episodes using a single extrastimulus, 22 of 52 (42%) episodes using double extrastimuli, and 40 of 66 (61%) episodes using burst right ventricular pacing. VT acceleration occurred in none of 49 attempts with a single extrastimulus, in eight of 52 (15%) attempts with double extrastimuli, and in 12 of 66 (18%) attempts using burst right ventricular pacing. During therapy, the frequency of either ventricular tachycardia termination or acceleration did not change regardless of the pacing termination method used. However, by prolonging the mean VT cycle length from 311.1 +/- 82.2 msec to 401.9 +/- 103.5 msec (p less than 0.01), drugs increased the overall frequency of VT termination. We conclude that: (1) pacing terminates VT more frequently if the VT cycle length is long and if right ventricular bursts are used, (2) burst right ventricular pacing increases the risk of VT acceleration, and (3) drugs increase the frequency of ventricular tachycardia termination by prolonging VT cycle length but do not affect frequency of VT acceleration.

Adult↗
PubMed1983

Prolongation of the Q-T interval in man during sleep.

Parasympathetic blockade shortens the duration of the Q-T interval and ventricular effective refractory period independent of heart rate change. Since relative parasympathetic effect increases during sleep, it was determined whether sleep was associated with a change in the Q-T interval. Fifteen patients receiving no drugs underwent 3 to 6 days of continuous electrocardiographic recordings. Tracings were sampled every 30 minutes and recorded at a paper speed of 25 mm/s. This provided 12,000 Q-T and R-R intervals that were measured. Comparison of R-R intervals that had similar durations during sleep and awake states revealed that the duration of the Q-T interval was longer during sleep in all 15 patients (p less than 0.001). Eight patients had sufficient range of overlap of R-R intervals to compare linear regression lines of Q-T intervals recorded while awake with Q-T intervals recorded while asleep. The regression lines during sleep exhibited a mean intercept change of 38 +/- 37 ms and mean slope change of -0.021 +/- 0.040 ms when compared with the regression lines during the awake state. The difference in Q-T interval between awake and sleep states was 19 +/- 7 ms when calculated at a heart rate of 60 beats/min. These statistical comparisons of the relationship of the Q-T interval to R-R interval indicate that the Q-T interval is longer during sleep than during the awake state at the same heart rate. Prolongation of the Q-T interval during sleep may reflect increased vagal tone or sympathetic withdrawal. These changes in repolarization may be related to the diurnal variation of some ventricular arrhythmias.

Adult↗