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Biomedical subjects

J J Heger

Publications and source records attributed to J J Heger.

At least 73 records · Page 4Linked to original sources
PubMed1983

Syncope and ventricular tachycardia in patients with ventricular preexcitation.

Four patients with ventricular preexcitation whose syncope initially was attributed to an arrhythmia utilizing the accessory pathway are presented. At electrophysiologic study, the electrophysiologic characteristics of the accessory pathways were considered unlikely to support a tachycardia of a rate sufficient to result in syncope. Programmed stimulation of the right ventricle, however, reproducibly induced ventricular tachycardia to which the syncope was subsequently attributed in 3 patients. The importance of identifying ventricular tachycardia as the cause of syncope in these patients is emphasized.

Adult↗
PubMed1983

Modulation of the Q-T interval by the autonomic nervous system.

Recent investigations have clarified some of the effects of the autonomic nervous system on duration and spatial distribution of the Q-T interval in humans. The use of atrial pacing to fix heart rate or 24-hour continuous electrocardiographic recording to develop a regression formula for individual patients has provided a means to interpret the effects of an intervention that alters both the heart rate and the Q-T interval. Drugs that affect the autonomic nervous system can influence Q-T interval directly or by changing rate. Bazett's formula to correct for rate may be misleading after certain drug interventions. For example, the Q-T interval during sinus rhythm or atrial pacing and the ventricular effective refractory period shorten after atropine plus propranolol, but corrected Q-T interval using Bazett's formula does not change. No change occurs in the Q-T interval during sinus rhythm or atrial pacing, or in ventricular effective refractory period after administration of propranolol although corrected Q-T interval using Bazett's formula markedly shortens. Q-T interval during sinus rhythm and atrial pacing and ventricular effective refractory period decrease after atropine but correct Q-T interval lengthens.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Reevaluation of enhanced atrioventricular nodal conduction: evidence to suggest a continuum of normal atrioventricular nodal physiology.

The syndrome of enhanced atrioventricular nodal (AVN) conduction has been defined arbitrarily by: AH interval during normal sinus rhythm (AH-NSR) less than or equal to 60 msec; shortest right atrial pacing cycle length (PCL) maintaining 1:1 AVN conduction (shortest PCL 1:1) less than or equal to 300 msec; and at the shortest PCL 1:1, an increase in the AH interval from AH-NSR (delta AH) less than or equal to 100 msec. We examined the relationship between AH-NSR, shortest PCL 1:1, and delta AH in 160 consecutively studied patients who did not have accessory AV pathways or second-degree AV block to determine whether a distinct subgroup of patients with unusually rapid AVN conduction properties could be identified. The frequency distribution of each of the variables was unimodal and continuous. Cluster analysis, combining the three variables, failed to reveal a distinct subgroup at the lower end of the spectrum. Sixty-six patients (41%) had AH-NSR less than or equal to 60 msec, 36 (23%) shortest PCL 1:1 less than or equal to 300 msec, 76 (48%) delta AH less than or equal to 100 msec, and 17 (11%) all three criteria. The shape of the AH vs atrial PCL curve was independent of shortest PCL 1:1. Neither delta AH nor the terminal slope of the curve for AH vs atrial PCL (measured over the 20-40 msec before Wenckebach block) was related to AH-NSR or shortest PCL 1:1. We conclude that a subgroup cannot be identified by AH-NSR, shortest PCL 1:1, and delta AH, and that enhanced AVN conduction as previously defined represents simply one end of the continuous spectrum of normal AVN physiology.

Adolescent↗
PubMed1983

Drug therapy of cardiac arrhythmias.

The authors provide an overview of the general features of pharmacokinetics and report the pharmacodynamic and pharmacokinetic interactions of selected antiarrhythmic drugs. Their clinical experience in the use of investigational antiarrhythmic drugs is also presented.

Amiodarone↗
PubMed1983

Clinical electrophysiology of ventricular tachycardia.

Programmed ventricular stimulation, electrophysiologic effects of various antiarrhythmic drugs, and the results of serial electrophysiologic testing in patients with ventricular arrhythmias are discussed. The use of discriminant analysis to predict the efficacy of antiarrhythmic drugs is also briefly analyzed.

Anti-Arrhythmia Agents↗
PubMed1982

Electrophysiology of oral encainide.

The electrophysiologic effects of oral encainide were assessed in 15 patients. Electrophysiologic studies were performed before and after 3 or more days of oral encainide therapy, 100 to 300 mg/day (mean 242 +/- 66). Patients received no other cardioactive drugs during this time. Encainide significantly (p less than 0.005) lengthened the following: A-H interval (74.5 +/- 21.5 to 105.5 +/- 39.1 ms, mean +/- standard deviation), the shortest atrial pacing cycle length maintaining 1:1 atrioventricular (A-V) nodal conduction (339.0 +/- 71.3 to 417.0 +/- 88.6 ms), H-V interval (47.5 +/- 7.8 to 67.1 +/- 12.9 ms), QRS interval (103.5 +/- 30.9 to 132.3 +/- 35.7 ms), right atrial (233.8 +/- 27.2 ms to 282.9 +/- 38.6 ms) and right ventricular (235.7 +/- 15.6 to 267.1 +/- 36.9 ms) effective refractory periods and Q-T interval (364.4 +/- 38.0 to 416.9 +/- 55.3 ms). The spontaneous sinus cycle length did not change significantly. In four patients who had accessory A-V muscle connections (two manifest, two concealed) encainide abolished anterograde conduction over the accessory pathway in two patients, and increased the retrograde effective refractory period and/or lengthened retrograde conduction time or blocked retrograde conduction in the accessory pathway, or all three variables, in all four patients. There was no correlation between the plasma encainide concentration obtained at the time of study and the magnitude of change in any electrophysiologic variable. It is concluded that (1) encainide depresses conduction in the A-V node, His-Purkinje system and accessory pathway, and increases refractoriness of the atrium, ventricle and accessory pathway, and (2) differences between these results and those of earlier studies using encainide in a single intravenous dose (which found no significant effects on A-V nodal conduction or atrial and ventricular refractoriness) may be explained in part by the effects of an active metabolite of encainide.

Administration, Oral↗
PubMed1982

Clinical transvenous cardioversion of recurrent life-threatening ventricular tachyarrhythmias: low energy synchronized cardioversion of ventricular tachycardia and termination of ventricular fibrillation in patients using a catheter electrode.

The purpose of this study was to test the efficacy, safety, and patient tolerance of transvenous cardioversion and defibrillation in patients who had recurrent ventricular tachyarrhythmias. In five of seven patients, a truncated exponential shock of 0.025 to 2.0 joules synchronized to the QRS complex terminated 47 episodes of recurrent sustained ventricular tachycardia (VT). Cardioversion threshold was less than or equal to 0.25 joule in three patients and 0.75 to 2.0 joules in two patients. Shocks of 0.75 joule and 2.0 joule failed to terminate VT in one patient each; higher energies were not tried because of hemodynamic decompensation. In one patient, a shock of 25 joules terminated ventricular fibrillation (VF) on three occasions, and in another patient a shock of 1.0 joule terminated atrial fibrillation on one occasion. Shocks less than or equal to 0.5 joule were well tolerated by the awake unsedated patient. One hundred forty of 141 synchronized shocks (including subthreshold shocks) produced no repetitive ventricular activity. In one seriously ill patient who had received multiple antiarrhythmic drugs and required balloon counterpulsation for hemodynamic support, on a single occasion each a synchronized transvenous shock and a synchronized conventional transthoracic shock produced ventricular flutter and ventricular fibrillation (VF), respectively. We conclude that synchronized transvenous cardioversion by a catheter electrode offers promise as a new therapeutic approach.

Aged↗
PubMed1982

Drug conversion of nonsustained ventricular tachycardia to sustained ventricular tachycardia during serial electrophysiologic studies: identification of drugs that exacerbate tachycardia and potential mechanisms.

Eleven of 83 patients who had ventricular tachycardia (VT) and underwent serial electrophysiologic study (EPS) had a more severe VT induced while receiving a particular antiarrhythmic drug as compared to control study. For all patients only nonsustained VT was initiated during control study, while sustained VT occurred during drug testing with disopyramide (2 patients), quinidine (2 patients), amiodarone (4 patients), and encainide (7 patients), although spontaneous arrhythmias appeared well-controlled prior to repeat testing. Pacing techniques used to induce sustained VT were the same as those used in the control study in eight patients and "less aggressive" in three patients. Almost all episodes of sustained VT resulted in substantial hypotension, especially in patients who were taking encainide. Drugs associated with sustained VT increased the median tachycardia cycle length by 112 msec (p less than 0.005) but increased the median ventricular effective refractory period by only 30 msec (p less than 0.02). Assuming re-entry was responsible for VT, we postulate that drugs facilitated initiation of sustained VT by prolonging activation time but only minimally increasing refractoriness of the tachycardia circuit.

Adult↗
PubMed1982

Clinical and electrophysiologic findings in patients with repetitive monomorphic ventricular tachycardia and otherwise normal electrocardiogram.

Natural history, structural substrate, electrocardiographic and electrophysiologic characteristics and therapy were evaluated in 18 patients who demonstrated repetitive ventricular tachycardia, defined as repeated episodes of ventricular tachycardia that had a uniform QRS configuration and normal sinus-conducted QRS complexes between the episodes of tachycardia. The patients were young (mean age 37 years) and frequently had a long history of arrhythmias before this evaluation; only two patients has a history of syncope and six were completely asymptomatic. Fourteen patients had no evidence of underlying structural heart disease, three had mitral valve prolapse and one had congestive cardiomyopathy. Episodes of ventricular tachycardia tended to occur in clusters over a 24 hour electrocardiographic recording period. Repetitive ventricular tachycardia was induced in two of nine patients by programmed electrical stimulation, and in seven patients incremental atrial and ventricular pacing suppressed spontaneous arrhythmia. In the one patient whose tachycardia was induced by incremental ventricular pacing there was an inverse relation between pacing cycle length and the interval from the last paced complex to the first complex of ventricular tachycardia, indicating there was overdrive suppression. At a follow-up time of 0.5 to 8 years no patient had died or had worsening of symptoms. Encainide completely eliminated episodes of ventricular tachycardia during acute treatment in five of six patients tested. Seven patients received no antiarrhythmic therapy and the arrhythmia appeared to have spontaneously resolved in four of these patients. Repetitive ventricular tachycardia appears to have distinct clinical and electrophysiologic characteristics. In this series the arrhythmia had a good prognosis and often required no treatment. The electrophysiologic features are consistent with a mechanism of automaticity.

Adolescent↗
PubMed1982

Value and limitations of clinical electrophysiologic study in assessment of patients with unexplained syncope.

We assessed the value of clinical electrophysiologic study using intracardiac recording and programed electrical stimulation in 34 patients who had unexplained syncope and/or presyncope. All patients had normal electrocardiograms, and no abnormality was detected by clinical examination, ambulatory electrocardiographic recording, or treadmill testing. The electrophysiologic results were diagnostic in four patients (11.8 percent) and led to appropriate therapy that totally relieved symptoms. The results were abnormal but not diagnostic in two patients (5.8 percent) and normal in the remaining 28 patients (82.4 percent). The patients were followed for a mean period of 15 months (range two to 44) after electrophysiologic testing. Sixteen patients (47 percent) had no further episodes in the absence of any intervention. In four patients (11.8 percent), a definitive diagnosis was made during follow-up. In seven patients, permanent pacing was instituted empirically with relief of syncope. Two patients continued to have syncopal spells. We conclude that the diagnostic yield of electrophysiologic testing is low in a patient population that has no electrocardiographic abnormality or clinical evidence of cardiac disease. Empirical permanent pacing in patients with symptoms continuing after our study appeared to be beneficial, but this result is difficult to evaluate because of the high incidence of spontaneous remission in this group. Persistent attempts to document electrocardiographic abnormalities during a typical episode of symptoms appears to be the only definitive way to confirm or exclude an arrhythmic cause of the symptoms.

Adult↗