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Biomedical subjects

E S Gang

Publications and source records attributed to E S Gang.

At least 37 records · Page 2Linked to original sources
PubMed1988

Subthreshold atrial pacing in patients with a left-sided accessory pathway: an effective new method for terminating reciprocating tachycardia.

This study investigated the possibility of terminating reciprocating atrioventricular (AV) tachycardia using subthreshold atrial pacing. Ten patients with a left-sided accessory pathway and sustained AV tachycardia underwent subthreshold atrial pacing from the coronary sinus site closest to insertion of the accessory pathway. In seven of these patients, the tachycardia could be reliably terminated with subthreshold atrial overdrive pacing. When pacing at a cycle length of 80 +/- 23% of the tachycardia cycle length, the minimal subthreshold current that was effective in tachycardia termination was 64 +/- 14% of threshold current and the maximal ineffective current was 49 +/- 17% of threshold (p less than 0.05). In all cases, the tachycardia was terminated by one or two instances of atrial capture that resulted in a premature atrial impulse (20 +/- 4% advancement of the atrial cycle) that blocked the AV node limb of the tachycardia. Anterograde conduction over the accessory pathway never occurred, either during the tachycardia or during subthreshold pacing after a return to normal sinus rhythm. No instances of atrial fibrillation were provoked by subthreshold pacing. Possible explanations for the intermittent atrial capture with critically placed subthreshold impulses include supernormal atrial conduction or summation of impulses at the atrial insertion site of the accessory pathway. It is concluded that subthreshold pacing is effective in selected patients with AV tachycardia due to an accessory pathway. Furthermore, because neither atrial fibrillation nor anterograde conduction over the accessory pathway is seen with subthreshold pacing, this modality may hold significant promise for permanent antitachycardia pacing in these patients.

Adult↗
PubMed1987

The signal-averaged electrocardiogram as a screening test for inducibility of sustained ventricular tachycardia in high risk patients: a prospective study.

The role of the signal-averaged electrocardiogram in predicting the induction of sustained monomorphic ventricular tachycardia in high risk patients was assessed prospectively in 100 consecutive patients. Presenting diagnoses were syncope (38 patients), nonsustained ventricular tachycardia (24 patients), sustained ventricular tachycardia (25 patients) and sudden cardiac arrest (13 patients). Using programmed ventricular stimulation, 71 patients (group I) did not have and 29 patients (group II) did have inducible sustained monomorphic ventricular tachycardia. Using the signal-averaged electrocardiogram with filtering (6 dB/octave) at high pass corner frequencies of 67 and 100 Hz, the two groups were compared. The signal-averaged electrocardiogram was considered abnormal if all of the following criteria were satisfied: 1) the total filtered QRS complex duration was greater than 120 ms, 2) the duration of the terminal QRS complex of less than or equal to 20 microV was greater than or equal to 30 ms, and 3) at least one deflection (late potential) was present in this region. Differences between groups I and II in these three measures were highly significant (p less than or equal to 0.001). The sensitivity and specificity of signal averaging for predicting the induction of sustained ventricular tachycardia were 93 and 94%, respectively. Stepwise logistic regression analysis identified the signal-averaged electrocardiogram as the best predictor of induction of sustained monomorphic ventricular tachycardia, independent of left ventricular ejection fraction, presence of ventricular aneurysm, myocardial infarction and other clinical variables (chi-square = 93.2, p less than 0.0001). The signal-averaged electrocardiogram is a sensitive and specific test for the induction of sustained monomorphic ventricular tachycardia, having independent predictive value.

Coronary Disease↗
PubMed1987

Decline in ventricular fibrillation threshold after successive premature extrastimuli: a possible explantation for the induction of ventricular fibrillation during programmed stimulation with multiple extrastimuli.

To examine the relation between the ventricular fibrillation threshold and the number of premature extrastimuli delivered to the right ventricle during programmed ventricular stimulation, a clinical stimulation protocol was performed in nine normal, anaesthetised, closed chest dogs. In addition, the ventricular fibrillation threshold was measured in each dog after a train of eight paced (S1) beats (VFT-S2), after a single premature extrastimulus (VFT-S3), and after two extrastimuli (VFT-S4). The VFT-V3 was 32% lower than the VFT-S2 (16(7) mA vs 24(9) mA, p less than 0.001). The VFT-S4, or the current required by the S4 extrastimulus to induce ventricular fibrillation, was 25% lower than the VFT-S3 (12(8) mA vs 16(7) mA, p less than 0.05). The cumulative reduction in the ventricular fibrillation threshold measured by the S1S2S3S4 stimulation protocol was approximately 50%. Although in most dogs the VFT-S4 was still considerably higher than twice threshold current intensity, the results of the study suggest that a possible mechanism for the induction of non-clinical ventricular fibrillation in the clinical electrophysiology laboratory may be the progressive lowering of the ventricular fibrillation threshold caused by the addition of multiple extrastimuli. This may be particularly relevant in patients with an already reduced fibrillation threshold.

Action Potentials↗
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↗
PubMed1987

Orthodromic tachycardia initiation dependent on 1:2 atrioventricular conduction in the presence of a left lateral bypass tract.

This report describes a patient who presented with atrial fibrillation associated with a rapid ventricular response (270 bpm) and wide QRS complexes. At the time of electrophysiology study, a left lateral bypass tract with both anterograde and retrograde conduction was demonstrated. Orthodromic tachycardia with atrial premature impulses was initiated and was dependent on two ventricular responses to one atrial impulse. Intravenous procainamide administration had little effect on anterograde or retrograde conduction in the accessory pathway; however, it prevented orthodromic tachycardia initiation with atrial premature impulses by prolonging atrial muscle refractoriness.

Adult↗
PubMed1987

Life-threatening postoperative pulmonary complications in patients with previous amiodarone pulmonary toxicity undergoing cardiothoracic operations.

Amiodarone therapy for cardiac arrhythmias is increasingly being recognized to be associated with pulmonary toxicity. In this report, we describe the case histories of four patients with previously diagnosed amiodarone pulmonary toxicity in whom the adult respiratory distress syndrome developed after cardiothoracic operations for malignant ventricular arrhythmias. Three patients underwent endocardial resection (two died), and a fourth patient had implantation of an automatic defibrillator unit. Radiographic changes and results of pulmonary function testing are evaluated during initial toxicity and preoperatively. These four patients (mean amiodarone dosage of 420 mg/day for 20 months) are compared to 13 other patients undergoing cardiothoracic operations with prior amiodarone treatment (one patient with preoperative pulmonary toxicity) in whom life-threatening postoperative pulmonary complications did not develop (mean dosage of 550 mg/day for 10 months). Mean preoperative serum amiodarone levels for the four patients were 1.5 micrograms/ml. In the two patients who died, desethylamiodarone levels were 510 and 4,400 micrograms/gm in pulmonary tissue. Histologic examination showed "honeycomb" appearance of the lung with prominent septae, alveolar foamy macrophages, and hyperplasia of alveolar lining cells, consistent with amiodarone pulmonary toxicity. Causes including pump-oxygenator time, oxygen toxicity, anesthetic agents, congestive heart failure, and pulmonary infection superimposed on amiodarone pulmonary toxicity are discussed with a review of the literature.

Aged↗
PubMed1986

Detection of late potentials on the surface electrocardiogram in unexplained syncope.

To assess the usefulness of signal averaging of the surface electrocardiogram for detecting hitherto undocumented ventricular tachycardia (VT) in patients with unexplained syncope, 24 such patients were evaluated by electrocardiography and programmed ventricular stimulation. The surface electrocardiograms of 15 normal volunteers and 22 patients with documented sustained VT were also examined. No study subject had a bundle branch block or a QRS duration longer than 120 ms. Sustained VT was recorded in 9 of the 24 patients with syncope (8 patients with inducible VT and 1 with a spontaneous episode of recorded sustained VT). The signal-processed electrocardiogram contained late potentials and a filtered QRS duration longer than 120 ms in 8 of these 9 patients (89% sensitivity). None of the remaining 15 patients had these electrocardiographic abnormalities. Similar results were found in the patients with previously documented sustained VT (82% sensitivity) and in normal volunteers (no instances of abnormal recordings). In patients with unexplained syncope, signal processing of the surface electrocardiogram may be a sensitive and specific noninvasive test for detecting a high-risk subset of patients prone to lethal ventricular tachyarrhythmias.

Adult↗
PubMed1986

Hemodynamic influences on sinus node recovery time: effects of autonomic blockade.

Ten patients with normal sinus node function were evaluated prospectively, to determine whether the decrease in blood pressure during rapid atrial pacing shortens the corrected sinus node recovery time. All patients had 30 seconds of atrial pacing at cycle lengths from 600 to 300 ms, with continuous arterial pressure monitoring, before and after intravenous administration of propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg). In the control state, a decrease in corrected sinus node recovery time was recorded with faster atrial pacing rates, which was significantly related to the initial drop in systolic blood pressure at the onset of atrial pacing. Specifically, as the initial pressure drop increased from 15 mm Hg or less to 16 to 45 and 45 to 100 mm Hg, corrected sinus node recovery time decreased from 272 +/- 79 to 205 +/- 70 ms (p less than 0.04) and to 134 +/- 120 ms (p less than 0.04), respectively. In contrast, after autonomic blockade, the corrected sinus node recovery time was prolonged, in a near linear fashion, as atrial pacing rates increased. The magnitude of blood pressure drop with atrial pacing did not differ significantly from that in the control state at similar pacing rates. These findings suggest that hypotension during rapid atrial pacing activates autonomic reflexes that significantly shorten the corrected sinus node recovery time. Autonomic blockade negates this effect and the corrected sinus node recovery time prolongs with faster atrial pacing.

Adult↗
PubMed1986

Wide QRS tachycardia due to AV nodal reentry and a "bystander" bypass tract with slow conduction properties.

An unusual mechanism for recurrent, wide QRS complex supraventricular tachycardia is described in this report. A 25-year-old man with normal PR and QRS intervals during sinus rhythm was shown to have preexcitation with a left bundle branch block pattern during tachycardia and during atrial pacing. Electrophysiologic studies demonstrated slow and decremental conduction properties in an accessory "bystander" AV pathway utilized for antegrade conduction during AV nodal reciprocating tachycardia. The differential diagnosis of this tachycardia is discussed in detail.

Adult↗
PubMed1985

Electropharmacologic testing in sustained ventricular tachycardia associated with coronary heart disease: value of the response to intravenous procainamide in predicting the response to oral procainamide and oral quinidine treatment.

Twenty patients with inducible, sustained ventricular tachycardia (VT) were prospectively evaluated to determine whether the response to intravenous procainamide administration, as assessed by programmed ventricular stimulation, predicted the response to oral procainamide and oral quinidine treatment. Six patients (30%) responded to intravenous procainamide (fewer than 10 beats of inducible VT). Ten of 20 patients (50%) responded to oral quinidine and 5 (25%) responded to oral procainamide. Mean drug serum levels were 11.3 +/- 2.1 micrograms/ml for intravenous procainamide, 5.4 +/- 0.8 micrograms/ml for oral quinidine and 11.7 +/- 3.4 micrograms/ml for oral procainamide. There was no significant difference in serum levels between those who responded and those who did not. Fifteen patients (75%) had a concordant drug response for intravenous and oral procainamide. Ten patients (50%) had a concordant response for intravenous procainamide and oral quinidine. Fifteen patients (75%) had a concordant drug response for oral procainamide and oral quinidine. Thus, in patients with sustained VT, the response to intravenous procainamide does not reliably predict the response to oral quinidine or oral procainamide, and serial day drug testing with these agents is necessary. Furthermore, high-dose quinidine therapy may be more effective in controlling VT in these patients than procainamide.

Administration, Oral↗
PubMed1985

Rate-dependent effects of procainamide on His-Purkinje conduction in man.

Microelectrode studies in isolated cardiac tissues have shown that the depressant effect of several antiarrhythmic drugs on the maximal upstroke velocity of the cardiac action potential is rate-dependent. To determine whether this effect of antiarrhythmic drugs is seen in humans, 14 patients undergoing atrial pacing at several rates were prospectively studied before and after the infusion of procainamide (15 mg/kg). The HV interval (His-Purkinje conduction rate) and the QRS duration (intraventricular conduction rate) were measured. Before procainamide infusion, atrial pacing did not significantly prolong the maximal HV interval (from 54 +/- 15 to 58 +/- 13 ms). After procainamide infusion (mean serum level 10.0 +/- 3 micrograms/ml) atrial pacing at an average of 5 pacing rates significantly prolonged the HV interval (from 67 +/- 18 to 80 +/- 20 ms, p less than 0.001). The extent of HV prolongation with atrial pacing after procainamide infusion was independent of the HV interval at rest before procainamide. The duration of the QRS complex also tended to prolong with atrial pacing after procainamide infusion, but this prolongation was not statistically significant. Thus, procainamide produces a rate-dependent depressant effect on His-Purkinje and intraventricular conduction, confirming observations made in isolated tissue preparations.

Adult↗
PubMed1985

Mode of stimulation versus response: validation of a protocol for induction of ventricular tachycardia.

Electrophysiologic studies were prospectively performed in 91 consecutive patients referred for evaluation of sustained ventricular tachycardia or sudden cardiac death. Fifty-two patients had a history of sustained ventricular tachycardia and 39 patients had a history of sudden cardiac death. The identical stimulation protocol was used in all patients. The stepwise protocol involved atrial pacing, burst ventricular pacing, single, double, and triple extrastimuli during ventricular pacing. Stimulation was performed at the right ventricular apex at two and five times diastolic threshold. Using this protocol, ventricular tachycardia was inducible in 48 (92%) of the 52 patients with a history of sustained ventricular tachycardia and in 28 (72%) of 39 patients with a history of sudden cardiac death (p less than 0.02). The use of a third extrastimulus increased the yield of inducible ventricular tachycardia by 37% in patients with a history of sustained ventricular tachycardia and by 25% in patients with a history of sudden cardiac death. Stimulation at five times diastolic threshold and stimulation from the right ventricular outflow tract added a 15% increment in overall yield of inducible ventricular tachycardia in patients with a history of sustained ventricular tachycardia, and a 26% increment in yield in patients with a history of sudden cardiac death. Forty-four (92%) of the 48 inducible patients in the sustained ventricular tachycardia group had inducible monomorphic ventricular tachycardia as compared to 19 (68%) of 28 patients in the sudden cardiac death group (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

The yield of programmed ventricular stimulation in mitral valve prolapse patients with ventricular arrhythmias.

A high-risk subset of patients with mitral valve prolapse (MVP) and a predisposition to sudden cardiac death (SCD) has been proposed. We analyzed the results of programmed ventricular stimulation (PVS) in 20 patients with MVP and ventricular arrhythmias (ventricular premature depolarization in 6, ventricular couplets in 2, nonsustained ventricular tachycardia [VT] in 7, ventricular fibrillation [VF] in 5) and in 12 "normal" control subjects. With the use of an identical stimulation protocol from the right ventricular apex (twice diastolic threshold, three extrastimuli), 9 of 20 MVP patients and 1 of 12 normal subjects had inducible ventricular arrhythmias (p less than 0.05). When more aggressive attempts at ventricular stimulation were used, an additional five MVP patients had positive responses to PVS while no normal subjects did. In the MVP group, the following arrhythmias were induced: nonsustained polymorphic VT in 10, VF in three, and ventricular flutter in one. In all but two patients, triple ventricular extrastimuli were required to elicit this response. Two of the 10 MVP patients undergoing electropharmacologic testing had a successful antiarrhythmic regimen identified, while 13 patients were discharged on empiric antiarrhythmic therapy. At a follow-up of 19.8 +/- 13.1 months, all 19 MVP patients who could be contacted were alive. Five patients had symptomatic recurrences at follow-up including two SCD survivors (VT in one and VF in one). In conclusion, it was found that the majority of MVP patients with ventricular arrhythmias have inducible ventricular tachyarrhythmias during PVS and are more susceptible to this than patients without structural heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Closed chest catheter ablation of an accessory pathway in a patient with permanent junctional reciprocating tachycardia.

This report describes a 23 year old woman with a lifelong history of permanent junctional reciprocating tachycardia refractory to conventional antiarrhythmic medications who was successfully treated with closed chest, transvenous selective ablation of a posteroseptal bypass tract. Two 100 J (stored) direct-current shocks were delivered to the region of the os of the coronary sinus using a quadripolar catheter positioned in the coronary sinus. At a 2 month follow-up interval, the patient is asymptomatic without recurrence of the tachycardia. It is concluded that in patients with permanent junctional reciprocating tachycardia, selective catheter ablation of a posteroseptal accessory pathway is a feasible alternative to a difficult pharmacologic regimen or to ablative surgery.

Adult↗
PubMed1985

Sinus node electrogram in patients with the hypersensitive carotid sinus syndrome.

Sinus node electrograms were obtained in two patients with unexplained syncope and the cardioinhibitory form of the hypersensitive carotid sinus syndrome. Direct recordings of sinus node potentials were obtained using a transvenous electrode catheter. Sinus node function was normal in both patients during standard electrophysiologic evaluation. Carotid sinus massage was performed in both patients and the sinus node electrogram was continuously recorded. After the onset of carotid sinus massage, prolongation of sinoatrial time, slowing of sinus rate of depolarization, sinoatrial exit block and finally sinus node arrest were recorded. After termination of carotid sinus massage, sinus node potentials did not precede the first atrial impulse; subsequent beats showed markedly prolonged sinoatrial times as well as changes in the P wave on the surface electrocardiogram. Sinus rate and sinoatrial time returned to control values gradually, as did the P wave configuration. Intravenous atropine (1.0 mg) abolished the abnormal response to carotid sinus massage. It is concluded that the application of carotid sinus massage in patients with the hypersensitive carotid sinus syndrome produces profound changes in sinoatrial conduction including sinoatrial exit block, as well as shifts in primary pacemaker site and sinus node arrest. These alterations in conduction and automaticity are reversible with atropine and may be secondary to denervation sensitivity to acetylcholine.

Aged↗
PubMed1984

Effects of timolol and propranolol on inducible sustained ventricular tachyarrhythmias in dogs with subacute myocardial infarction.

Timolol and propranolol reduce the incidence of cardiac death after myocardial infarction (MI). To explore possible mechanisms of this reduction in mortality, the antiarrhythmic effects of these 2 beta blockers were compared in a dog model of inducible sustained ventricular tachycardia (VT) or fibrillation (VF) 4 to 6 days after experimental closed-chest MI. Dogs with inducible VT or VF underwent drug studies with timolol and propranolol; the sequence of drug administration was randomized. Timolol doses were 0.1, 0.3, and 1.0 mg/kg; propranolol doses were 1.0, 3.0 and 10.0 mg/kg. Timolol and propranolol were equally effective in abolishing inducible VT or VF: 77% of instances of inducible VT or VF responded to 1 or both beta blockers. The VF threshold was significantly elevated by both timolol and propranolol; the elevation in the VF threshold was significantly greater in "responders," i.e., dogs in whom VT was prevented by beta blockade (15 +/- 9 vs 8 +/- 9 mA, p less than 0.05). The ventricular effective refractory period was prolonged by both drugs; again, more so in the responders than in the nonresponders (16 +/- 9 vs 8 +/- 14 mA, p less than 0.05). The QTc interval was not significantly affected by either beta blocker. Among the responders, no difference was detected between timolol and propranolol in the extent to which the effective refractory period was prolonged or the VF threshold elevated. However, the highest dose of propranolol decreased the mean blood pressure significantly more than the comparable dose of timolol. In conclusion, timolol and propranolol are equally effective in abolishing inducible VT or VF in the dog after subacute MI.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗