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Biomedical subjects

W J Mandel

Publications and source records attributed to W J Mandel.

At least 73 records · Page 4Linked to original sources
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

Hemodynamic benefits of synchronized 1:1 atrial pacing during sustained ventricular tachycardia with severely depressed ventricular function in coronary heart disease.

The hemodynamic effects of atrial pacing were studied in 8 patients who had ventricular tachycardia (VT) during electrophysiologic testing. These patients had chronic recurrent VT associated with organic heart disease and depression of left ventricular function (ejection fraction = 0.23 to 0.35). Hemodynamic variables were recorded during sinus rhythm (58 to 103 beats/min), pacing-induced VT (133 to 214 beats/min) and synchronized 1:1 triggered atrial pacing (atrium paced, ventricle sensed and triggered mode) during VT. For the latter, the ventriculoatrial coupling interval was adjusted to produce a maximal blood pressure response; the optimal interval was observed to be between 60% and 73% of the RR interval. Mean arterial blood pressure decreased after the onset of VT (90 +/- 11 to 79 +/- 14 mm Hg, p less than 0.05) but increased again when atrial pacing was added, to 98 +/- 12 mm Hg. Cardiac index decreased during VT (2.2 +/- 0.5 to 1.8 +/- 0.5 liters/min/m2 p less than 0.05), but in each case improved by the addition of atrial pacing, to 1.9 +/- 0.5 liters/min/m2. Evidence from pressure recordings suggested that optimal atrial pacing resulted in atrial contraction in early left ventricular diastole. Thus, appropriately timed atrial pacing during VT can result in significant increases in blood pressure and a consistent increase in cardiac index. In addition to offering insight into the mechanisms of hemodynamic compromise during VT, the clinical use of this technique may be to improve hemodynamic values in patients with hemodynamically unstable VT.

Aged↗
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

Spontaneous ventricular tachycardia associated with isolated right ventricular infarction, one day after right coronary artery occlusion in the dog: studies on the site of origin and mechanism.

The electrophysiologic and arrhythmic properties of isolated infarcted right ventricle (RV) were studied in 17 dogs during the first 24 hours after complete occlusion of the right coronary artery (RCA). During the 16-to-20-hour post occlusion period, spontaneously occurring sustained monomorphic ventricular tachycardia (VT) was present in all 17 dogs. Overdrive ventricular pacing (cycle lengths 200 to 250 msec) caused significant suppression of the VT when the rate of the VT was slower than 150 bpm (range 120 to 145 bpm) (n = 9), but had negligible effect when VT rate was higher than 150 bpm (range 160 to 245 bpm (n = 8). Overdrive pacing could not terminate either the slow or the fast type of VT. Bipolar intramural electrograms have showed electrical activity in the infarcted RV zone to precede Q wave of the VT by 15.4 +/- 5.8 msec regardless of VT rate. Microelectrode studies on isolated RV endocardial infarcted tissues 24 hours after RCA occlusions have shown the presence of spontaneous repetitive activity at a rate of 87 +/- 47 bpm, which was overdrive suppressed in dogs with slow VT, and spontaneous activity at a rate of 115.2 +/- 36 bpm (p less than 0.05) which was not overdrive suppressed in dogs with fast VT. Maximum diastolic potential, action potential amplitude, and Vmax of surviving subendocardial Purkinje fibers (SEPF) in the infarct zone were slightly but significantly depressed (p less than 0.05), and they manifested enhanced phase 4 depolarization, giving rise to automatic impulse initiation. Although action potential duration of these fibers was somewhat prolonged (p less than 0.05), no conduction delay occurred. Histopathologic examinations have shown necrosis of the basal two thirds of the RV, with no left ventricular involvement. Electron microscopy revealed lipid accumulation in the surviving SEPF as the sole abnormality. We conclude (1) that occlusion of the RCA in the dog is associated with high survival rate despite extensive necrosis involving exclusively the RV and (2) that VT seen during the 20 to 24 hours after occlusion arise in the infarcted zone of the RV, by an enhanced automatic mechanism in the surviving SEPF, possibly caused by cytoplasmic lipid accumulation. This model, by virtue of its high survival rate and frequency of late VTs, should be useful in providing clues to determine factors involved in the genesis of early VT/VF and for the evaluation of new pharmacologic agents during the 20- to 24-hour VT period.

Animals↗
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↗
PubMed1985

Evaluation of amiodarone therapy in the treatment of drug-resistant cardiac arrhythmias: long term follow-up.

The clinical efficacy of amiodarone in the management of patients with complex cardiac arrhythmias refractory to therapy with two or more conventional or other investigational anti-arrhythmic agents was studied by long-term follow-up of patients who had received the drug for a period of at least three months. A total of 181 patients, classified into four groups (Group 1--supraventricular arrhythmias, n = 42; Group 2--frequent VPBs, n = 46; Group 3--nonsustained V-tach, n = 16; and Group 4--sustained V-tach, n = 77) received a daily maintenance dose of 200-800 mg of Amiodarone for a period of up to 30 months. There were a total of 26 deaths (14%). Ten of these were classified as probable arrhythmic deaths; however, all had either good or excellent response to therapy over a mean follow-up period of 14.9 months prior to death. The drug had to be permanently discontinued due to side effects only in three patients and in the majority of patients with side effects symptoms could be alleviated with adjustment of dosage, thyroid replacement therapy or transient cessation of therapy. We conclude that amiodarone is highly effective in the management of high-risk patients with complex refractory cardiac arrhythmias and that close monitoring and prompt recognition of side effects and appropriate adjustment of dosage or institution of supplemental or replacement therapy (in less than 5% of patients) will allow continuation of amiodarone. The benefit of suppression of symptomatic arrhythmias and the potential of prevention of sudden death, far outweighs the incidence of severe side effects.

Adolescent↗
PubMed1984

Electrophysiologic and hemodynamic effects of propafenone, a new antiarrhythmic agent, on the anesthetized, closed-chest dog: comparative study with lidocaine.

The relative hemodynamic and electrophysiologic effects of a new antiarrhythmic drug, propafenone, and lidocaine were evaluated in eight closed-chest, anesthetized dogs. Propafenone (4 mg/kg intravenously) significantly (p less than 0.05) lowered aortic and pulmonary systolic pressures and caused a rise in heart rate (p less than 0.05). Cardiac output decreased from 4.5 +/- 1 to 3.8 +/- 0.7 L/min (p less than 0.05) during atrial pacing at 400 msec cycle length. Propafenone had no effect on pulmonary and aortic diastolic pressures. Lidocaine (5 mg/kg intravenously) caused a significant (p less than 0.05) decrease in aortic systolic pressure and a rise in heart rate. Lidocaine had no significant effect on the other measured hemodynamic parameters. Propafenone, unlike lidocaine, significantly (p less than 0.05) increased atrioventricular nodal functional refractory period and right ventricular endocardial (apex) cathodal (0.5 +/- 0.1 mA to 1.9 +/- 0.3 mA) and bipolar (1.4 +/- 0.3 to 2.2 +/- 0.4 mA) diastolic excitability threshold. Propafenone, unlike lidocaine, also caused a significant (p = 0.05) intraatrial conduction delay; however, neither drug caused conduction slowing in the His-Purkinje system. Both drugs had no effect on sinus nodal recovery time and on the effective refractory period of the right ventricular endocardium (apex). Mean plasma propafenone levels during hemodynamic and electrophysiologic measurement ranged between 3.2 +/- 1.8 micrograms/ml and 1.7 +/- 1.1 micrograms/ml. All of the propafenone-induced effects were reversible within 90 minutes. We conclude that propafenone differs from lidocaine in its atrial, AV nodal, and ventricular electrophysiologic properties, and thus these may explain propafenone's greater efficacy over lidocaine against both certain atrial and ventricular arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1984

Verapamil effects in AV node reentry tachycardia with intermittent supra-Hisian AV block.

The electrophysiologic details of two patients with atrioventricular (AV) node reentry tachycardia with intermittent 2:1 supra-Hisian block are presented. Both patients had clear evidence for atrial arrhythmias as well, emphasizing the need for a careful diagnostic analysis. Evidence supporting a diagnosis of AV node reentry tachycardia included: (1) short ventriculoatrial (VA) coupling intervals, (2) normal retrograde sequence of atrial activation, (3) dependence on critical AV node conduction times for initiation of tachycardia by atrial pacing, (4) ability to pace and capture the atria or ventricles without interrupting the tachycardia, and (5) fixed VA coupling intervals despite changes in tachycardia cycle length. Ten milligrams of verapamil was administered during sustained supraventricular tachycardia with 1:1 AV conduction, but despite prompt termination of tachycardia in both cases, 2:1 AV block was not induced. Atrial echoes could still be induced after verapamil, and diagnostic features (3) and (5) were particularly evident after the drug. Further analysis confirmed that verapamil did not have any observable effects on the likely site for supra-Hisian block--that is, the "final common pathway" of the AV node. This would support a contention that verapamil may have a selective effect on tissues within the confines of the AV node.

Adult↗
PubMed1984

The relationship between ventricular arrhythmias and ischemia-induced conduction delay in closed-chest animals within 24 hours of myocardial infarction.

To investigate the myocardial conduction characteristics of premature impulses during the first 24 hours following coronary ligation and its relationship to late infarction ventricular arrhythmias, transmural electrodes were positioned in the normal and ischemic myocardium in nine dogs. Cardiac conduction in ischemic myocardium was delayed 15 minutes post coronary occlusion both in the epicardium and endocardium, both in the anterograde (base to apex) and retrograde (apex to base) direction, and was maintained at the same level throughout the experiment. Conduction across the border of ischemic myocardium from ischemic to the normal segment was also delayed, especially in the endocardium. Spontaneous ventricular arrhythmias recorded on Holter tapes showed significant increase in the number of premature ventricular complexes and ventricular tachyarrhythmias 9 hours after infarction. Thus our findings suggest that spontaneous arrhythmias occurring in the late phase of acute myocardial infarction (AMI) are independent of the ischemia-induced conduction delay and an alternate mechanism such as abnormal automaticity may be responsible for late ventricular arrhythmias.

Animals↗
PubMed1984

Prognosis after sudden cardiac death without associated myocardial infarction: one year follow-up of empiric therapy with amiodarone.

Thirty-three consecutively referred patients with cardiac arrest from ventricular arrhythmias unassociated with a new acute myocardial infarction (AMI) were commenced on amiodarone therapy and followed for a minimum of 12 months. The dose of amiodarone was adjusted to maximum tolerance and not according to the incidence of asymptomatic ventricular premature complex activity. Eight patients died including five sudden deaths. Five out of the eight deaths occurred either within 3 months of therapy or when the dose of amiodarone was less than 400 mg/day. The majority of patients were found to have corneal microdeposits or either thyroid or liver function abnormalities, although none had any clinical manifestation. Ten patients had neurologic side effects. In summary, although the overall cardiac mortality seemed to be reduced by amiodarone therapy and the drug appears to be well tolerated by patients, its role in the prophylaxis against recurrent ventricular fibrillation may be enhanced by a regimen of higher loading and maintenance doses.

Adult↗