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Biomedical subjects

W M Miles

Publications and source records attributed to W M Miles.

At least 55 records · Page 3Linked to original sources
PubMed1987

Supernormal conduction in accessory atrioventricular connections.

Prospective electrophysiologic evaluation of 74 patients with ventricular preexcitation revealed 4 patients who had supernormal anterograde conduction over an accessory atrioventricular pathway. In each patient, anterograde conduction over the accessory pathway was present at relatively slow sinus rates, but the accessory pathway anterograde effective refractory period was substantially prolonged. During premature atrial stimulation, a "window" of supernormal conduction was identified at which closely coupled atrial extrastimuli conducted over the accessory pathway, whereas longer premature intervals resulted in accessory pathway block. Causes other than supernormal conduction to explain this phenomenon, for example, phase 4 block, were unlikely in each case. Although the mechanism of supernormal conduction in humans is unknown, the electrophysiologic findings in our patients are similar to those reported in patients with supernormal conduction in the His-Purkinje system.

Adult↗
PubMed1987

Electrophysiologic and antiarrhythmic effects of oral encainide in patients with atrioventricular nodal reentry or nodoventricular reentry.

Three patients with drug-resistant atrioventricular (AV) nodal reentrant tachycardia and two patients with reciprocating tachycardia associated with nodoventricular pathways received oral encainide after a control drug-free electrophysiologic study. In one patient with AV nodal reentry, encainide prolonged anterograde AV nodal conduction, produced complete ventriculoatrial (VA) block, and prevented tachycardia induction. Encainide had no effect on AV or VA conduction in the second patient with AV nodal reentry, and tachycardia with similar cycle length was still induced. The third patient was not studied while receiving encainide, but spontaneous AV nodal reentrant tachycardia occurring multiple times daily was abolished. In both patients with nodoventricular pathways, anterograde AV nodal and VA conduction were prolonged by encainide and tachycardia was no longer inducible. Two patients with AV nodal reentry were given long-term encainide therapy and have been free of recurrent arrhythmias for 16 and 30 months. One patient with a nodoventricular pathway has been without arrhythmia recurrence after 73 months of encainide therapy; the other patient required addition of propranolol to encainide because of recurrent tachycardia. We conclude that encainide can prolong anterograde AV nodal and VA conduction and prevent induced and spontaneous tachycardia in some patients with drug-resistant and highly symptomatic AV nodal or nodoventricular reentry.

Administration, Oral↗
PubMed1987

Pharmacokinetic and electrophysiologic interactions of amiodarone and procainamide.

The effects of amiodarone on the pharmacokinetic and electrophysiologic properties of procainamide were examined in eight patients treated for recurrent ventricular arrhythmias who received intravenous procainamide, 6 to 15 mg/kg, at control and after 1 to 2 weeks of oral amiodarone treatment. Compared with control, procainamide plasma clearance decreased from 0.43 +/- 0.12 L/kg-hr to 0.33 +/- 0.12 L/kg-hr (P less than 0.01), plasma elimination half-life increased from 3.77 +/- 0.64 hours to 5.21 +/- 0.42 hours (P less than 0.01), and volume of distribution was unchanged from 2.31 +/- 0.74 L/kg to 2.47 +/- 0.90 L/kg during amiodarone treatment. As single agents, intravenous procainamide and oral amiodarone produced equivalent increases in QRS duration, rate-corrected QT interval, right ventricular effective refractory period, and cycle length of induced ventricular tachycardia. After the addition of intravenous procainamide to amiodarone the QRS duration, rate-corrected QT interval, and, in six of eight patients, ventricular tachycardia cycle length were significantly increased compared with control or either drug alone, suggesting additive electrophysiologic effect. However, acceleration of induced ventricular tachycardia occurred in one patient with combined treatment, suggesting a potential for adverse electrophysiologic interactions. These findings indicate that amiodarone has pharmacokinetic and electrophysiologic interactions with procainamide and suggest that the intravenous dose of procainamide be reduced by 20% to 30% during concurrent drug administration.

Aged↗
PubMed1986

Encainide for treatment of supraventricular tachycardias associated with the Wolff-Parkinson-White syndrome.

Thirty-three patients with supraventricular tachycardia associated with the Wolff-Parkinson-White syndrome were treated with encainide for 26 months (mean). Encainide at a mean dosage of 187 mg/day abolished or markedly decreased episodes of palpitations in 24 of 33 (73%), and no patient had syncope or required cardioversion while receiving the drug. Encainide was well tolerated and was discontinued in only 2 patients because of side effects (6%). Only 1 patient (3%) had a proarrhythmic effect while taking encainide (ventricular tachycardia). Fourteen of 16 patients (88%) with atrial fibrillation continue receiving encainide. Episodes of palpitations have been abolished or markedly decreased and no patient has had syncope or required cardioversion. All 14 of these patients had either anterograde block in the accessory pathway during atrial fibrillation or greater than or equal to 75 ms increase in the shortest R to R interval formed by 2 preexcited QRS complexes. Encainide prolonged refractory periods of the atrial (p = 0.064) and ventricular (p = 0.061) muscle. It prolonged the cycle length at which 1:1 conduction of the accessory pathway in both the anterograde and retrograde directions occurred (both, p less than 0.001). Induction of atrioventricular-reciprocating tachycardia (AVRT) was prevented in 36% of patients at repeat electrophysiologic study. The AVRT cycle length increased 112 ms (mean, p less than 0.001) in those patients in whom AVRT was still inducible. The loss of delta waves recorded with the 12-lead scalar electrocardiogram during encainide therapy was a significant predictor of anterograde accessory pathway block (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Subthreshold conditioning stimuli prolong human ventricular refractoriness.

This study tested whether a subthreshold stimulus (Sc) inserted before a premature stimulus prolonged the right ventricular effective refractory period in humans, and whether the degree of effective refractory period lengthening was influenced by heart rate, Sc current intensity or Sc pulse duration. Sc at current intensity 10 mA and pulse width 2 ms prolonged mean effective refractory period from 255 ms to 277 ms (p less than 0.001, n = 20). The increase in effective refractory period was similar in 6 patients studied at pacing cycle lengths 600 (259 to 289 ms) and 400 ms (236 to 258 ms). When Sc current intensities were varied at 2, 5 or 10 mA at a constant pulse duration of 100 ms the effective refractory period progressively prolonged by 6, 40 and 81 ms respectively (p less than 0.02, n = 6). The pulse duration of Sc at a constant current of 10 mA significantly influenced effective refractory period prolongation. With Sc pulse durations of 2, 10, and 100 ms the effective refractory period prolonged by 16, 33 and 66 ms respectively (p less than 0.01, n = 7). Thus, subthreshold impulses prolong the effective refractory period in human right ventricular myocardium. The prolongation of effective refractory period depended on Sc current intensity and pulse duration but was independent of heart rate at the cycle lengths tested. The use of subthreshold stimuli as antiarrhythmic therapy may be feasible in some patients.

Adult↗
PubMed1986

Survivors of cardiac arrest: prevention of recurrence by drug therapy as predicted by electrophysiologic testing or electrocardiographic monitoring.

Sixty-two patients (44 men and 18 women, aged 15 to 75 years) resuscitated from at least 1 cardiac arrest unrelated to acute myocardial infarction were studied. No patient was taking antiarrhythmic drugs at the time of the initial cardiac arrest. Thirty-five patients had coronary artery disease (CAD) and 27 did not. Before drug therapy, control electrophysiologic studies induced ventricular tachycardia (VT) in 43 of 58 patients (74%) (30 of 35 with CAD and 17 of 27 without CAD). At control continuous electrocardiographic monitoring for 48 hours or longer, only 19 of 62 patients (31%) had spontaneous VT, 5 of whom had no VT induced at control electrophysiologic study. Mean follow-up was 22 months. Fourteen of 41 patients, 8 of 25 with and 6 of 16 without CAD, had VT suppressed with drugs during serial electrophysiologic testing, and none had a recurrent arrhythmic event. VT was suppressed in 12 of 14 patients receiving conventional drugs. Of 27 patients with VT induced during all drug studies, 6 died from cardiac arrest and 4 had recurrent VT. Drug efficacy in 20 patients was guided by continuous electrocardiographic monitoring, and 4 of 9 patients in whom VT and ventricular pairs were suppressed by drug therapy, as documented by continuous electrocardiographic monitoring for 48 hours or longer, died of cardiac arrest. Overall, 26 patients were discharged receiving amiodarone therapy, and 5 died of cardiac arrest and 3 had recurrent sustained VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Determination of the earliest site of ventricular activation in Wolff-Parkinson-White syndrome: application of digital continuous loop two-dimensional echocardiography.

Surgical and transcatheter ablation of accessory atrioventricular (AV) connections (Wolff-Parkinson-White syndrome) requires accurate localization of the accessory pathway. In a canine model of endocardial pacing, a continuous loop two-dimensional echocardiographic technique was developed for determining the earliest site of ventricular activation. This technique was then used to localize accessory AV connections in patients. Echocardiographic images were acquired on videotape and converted to a digital continuous loop format, from which the earliest site of systolic motion was determined. In six dogs, using six distinct endocardial sites, two blinded observers accurately identified the earliest site of ventricular activation in 31 (86%) of 36 and 32 (89%) of 36 locations. Determination of the earliest site of ventricular activation with the continuous loop digital technique was superior to standard analog analysis in overall accuracy (p less than 0.02) and in intraobserver variability (p less than 0.004). After validation of this technique, 21 patients with 22 accessory AV connections with anterograde conduction were studied. The earliest site of mechanical activity was determined during sinus (10 patients) or atrial paced (11 patients) rhythms by two blinded observers and compared with electrophysiologic mapping and surface electrocardiograms. Digitally processed echocardiograms correctly localized the earliest site of ventricular activation in 18 of 22 connections and predicted an adjacent location in the remaining 4.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Alteration of human right bundle branch refractoriness by changes in duration of the atrial drive train.

We studied the effect of drive train duration on human right bundle branch refractoriness. Seven patients with a QRS duration of 0.10 sec or less and no preexcitation had functional right bundle branch block induced reproducibly with premature atrial stimulation. Refractoriness of the right bundle branch was defined as the longest H1H2 interval resulting in right bundle branch block and was determined in each patient at a constant pacing cycle length but at five to seven different atrial drive train durations varying from four to 99 complexes. In all seven patients, right bundle branch refractoriness decreased with increasing drive train duration (mean 15 msec). One-third of this decrease (5.0 msec) occurred between drive train durations of four and eight complexes, and close to two-thirds (9.3 msec) occurred between drive train durations of eight and 64 complexes. Very little further decrease (0.7 msec) occurred between 64 and 99 complexes. We conclude that right bundle branch refractoriness shortens progressively as the preceding drive train duration increases. This phenomenon may in part explain the disappearance of functional right bundle branch block during supraventricular tachycardia after a variable number of complexes without a change in cycle length of tachycardia.

Adult↗
PubMed1986

The preexcitation index: an aid in determining the mechanism of supraventricular tachycardia and localizing accessory pathways.

In this study we sought to determine whether characteristics of ventricular-induced atrial preexcitation during reciprocating tachycardia could help differentiate atrioventricular (AV) nodal reentry from orthodromic AV reentry using an accessory pathway and to identify the site of accessory pathways in patients with Wolff-Parkinson-White syndrome. Fifty-five patients with orthodromic AV reciprocating tachycardia and 22 patients with AV nodal reentrant tachycardia were studied with standard electrophysiologic techniques. There were 24 left free wall, 23 posterior septal, seven anterior septal, and one right free wall accessory pathways. Progressively premature right ventricular complexes (V2) were introduced during reciprocating tachycardia (V1V1). The V1V1 interval during tachycardia minus the longest V1V2 at which atrial preexcitation occurred defined a preexcitation index (PI). Atrial preexcitation occurred in 49 of 55 (89%) patients with AV reentry compared with only three of 22 (14%) patients with AV nodal reentry (p less than .001). In the three patients with AV nodal reentry who demonstrated atrial preexcitation, the PI was distinct from that of the septal pathways and was in the upper range of values for left free wall pathways. The percentage of tachycardias demonstrating atrial preexcitation was not different between the free wall and septal pathways, but His bundle activation was visible at the time of atrial preexcitation in only six of 17 (35%) left free wall compared with 13 of 16 (81%) posterior septal and seven of seven (100%) anterior septal pathways (p less than .05 free wall vs posterior or anterior septal).(ABSTRACT TRUNCATED AT 250 WORDS)

Atrioventricular Node↗
PubMed1986

The implantable transvenous cardioverter: long-term efficacy and reproducible induction of ventricular tachycardia.

We followed 11 patients for 5 to 27 months (mean 14.9) after implantation of a permanent transvenous low-energy synchronized cardioverter to evaluate both long-term reproducibility of ventricular tachycardia (VT) induction via noninvasive programmed electrical stimulation with the cardioverter and efficacy of cardioversion. Induction and termination of VT were attempted at implantation and approximately every 3 months thereafter. All patients had coronary artery disease and were receiving antiarrhythmic drug therapy (amiodarone in eight). VT cycle length, morphology, and mode of induction were reproducible on multiple occasions in nine patients; clinical VT was induced inconsistently in two patients. Multiple VT episodes in five patients had one morphology, whereas two morphologies occurred in six patients. Synchronization of the shock within the QRS complex and right ventricular effective refractory periods determined via the cardioverter remained constant over the follow-up period. VT was terminated on every occasion in nine patients and on eight of nine occasions in one patient. Tachycardia was accelerated on three of five occasions in one patient. Consistently effective cardioversion energy (0.2 to 2.0 J) increased modestly in four patients. We conclude that patients with inducible monomorphic VT usually have sustained VT with similar characteristics inducible over a period of time and cardioversion and sensing functions of the cardioverter remain relatively stable over time.

Aged↗
PubMed1986

Supraventricular tachycardia in patients without overt preexcitation.

In this article, the authors discuss the features and differential diagnosis of supraventricular tachycardia with a regular ventricular rate that occurs in patients without overt preexcitation during sinus rhythm. In the authors' experience, the two most common mechanisms of these tachycardias are reentry within the atrioventricular node (AV nodal reentry) and atrioventricular reentry using a concealed accessory pathway for retrograde conduction and the AV node/His-Purkinje system for antegrade conduction (AV reentry). Sinus nodal reentry, intra-atrial reentry, automatic atrial tachycardia, and nonparoxysmal junctional tachycardia account for the remaining episodes of regular supraventricular tachycardia. Therapy for AV and AV nodal reentry is also discussed.

Diagnosis, Differential↗
PubMed1985

Amiodarone treatment in patients with ventricular arrhythmias.

Amiodarone has been used in the therapy of supraventricular and ventricular tachycardia, and has often been categorised as a class III rather than a class I agent. However, in patients with ventricular arrhythmias, amiodarone 800mg daily for 14 days prolonged the right ventricular effective refractory period by a mean of 18.8 msec (p less than 0.05), and HV interval by a mean of 5.2 msec (p less than 0.05), these changes being similar to those noted with drugs such as quinidine, procainamide, disopyramide and encainide. The antiarrhythmic efficacy of amiodarone was evaluated in 196 patients with recurrent sustained ventricular tachycardia, recurrent ventricular fibrillation or recurrent nonsustained ventricular tachycardia. Coronary artery disease, dilated (congestive) cardiomyopathy, or other forms of heart disease were present in most patients. After 1 month of therapy, 177 patients continued to receive amiodarone and, during the remainder of the follow-up period, 139 patients had no recurrence of spontaneous ventricular tachycardia or ventricular fibrillation. Sudden cardiac death occurred in 15 patients after a mean treatment period of 10.4 months. Overall, amiodarone was an effective form of therapy in patients with ventricular tachycardia and ventricular fibrillation.

Adolescent↗
PubMed1984

Antiarrhythmic and electrophysiologic effects of oral propafenone.

Twenty-six patients had ventricular tachycardia initiated at control electrophysiologic study and had a repeat study during oral propafenone therapy. Ten patients had had sustained ventricular tachycardia, 6 cardiac arrest and 10 symptomatic, nonsustained ventricular tachycardia. Twenty-two patients had heart disease, 18 of whom had coronary artery disease. During propafenone therapy, ventricular tachycardia could not be initiated during programmed ventricular stimulation in 5 patients, and in 21 patients the cycle length of induced ventricular tachycardia increased from 246 +/- 42 ms at control to 355 +/- 96 ms (p less than 0.001). Seventeen patients were discharged with propafenone therapy and have been followed for a mean of 11 months. No symptomatic ventricular tachycardia recurred in the 5 patients without inducible ventricular tachycardia during drug treatment. Six of 12 patients with inducible ventricular tachycardia during the drug study have remained asymptomatic. In conclusion, propafenone substantially prolongs the cycle length of ventricular tachycardia, and initiation of ventricular tachycardia by programmed ventricular stimulation at drug study does not preclude a favorable clinical outcome.

Adult↗