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Biomedical subjects

W N Brodine

Publications and source records attributed to W N Brodine.

6 recordsLinked to original sources
PubMed1992

Slowing of ventricular tachycardia as a possible endpoint for serial drug testing at electrophysiological study.

Certain patients who cannot be rendered noninducible by serial drug testing during electrophysiology study demonstrate significant slowing of their ventricular tachycardia rate with selected agents. We evaluated the characteristics and outcome of 19 such patients to assess whether this slowing could be considered an acceptable endpoint for treatment. This group consisted of 14 males and 5 females (mean age 63 +/- 9) with a mean ejection fraction of 28 +/- 13% and inducible sustained ventricular tachycardia. Sixteen patients had known coronary artery disease and 13 had prior myocardial infarction. The other three patients had idiopathic cardiomyopathy. Serial drug testing during an electrophysiology protocol that used up to three extrastimuli at two or three cycle lengths at two right ventricular sites was used to select a medication regimen that provided optimal ventricular tachycardia slowing without limiting side effects. Five patients were treated with amiodarone, three with Ic agents (all with ejection fraction greater than 30%), and the remainder with Ia and Ib agents alone or in combination. Mean initial ventricular tachycardia rate was 219 +/- 26 beats/min with posttreatment ventricular tachycardia rate 137 +/- 17 (mean initial cycle length 278 +/- 35 msec, posttreatment 443 +/- 53 msec). Two groups were identified, those who had recurrent (although well-tolerated) ventricular tachycardia (group I, n = 8, mean time to recurrence = 15 months), and those who did not (group II, n = 11, mean follow-up 22 months). Overall sudden death rate was 5%, while total mortality was 11% (all mortality in group I).(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone↗
PubMed1990

Simultaneous, multiple point mapping during surgery for Wolff-Parkinson-White syndrome without the use of a computer.

Epicardial mapping of patients undergoing surgical correction of the Wolff-Parkinson-White syndrome is usually accomplished by using a single point probe. This somewhat tedious and time consuming method has been streamlined by computer-based systems allowing multiple simultaneous point maps to be developed either by electrodes applied as a band around the atrioventricular groove or a sock over the ventricle. Because the computer technology required to access, analyze, and display this data is not widely available, a system was devised to display ten simultaneous electrograms from a wrap of ten electrodes placed about the atrial or ventricular side of the atrioventricular groove. Using this technique three patients undergoing surgery for accessory pathway removal were accurately and quickly mapped allowing surgical cure of the preexcitation in each case.

Electrocardiography↗
PubMed1983

Dual atrioventricular nodal pathways associated with a gap phenomenon in atrioventricular nodal conduction.

A 67 year old man underwent electrophysiologic study for evaluation of syncope. During atrial pacing at a basic cycle length of 600 ms, atrial premature stimuli were introduced at progressively shorter coupling intervals. The graph of atrial coupling intervals versus corresponding His bundle responses revealed an abrupt increase in atrioventricular (AV) nodal conduction time with coupling intervals from 320 to 340 ms. In an atrial coupling interval of less than 320 ms, conduction was again rapid until the effective refractory period of the atrium was reached. These unique findings are compatible with dual pathways and a gap phenomenon within the AV node.

Aged↗
PubMedDate not supplied

Serial electrophysiologic effects of bretylium in man and their correlation with plasma concentrations.

The serial electrophysiologic effects of bretylium were studied in 10 patients undergoing cardiac catheterization before giving the drug, at the end of bretylium tosylate-loading infusion (5 mg/kg/15 min), and after 1 h of intravenous drug maintenance (1.5 mg/min). Mean blood pressure increased during drug loading from 93.6 +/- 10.9 mm Hg to 121.1 +/- 16.2 mm Hg (p less than 0.01, t = 15 min) but returned toward control (100.9 +/- 18.7 mm Hg, p = NS) during drug maintenance (t = 75 min). Small changes in PR, QRS, QTc, AH, and HV intervals during spontaneous and paced rhythms were not significant. Comparison of the control electrophysiologic study with early and late postdrug studies showed no significant changes in corrected sinus node recovery times and in Wenckebach cycle lengths, but small decreases in refractory periods occurred. After drug loading, decreases in mean effective refractory periods of atrium, AV node, and right ventricle of 12, 2, and 16 ms, respectively, occurred (p = NS); during drug maintenance (t = 75 min), these refractory periods had decreased with respect to control by 21, 36, and 13 ms, respectively (p less than 0.05, 0.05, and 0.01). Functional refractory period of the AV node decreased at 75 min by 31 ms (p less than 0.01). The observed shortening of refractory periods contrasts with the direct effects of bretylium in isolated ventricular muscle and Purkinje fibers, which consist of prolongation of effective refractory periods and action potential duration. Thus, indirect (adrenergic) effects may be more important to overall clinical electrophysiologic actions not only acutely during loading but also during at least the first 60-90 min of maintenance therapy, which spans the expected time of initial clinical antifibrillatory response.

Adult↗