Biomedical subjects
D Wu
Publications and source records attributed to D Wu.
Effects of oral verapamil in patients with atrioventricular reentrant tachycardia incorporating an accessory pathway.
In 14 patients with atrioventricular reentrant tachycardia incorporating an accessory pathway, electrophysiologic studies were performed before and serially at 0.5--1-hour intervals for 6 hours after the fourth dose of 80 mg of oral verapamil given every 6 hours. Verapamil increased both the longest atrial paced cycle length producing type 1 atrioventricular block and the effective refractory period of the atrioventricular conduction system at all measurements. Before verapamil, sustained tachycardia could be induced in all 14 patients. After verapamil, six patients had induction of echo beats alone at all measurements, and in eight patients nonsustained or sustained tachycardia could be induced, particularly after the fourth hour. Follow-up study with oral verapamil at the same dosage in 13 patients for 7 +/- 5 months (+/- SD) revealed that the six patients with induction of echo beats alone have been free of symptomatic arrhythmia, while six of the remaining eight patients had occasional attacks of sustained tachycardia. Thus, oral verapamil increases atrioventricular nodal refractoriness, with an effect lasting up to 6 hours. Electrophysiologic study performed 5-6 hours after verapamil can be used to predict clinical responses in patients with atrioventricular reentrant tachycardia.
Effects of acebutolol on paroxysmal atrioventricular reentrant tachycardia in patients with manifest or concealed accessory pathways.
Electrophysiologic studies before and after administration of 50 mg of intravenous (IV) acebutolol were performed in 20 patients. Four of the 20 had persistent preexcitation, two had intermittent preexcitation, and 14 had a concealed retrogradely conducting accessory pathway (AP). Acebutolol depressed anterograde AP conduction with loss of preexcitation in one patient and increased the effective refractory period of AP in the remaining three; in most, it depressed anterograde normal pathway conduction. The longest atrial paced cycle length producing atrioventricular (AV) nodal block increased from 290 +/- 7 to 39 +/- 6 msec (mean +/- SEM) after acebutolol (p less than 0.01). Acebutolol had no significant effect on retrograde AP conduction. Sustained AV reentrant tachycardia was inducible in all 20 patients before acebutolol and in 19 after acebutolol. The cycle length of tachycardia increased from 323 +/- 8 to 352 +/- 8 msec after acebutolol (p less than 0.01), reflecting an increment of A-H interval from 148 +/- 8 to 174 +/- 9 msec (p less than 0.01). Electrophysiologic studies were reported after 800 mg of oral acebutolol given in four divided doses at six-hour intervals in eight patients. The results were comparable to those of IV acebutolol. Thus, acebutolol depresses AV nodal conduction and slows the rate of AV reentrant tachycardia, but is generally ineffective in inhibiting the induction of sustained tachycardia. It occasionally depresses anterograde AP conduction.
[Investigation on Machado's reconstruction after pancreatoduodenectomy].
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Dual atrioventricular nodal pathways: a reappraisal.
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Effects of oral disopyramide phosphate on induction and sustenance of atrioventricular reentrant tachycardia incorporating retrograde accessory pathway conduction.
We performed electrophysiologic studies before and after oral administration of disopyramide phosphate, 200 mg every 6 hours, in 20 patients with atrioventricular (AV) reentrant tachycardia using a retrogradely conducting accessory pathway. Disopyramide markedly depressed retrograde accessory pathway conduction by increasing the mean ventricular paced cycle length that produced ventriculoatrial block (less than or equal to 287 +/- 4 to greater than or equal to 392 +/- 22 msec, p less than 0.01); it also depressed antegrade normal pathway AV conduction by increasing the atrial paced cycle length that produced AV block (287 +/- 9 to 328 +/- 7 msec, p less than 0.01). In 14 patients, tachycardia could not be induced or sustained after disopyramide phosphate. In 13 patients, this reflected depression of the retrograde limb with either absence of atrial echoes (nine patients) or induction of nonsustained tachycardia that terminated after the QRS complex (four patients), and in one, it reflected depression of the antegrade limb with induction of a single atrial echo not followed by a QRS response. In six patients, sustained tachycardia could still be induced after disopyramide. Oral disopyramide phosphate is effective in preventing induction of sustained AV reentrant tachycardia in most patients. This effect is achieved by depression of the retrograde limb of the reentrant circuit.
Digoxin, propranolol, and atrioventricular reentrant tachycardia in the Wolff-Parkinson-White syndrome.
In 22 patients with atrioventricular reentrant tachycardia incorporating a retrogradely conducting accessory pathway, electrophysiologic studies were done before and after oral digoxin, 1.25 mg, and propranolol, 160 to 240 mg, each given in 4 divided doses at 6-hour intervals. Before digoxin and propranolol, all 22 patients had induction of sustained tachycardia. After the medication six patients lost the ability to induce atrial echo and one lost the ability to sustain tachycardia due to an increased retrograde accessory pathway or atrial refractoriness or both. Six patients lost the ability to induce or sustain tachycardia due to increased atrioventricular nodal refractoriness. In the remaining nine patients with inducible sustained tachycardia, cycle lengths of tachycardia were prolonged. These findings suggest that combined use of oral digoxin and propranolol is useful in selected patients with atrioventricular reentrant tachycardia.
Percutaneous transluminal coronary angioplasty--a case report.
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Clinical observation and experimental study on 300 anorectic children treated with stomachic granules.
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The development of microwave power applications in China.
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[Acute renal failure following wasp stings ].
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Evaluation of an effective antiarrhythmic regimen using sequential electrophysiologic and exercise tests in a patient with post-infarction recurrent sustained ventricular tachycardia.
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Significance of bundle branch or fascicular block complicating acute myocardial infarction.
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Determinants of sustained slow pathway conduction and relation to reentrant tachycardia in patients with dual atrioventricular nodal transmission.
In 24 patients with dual atrioventricular (AV) nodal pathways, multiple incremental atrial pacing studies were performed to obtain atrial (A) to His (H) basic driven (A1 and H1) and extrastimulus (A2 and H2) intervals. Discontinuous A1-A2 and H1-H2 intervals were analyzed for relations between initial coupling times and subsequent A-H responses, and to examine curves of sequential paced cycle lengths (A-A intervals) versus A-H intervals. Seventeen patients showed sustained slow pathway (SP) conduction with demonstration of discontinuous A-A and A-H curves. Sustained SP conduction occurred at critical atrial paced rates when the first paced beat was blocked in the fast pathway (FP) with conduction via the SP. Eleven of these 17 patients had inducible sustained supraventricular tachycardia (SVT). A-H interval during SVT in these 11 patients was closely related to SP A-H interval during atrial pacing at the paced rate comparable to SVT rate (r = +0.89, p less than 0.001). The seven remaining patients showed continuous A-A and A-H curves. In three of these seven patients, sustained SVT was inducible, suggesting ability to sustain SP conduction. All of these three patients had continuous A1-A2 and H1-H2 curves during sinus rhythm so that the first atrial paced beat could not be blocked in the FP for subsequent SP conduction. In the other four of the remaining seven patients, despite block of the first atrial paced beat in the FP with SP conduction, the second paced beat was blocked in the SP so that all subsequent beats resumed FP conduction. In conclusion, sustained SP conduction in patients with dual AV nodal pathways requires (1) an initiating beat being blocked in the FP, (2) a critical rate cycle length, and (3) the ability of SP for repetitive conduction at critical rates.
Effects of quinidine on atrioventricular nodal reentrant paroxysmal tachycardia.
Electrophysiologic studies were performed in 14 patients with atrioventricular nodal reentrant paroxysmal tachycardia (PSVT) before and after oral administration of 1.2-1.6 g quinidine sulfate over a 24-hour period (0.3-0.4 g every 6 hours). Studies were performed after 0.5-1 mg i.v. atropine before and after quinidine. All 14 patients had induction of sustained PSVT before quinidine, with or without atropine. After quinidine, 11 patients lost the ability to induce echoes or sustain PSVT, reflecting depression of the retrograde pathway with either absence of atrial echoes (six patients) or induction of nonsustained PSVT, with termination of echoes or PSVT occurring after QRS (block in retrograde pathway) (five patients). In only one of these 11 patients was sustained PSVT inducible after addition of atropine. All 11 were discharged on the same dose of quinidine. In three patients, quinidine was discontinued because of side effects. Follow-up in the remaining eight patients for 8 +/- 2 months showed no recurrence of sustained PSVT. Three of the 14 patients had induction of sustained PSVT after quinidine. Ventricular paced cycle length producing ventriculoatrial block was 314 +/- 7 msec (mean +/- SEM) before and 392 +/- 13 msec after quinidine (p less than 0.01) in the 14 patients, suggesting depression of the retrograde pathway with quinidine. In summary, quinidine inhibited induction of sustained atrioventricular nodal reentrant tachycardia with depression of the retrograde pathway. It is very effective in preventing recurrence of PSVT in most patients.
Exercise-triggered paroxysmal ventricular tachycardia. A repetitive rhythmic activity possibly related to afterdepolarization.
Electrophysiologic study, isoproterenol infusion, and serial treadmill exercise tests before and after administration of propranolol, verapamil, lidocaine, and procainamide were done in three patients with exercise-triggered ventricular tachycardia. In all three patients, organic heart diseases were absent. Ventricular tachycardia was reproducibly provoked with exercise and with isoproterenol infusion. Propranolol (tested in three patients) and lidocaine (tested in two patients) effectively prevented exercise provocation of tachycardia. Verapamil terminated tachycardia in all three patient and successfully prevented exercise provocation of tachycardia in only two patients. Procainamide was ineffective in one patient and was partially effective in two patients. In the latter two patients, ventricular ectopies, couplets, and short salvos remained provocable with exercise. Electrical stimulations with incremental ventricular pacing and ventricular extrastimulus testing failed to induce tachycardia in all three patients. These findings strongly suggest that repetitive rhythmic activities related to the catecholamine-sensitive afterdepolarizations are probably responsible for the exercise-triggered ventricular tachycardia.