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Biomedical subjects

D Wu

Publications and source records attributed to D Wu.

At least 577 records · Page 32Linked to original sources
PubMed1985

Frequency and significance of induced sustained ventricular tachycardia or fibrillation two weeks after acute myocardial infarction.

Electrophysiologic study, 24-hour ambulatory electrocardiographic monitoring, treadmill exercise test and angiographic evaluations were performed in 45 patients 14 +/- 3 days (mean +/- standard deviation) after acute myocardial infarction. Electrophysiologic study protocol included burst ventricular pacing and 1 to 3 ventricular extrastimuli at 2 cycle lengths from right ventricular apex, right ventricular outflow and left ventricle. Sustained monomorphic ventricular tachycardia (VT) (13 patients) or ventricular fibrillation (VF) (7 patients) was induced in 20 patients (44%) (group I). In these 20 patients, VT/VF was inducible with 2 extrastimuli in 10 patients, 3 extrastimuli in 9 patients and burst pacing in 1 patient. In the remaining 25 patients (56%), induction of no fewer than 7 ventricular beats were noted (group II). Severe left ventricular (LV) wall motion abnormalities occurred in 70% of group I patients and 22% of group II patients (p less than 0.005). There was no difference in the site of infarction, frequency and grade of ventricular ectopic rhythm on ambulatory electrocardiographic monitoring, double product on submaximal exercise, LV ejection fraction, and number of obstructed coronary arteries (70% or greater) (p greater than 0.1) between group I and group II patients. During a mean follow-up of 10 +/- 3 months, 1 patient in each group died suddenly, and in 1 group I patient spontaneous sustained VT developed which was identical in morphologic configuration to that induced during electrophysiologic study. In conclusion, electrical induction of sustained VT or VF during electrophysiologic study is common in patients 2 weeks after acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Inflammatory response induced by intrapleural injection of antiserum to IgE in rat. An evaluation of the role of histamine.

Intrapleural injection of antiserum to rat IgE (anti-IgE) into rats resulted in release of histamine from mast cells and rapid effusion of fluid and plasma proteins into the pleural cavity. By 4 hr this was followed by infiltration of neutrophils. These responses were dependent on the amount of anti-IgE injected, and maximal responses were greater than those obtained with compound 48/80. The effusion of fluid and protein, but not the infiltration of cells, was partially suppressed by prior treatment with the H1 histamine receptor antagonist mepyramine (5 mg/kg, s.c.) or the H2 antagonist metiamide (100 mg/kg, s.c.) and was almost totally suppressed (85-88%) when both drugs were administered simultaneously. Neither methysergide (1 and 4 mg/kg, s.c.) nor indomethacin (5 and 10 mg/kg, i.v.) had an effect on the responses to anti-IgE. Although it seemed likely that histamine was a primary mediator of increased vascular permeability, the intrapleural injection of histamine agonists or histamine in large amounts (50 micrograms) provoked a much less intense response than did anti-IgE. The effects of injected histamine may not, therefore, mimic those induced by histamine released from mast cells in situ. The intrapleural injection of histamine releasers such as anti-IgE may serve as a useful model to test the therapeutic efficacy of antihistamine drugs. The present results also confirm previous reports that localized neutrophil infiltration occurs after mast cell degranulation.

Animals↗
PubMed1985

Determinants of simultaneous fast and slow pathway conduction in patients with dual atrioventricular nodal pathways.

Double His bundle and ventricular responses to a single atrial impulse caused by a simultaneous fast and slow pathway conduction was observed during electrophysiologic study in three patients with dual-pathway atrioventricular nodal reentrant paroxysmal supraventricular tachycardia. In patient No. 1 this phenomenon occurred during rapid atrial pacing, in patient No. 2 during both rapid atrial pacing and delivery of a single atrial extrastimulus, and in patient No. 3 during delivery of double atrial extrastimuli. Retrograde unidirectional block in the slow pathway was suggested by retrograde induction of tachycardia at a long ventricular paced cycle length and/or long ventricular coupling interval in all three patients. Our findings suggest that major determinants of this phenomenon include: a sufficient conduction delay in the slow pathway so that the distal tissue is able to respond for the second time, and a retrograde unidirectional block in the slow pathway so that the fast pathway impulse will not enter and collide with the oncoming slow pathway impulse.

Atrioventricular Node↗
PubMed1985

Preparative isolation of peroxisomes from liver and kidney using metrizamide density gradient centrifugation in a vertical rotor.

A method for the preparative isolation of peroxisomes from the livers of rat, guinea pig, and mouse, and also from rat kidney is described. The light mitochondrial fraction, i.e., particles sedimenting between 33,000 and 250,000g-min, or the postnuclear supernatant of liver or kidney, is subjected to a 20-50% Metrizamide density gradient ultracentrifugation in a vertical rotor. After centrifugation, the peroxisomes (marker enzyme catalase and dihydroxyacetone phosphate acyltransferase) sedimented as a band near the bottom of the tube (rho = 1.22 g/ml). From the distribution of different marker enzymes and also from the morphometric examinations, it was demonstrated that the isolated peroxisomes are not contaminated with lysosomes, mitochondria, or microsomes.

Animals↗
PubMed1985

Double atrial responses to a single ventricular impulse due to simultaneous conduction via two retrograde pathways.

Electrophysiologic studies were performed in two patients. In one patient (Case 1) with ventricular pre-excitation and paroxysmal supraventricular tachycardia, studies after diltiazem administration showed two QRS responses to a single atrial stimulus during atrial pacing at a cycle length of 300 ms. The first QRS response with full pre-excitation and short PR interval was consistent with accessory pathway conduction, while the second QRS response with a normal duration and an atrio-His bundle interval of 350 ms was consistent with normal pathway conduction. The second QRS response was followed by initiation of supraventricular tachycardia. Studies after verapamil administration on a separate day disclosed two atrial responses to a single QRS complex during ventricular pacing at cycle lengths between 330 and 280 ms, suggesting simultaneous retrograde accessory and normal pathway conduction. In Case 2 with a supraventricular tachycardia using a fast atrioventricular nodal pathway for anterograde and a slow ventriculoatrial pathway for retrograde conduction, two atrial responses to a single QRS complex were observed during ventricular pacing at cycle lengths between 500 and 400 ms. The first atrial response showed a stimulus to atrial interval of 120 ms and an atrial activation sequence with the low septal right atrium being earlier than other atrial sites, suggesting retrograde fast pathway conduction. The second atrial response showed a stimulus to atrial interval of 505 ms and an atrial activation sequence with low septal right atrium being simultaneous with the proximal coronary sinus, suggesting retrograde slow pathway conduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Pseudosimultaneous fast and slow pathway conduction: a common electrophysiologic finding in patients with dual atrioventricular nodal pathways.

Two ventricular responses following termination of rapid atrial pacing were noted in 24 of 87 patients with dual atrioventricular (AV) nodal pathways and supraventricular tachycardia. In all 24 patients, the AH intervals of the first and second ventricular responses were comparable with those of the fast and slow pathways, respectively. Careful analysis of the whole pacing sequence revealed that, in 21 patients, this phenomenon resulted from sustained slow pathway conduction with long AH intervals. In these patients, as the AH interval of each paced beat was progressively lengthened during pacing, the corresponding His bundle and ventricular responses were pushed one cycle behind the current atrial paced beat, so that the last paced beat was followed by two His bundle and ventricular responses. In only three patients did double ventricular responses result from simultaneous fast and slow pathway conduction. One of these three patients also showed two ventricular responses resulting from sustained slow pathway conduction. Several factors predispose to the occurrence of this phenomenon in patients with dual AV nodal pathways. These include an ability to sustain slow pathway conduction, a longer slow pathway AH interval, a shorter sinus AH interval (fast pathway) and a shorter atrial paced cycle length that sustains slow pathway conduction. In conclusion, sustained slow pathway conduction with resultant long AH intervals is the mechanism of two ventricular responses following termination of atrial pacing in most patients with dual AV nodal pathways. This phenomenon should be distinguished from the rare occurrence of double ventricular responses to an atrial impulse due to simultaneous fast and slow pathway conduction.

Adolescent↗
PubMed1985

Termination of paroxysmal supraventricular tachycardia with a single oral dose of diltiazem and propranolol.

The efficacy of a single oral dose combination of 120 mg diltiazem and 160 mg propranolol in terminating paroxysmal supraventricular tachycardia (PSVT) was evaluated in 15 patients. All 15 patients underwent electrical induction of PSVT that lasted longer than 15 min, and all underwent randomized crossover placebo and diltiazem and propranolol studies on 2 consecutive days. On each day PSVT was induced and placebo or diltiazem and propranolol was administered 15 min later. Electrical conversion of PSVT was performed when severe symptoms occurred or at the end of 240 min. With placebo PSVT lasted 164 +/- 89 (mean +/- SD) min; four patients had spontaneous conversion. With diltiazem and propranolol PSVT lasted 39 +/- 49 min (p less than .001); 14 patients had spontaneous conversion in an average of 27 +/- 15 min. None of the 14 patients had electrical reinduction of sustained PSVT after conversion. The sinus nodal recovery time during spontaneous or electrical conversion of PSVT was 911 +/- 459 msec with placebo and 1076 +/- 270 msec with diltiazem and propranolol (NS). Two patients developed transient second-degree atrioventricular block and junctional rhythm while on diltiazem and propranolol. Serum diltiazem and propranolol levels (ng/ml) after diltiazem and propranolol in five patients were, respectively, 49 +/- 26 and 108 +/- 101 at 15 min, 232 +/- 147 and 228 +/- 148 at 30 min, 254 +/- 169 and 370 +/- 393 at 45 min, 280 +/- 115 and 209 +/- 189 at 60 min, 188 +/- 72 and 268 +/- 264 at 120 min, and 118 +/- 57 and 265 +/- 148 at 240 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Serial electrophysiologic studies of the effects of oral diltiazem on paroxysmal supraventricular tachycardia.

In 16 patients with paroxysmal supraventricular tachycardia, electrophysiologic studies were done before and serially at hourly intervals for eight hours after the third oral dose of 90 mg diltiazem given every eight hours. Diltiazem increased both the longest atrial paced cycle length producing type 1 atrioventricular block and the effective refractory period of the atrioventricular conducting system at all measurements. Before diltiazem, all 16 patients had induction of sustained tachycardia. After diltiazem, sustained tachycardia could not be induced in ten patients at any measurements; in these patients, either echo or nonsustained tachycardia was induced. In the remaining six patients, sustained tachycardia was induced, particularly after six hours. Follow-up observations in 12 patients receiving the same dosage of oral diltiazem for 6 +/- 2 months (mean +/- SD), showed that of the eight patients in whom electrophysiologic testing induced either echo or nonsustained tachycardia, six were asymptomatic and two experienced transient palpitation. Of the other four patients with induction of sustained tachycardia, three had transient palpitation and one had occasional attacks of sustained tachycardia requiring modification of therapy. Thus, oral diltiazem increases atrioventricular nodal refractoriness, with an effect lasting up to eight hours. It is an effective agent for the prophylaxis of paroxysmal supraventricular tachycardia.

Administration, Oral↗
PubMed1984

Usefulness of intravenous diltiazem in predicting subsequent electrophysiologic and clinical responses to oral diltiazem.

Diltiazem, 0.25 mg/kg, was given intravenously during induced tachycardias in 6 patients with atrioventricular (AV) nodal reentrant tachycardia (group I) and in 24 patients with AV reentrant tachycardia incorporating a retrogradely conducting accessory pathway (group II). In all 6 group I and in 15 of 24 group II patients, tachycardias terminated within 1 minute after diltiazem administration, with a weak link in the anterograde direction. In 3 other patients in group II, tachycardias were terminated by a premature ventricular complex within 1 minute. In the remaining 6 patients in group II, in whom tachycardias failed to terminate, rates of tachycardias decreased as a result of suppression of anterograde AV nodal conduction by diltiazem. Electrophysiologic studies were performed subsequently 2 hours after the third dose of 90 mg of diltiazem, which was given orally at 8-hour intervals. In 18 responders to intravenous diltiazem who were subjected to oral diltiazem testing, sustained supraventricular tachycardia (SVT) could be induced in only 2. Of the 6 nonresponders, sustained tachycardias could not be induced in 3. Twelve patients, including 11 responders and 1 nonresponder to intravenous diltiazem who responded to oral diltiazem testing, were discharged with oral diltiazem therapy, 90 mg every 8 hours, with follow-up periods of 2 to 13 months (mean 7 +/- 4 [+/- standard deviation]). The frequency of recurrent SVT decreased significantly; 8 patients were free of tachycardias and 4 had occasional recurrences of SVT that required no hospital visit. In conclusion, intravenous diltiazem is effective in terminating SVT. Termination of SVT by intravenous diltiazem predicts subsequent electrophysiologic and clinical responses to oral diltiazem.

Administration, Oral↗
PubMed1984

Determinants of tachycardia induction using ventricular stimulation in dual pathway atrioventricular nodal reentrant tachycardia.

Factors determining tachycardia induction using ventricular stimulation in atrioventricular (AV) nodal reentrant tachycardia utilizing the slow pathway for anterograde and the fast pathway for retrograde conduction were analyzed in 53 patients. Sixteen patients had tachycardia induced by ventricular stimulation. In 15, tachycardia was inducible with incremental ventricular pacing. In 4 of these 15 patients, the tachycardia was also induced with V1V2 testing, while in 11 patients, the tachycardia was not induced with V1V2 testing. In 9 of the latter 11 patients, tachycardia could be induced with V1V2V3 testing, suggesting that the retrograde effective refractory period (ERP) of the right bundle (RB) or the relative refractory period of the His-Purkinje system (HPS) was the limiting factor for tachycardia induction during V1V2 testing. In the remaining one patient, tachycardia was induced with V1V2V3 testing, which provoked a premature ventricular beat, leading to tachycardia induction. Tachycardia was not induced by ventricular stimulation in 37 patients. Factors deterring tachycardia induction in these patients may be related to the retrograde ERP or functional refractory period (FRP) of the HPS, the retrograde ERP of the fast pathway, and an insufficient conduction delay of the circuit (retrograde fast and anterograde slow pathway) to allow anterograde conduction of the slow pathway. In conclusion, AV nodal reentrant tachycardia can be induced by ventricular stimulation in approximately 30% of patients with incremental ventricular pacing and/or ventricular extrastimulus testing. Induction of tachycardia with ventricular stimulation, nevertheless, is frequently limited by the retrograde FRP or ERP of the HPS, the retrograde ERP of the fast pathway, and possibly by an insufficient conduction delay of the circuit.

Adolescent↗
PubMed1983

Idiopathic paroxysmal ventricular tachycardia with a QRS pattern of right bundle branch block and left axis deviation: a unique clinical entity with specific properties.

Electrophysiologic evaluation before and after the serial administration of verapamil, lidocaine, propranolol, and procainamide was undertaken in 4 young, asymptomatic patients with recurrent, sustained ventricular tachycardia (VT). No patient had obvious organic heart disease. The electrocardiogram during sinus rhythm showed S-T depression and T-wave inversion over the inferior and lateral precordial leads in 3 patients. QRS morphologic characteristics during episodes of VT showed a pattern of right bundle branch block and left axis deviation. In all 4 patients, VT could be both induced and terminated with electrical stimulation. Verapamil terminated VT and prevented the induction of sustained VT in 3 patients, and markedly slowed the rate of VT in 1 patient. Procainamide effectively prevented the induction of sustained VT in 2 patients, and although ineffective in preventing induction in 2 patients, it slowed the rate of tachycardia in both. Lidocaine and propranolol did not prevent the induction of VT in any patient. These findings suggest that slow-response tissues may be involved in the genesis of VT in these patients, and that VT in these patients may represent a unique clinical entity with distinct electrocardiographic, electrophysiologic, and electropharmacologic properties.

Adult↗
PubMed1983

Effects of oral diltiazem in paroxysmal supraventricular tachycardia.

Electrophysiologic studies were performed before and 2 hours after the oral administration of 270 mg of diltiazem in 3 divided doses at 8-hour intervals in 36 patients with paroxysmal supraventricular tachycardia (SVT). Before diltiazem, all 36 patients had induction of sustained SVT: 24 with atrioventricular (AV) reentrance incorporating an accessory pathway (Group 1) and 12 with AV nodal reentrance (Group 2). After diltiazem, 20 patients in Group 1 lost the ability to induce or sustain SVT because of increased anterograde normal pathway refractoriness in 19 patients and increased retrograde accessory pathway refractoriness in 1. Eight patients in Group 2 could no longer induce or sustain SVT because of increased anterograde slow pathway refractoriness in 2 patients and increased retrograde fast pathway refractoriness in 6. Diltiazem concentration in the blood, measured in 29 patients, was 156 +/- 75 ng/ml (mean +/- standard deviation). Fifteen patients, 2 with and 13 without induction of sustained SVT after diltiazem, were discharged on the same dosage of diltiazem and followed up 5 +/- 3 months. The former 2 patients had attacks of sustained SVT, whereas the latter 13 have been free of sustained SVT. In conclusion, oral diltiazem prevents induction and sustenance of paroxysmal SVT in most patients and may be used as an alternative agent for the prophylaxis of SVT.

Administration, Oral↗