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Biomedical subjects

D Wu

Publications and source records attributed to D Wu.

At least 667 records · Page 37Linked to original sources

Quantification of human atrioventricular nodal concealed conduction utilizing S1S2S3 stimulation.

We studied antegrade concealed conduction of atrial extrastimuli (A2) that blocked in the atrioventricular (AV) node in eight subjects, using a third extrastimulus (A3), coupled at decreasing coupling intervals to A2. Three A1-A2 intervals were tested in each subject: late (just shorter than AV nodal effective refractory period), intermediate, and early (just longer than atrial functional refractory period). The curves relating the following variables were constructed for each A2: A1-A3, H1-H3 and A2-A3, A3-H3. The former was compared to the control A1-A2, H1-H2 curve. Concealment of A2 was demonstrated in all eight subjects at the three tested values of A1-A2. The A2-A3, A3-H3 curve allowed analysis of AV nodal conduction time (A3-H3) and AV nodal recovery time (defined as the shortest A2-A3 at which the impulse conducted to the His bundle) at identical values of A2-A3. In all subjects the timing of blocked A2 had minimal effect on both AV nodal conduction time and recovery time. In five of the eight subjects a late A2 sporadically conducted to the His bundle. Conduction of A2 to the His bundle resulted in marked lengthening of both AV nodal conduction and recovery times. Concealed conduction of A2 was always demonstrated, but the degree of concealment was relatively fixed, whether A2 was an early, intermediate, or late blocked premature beat. Slow conduction of A2 had a much greater effect than concealment of A2 on subsequent impulse conduction.

Aged↗

Angina-like syndrome with diazoxide therapy for hypertensive crisis.

In 14 patients with hypertensive crisis treated with diazoxide, close monitoring of blood pressure, heart rate, and symptoms was performed. Standard 12-lead electrocardiograms were recorded before and after diazoxide. All patients showed a significant fall in blood pressure after drug administration. Seven patients (50%) showed significant ST-T changes after diazoxide. Six patients (43%) developed substernal discomfort demonstrated by substernal pain of tightness. Five patients (35%) had both chest discomfort and ST-T changes. One of these patients with substernal pain and ST elevation had evidence of acute myocardial infarction with serial enzyme studies. In the patients with significant ST-T changes, the average fall in blood pressure was significantly greater than the average fall in blood pressure in the patients without significant ST-T changes. These findings suggest that both ST-T changes and substernal discomfort were due to myocardial ischemia secondary to a sudden severe drop in blood pressure.

Adolescent↗

Sinus nodal responses to atrial extrastimuli in patients without apparent sinus node disease.

In 36 patients without sinus node disease scanning with an atrial extrastimulus (A2) was performed during sinus rhythm with the sinus cycle length measured in milliseconds. Zones of nonreset due to interference, reset, interpolation and sinus echoes were defined by noting the timing of the first response after A2. Zones were defined in terms of their longest and shortest A1-A2 coupling intervals (in milliseconds). A zone of nonreset was found in 12 of 12 patients in whom A2 was delivered late. The mean cycle length in these 12 patients was 779 msec, with a mean zone of nonreset of 779 to 585 msec (25 percent of cycle length). All 36 patients (100 percent) had a zone of reset. The mean cycle length in these 36 patients was 803 msec with a zone of reset from 692 to 319 msec (46 percent of cycle length). Seven of 36 patients (19 percent) had a zone of interpolation. The mean cycle length in these seven patients was 754 msec, with a mean zone of interpolation of 344 to 279 (9 percent of cycle length). Four of 36 patients (11 percent) had a zone of sinus echoes. The mean cycle length in these four patients was 870 msec, with a mean zone of echoes from 350 to 313 msec (4 percent of cycle length). Calculated sinoatrial conduction time ranged from 40 to 153 msec (mean +/- standard deviation 92 +/- 30 msec). Shortening of the cycle length with atrial pacing increased the number of patients with zones of interpolation and echoes. In conclusion, zones of nonreset and reset are found in all patients with normal sinus nodal function, whereas zones of interpolation and echoes are much less common. Sinoatrial conduction time is surprisingly long in patients without apparent sinus node disease.

Adult↗

Chronic right bundle branch block and left posterior hemiblock. Clinical, electrophysiologic and prognostic observations.

Twenty-one patients with long-term right bundle branch block and left posterior himiblock were studied electrophysiologically and then followed up prospectively. The group consisted of 19 men and 2 woman aged 61 +/- 2.7 years (mean +/- standard error of the mean). The majority of patients had either hypertensive cardiovascular disease (48 percent) or primary conduction disease (33 percent). Initial electrophysiologic studies revealed A-H intervals of 58 to 152 msec (mean 98 +/- 7.7) and H-V intervals of 40 to 80 msec (mean 52 +/- 2.1). Six patients (29 percent) had prolonged H-V intervals. The follow-up period ranged from 91 to 1,231 days (mean 671 +/-68). Three of 21 patients (14 percent) needed a permanent pacemaker after development of the following symptomatic conduction disease: sinoatrial block on day 3 of follow-up; second degree atrioventricular (A-V) block, site undetermined, on day 118; and second degree A-V block proximal to the His bundle on day 398. One patient died suddenly (on day 571), and two others died of noncardiac causes. In conclusion, combined right bundle branch block and left posterior hemiblock was associated with less trifascicular disease than reported previously. The clinical course of most of the patients was benign and the incidence of sudden death was relatively small. Symptomatic conduction disease occurred but could be definitely related to trifascicular disease in only one patient. These short-term data suggest that prophylactic pacemaker insertion is not routinely indicated in patients with chronic right bundle branch block and left posterior hemiblock.

Adult↗

Alternating Wenckebach periodicity: A common electrophysiologic response.

Alternating Wenckebach periods are defined as episodes of 2:1 atrioventricular (A-V) block in which conducted P-R intervals progressively prolong, terminating in two or three blocked P waves. In this study, His bundle recordings were obtained in 13 patients with pacing-induced alternating Wenckebach periods. Three patterns were noted: Pattern 1 (one patient with a narrow QRS complex) was characterized by 2:1 block distal to the H deflection (block in the His bundle) and Wenckebach periods proximal to the H deflection, terminating with two blocked P waves. Pattern 2 (four patients) was characterized by alternating Wenckebach periods proximal to the His bundle, terminating with three blocked P waves. Pattern 3 (eight patients) was characterized by alternating Wenckebach periods proximal to the His bundle, terminating with two blocked P waves. Alternating Wenckebach periods are best explained by postulating two levels of block. When alternating Wenckebach periods are terminated by three blocked P waves (pattern 2), the condition may be explained by postulating 2:1 block (proximal level) and type I block (distal level). When alternating Wenckebach periods are terminated by two blocked P waves (patterns 1 and 3), the condition may be explained by postulating type I block (proximal level) and 2:1 block (distal level). Pattern 1 reflects block at two levels, the A-V node and His bundle. Patterns 2 and 3 most likely reflect horizontal dissociation within the A-V node.

Adult↗

H-V interval in patients with bifascicular block (right bundle branch block and left anterior hemiblock). Clinical, electrocardiographic and electrophysiologic correlations.

Electrophysiologic studies were performed in 119 adults with chronic bifascicular block manifested by right bundle branch block and left anterior hemiblock. The H-V interval was normal in 86 patients and prolonged in 33. The following clinical variables were more frequent (P less than 0.05) in patients with a prolonged H-V interval: cardiac third sound, mitral systolic murmur, cardiomegaly on chest roentgenogram, congestive heart failure and cardiac functional class III or IV (New York Heart Association criteria). The following differences in the electrocardiographic and electrophysiologic findings were found: Patients with a prolonged H-V interaval had a longer mean P-R interval, QRS duration and A-H interval (P less 0.02). All patients were followed up prospectively in a cardiac conduction disease clinic after initial evaluation. The mean follow-up periods were (mean plus or minus standard error of the mean) 514 plus or minus 49 and 563 plus or minus 34 days for the patients with a prolonged and normal H-V interval, respectively. Progression of conduction disease occurred in three patients (4 percent) with a normal H-V interval and in four (12 percent) with a prolonged interval. The cumulative 3 year mortality rate for the entire group was 25 percent. The patients with a prolonged H-V interval had a higher cumulative 2 year mortality rate than those with a normal H-V interval but the difference was not statistically significant. In summary, a prolonged H-V interval was often associated with serious myocardial dysfunction and a high mortality rate. The risk of progression of conduction disease was slight with either a prolonged or a normal H-V interval during this relatively short follow-up period.

Adolescent↗

Limitation of the surface electrocardiogram in diagnosis of atrial arrhythmias. Further observations on dissimilar atrial rhythms.

Electrophysiologic studies with recordings of multiple intracavitary electrograms were performed in two patients with atrial dysrhythmias. In Case 1 the arrhythmic pattern in the surface electrocardiogram resembled atrial flutter. Electrophysiologic studies revealed the arrhythmia to be paroxysmal left atrial tachycardia, with separation of left and right atrial components of the P wave by an isoelectric period secondary to marked interatrial conduction delay. In Case 2 the surface electrocardiogram indicated paroxysmal atrial tachycardia with block. Electrophysiologic studies revealed right atrial standstill with atrial inexcitability and two dissimilar rhythms involving the left atrium. The electrocardiograms did not accurately reflect atrial arrhythmias in these two patients and only multiple direct recordings permitted the correct diagnoses. New electrophysiologic observations concerning intraatrial block and dissimilar atrial rhythms are presented.

Aged↗

Dual atrioventricular nodal pathways. A common electrophysiological response.

Evidence of dual atrioventricular nodal pathwats (a sudden jump in H1-H2 at critical A1-A2 coupling intervals) was shown in 41 out of 397 patients studied with atrial extrastimulus techniques. In 27 of these 41, dual pathways were demonstrable during sinus rhythm, or at a cycle length close to sinus rhythm (CL1). In the remaining 14, dual pathways were only demonstrated at a shorter cycle length (CL2). All patients with dual pathways at cycle length who were also tested at cycle length (11 patients) had dual pathways demonstrable at both cycle lengths. In these 11 patients both fast and slow pathway effective refractory periods increased with decrease in cycle length. Twenth-two of the patients (54%) had either an aetiological factor strongly associated with atrioventricular nodal dysfunction or one or more abnormalities suggesting depressed atrioventricular nodal function. Dvaluation of fast pathway properties suggested that this pathway was intranodal. Seventeen of the patients had previously documented paroxysmal supraventricular tachycardia (group 1). Eight patients had recurrent palpitation without documented paroxysmal supraventricular tachycardia (group 2), and 16 patients had neither palpitation nor paroxysmal supraventricular tachycardia (group 3). Echo zones were demonstrated in 15 patients (88%) in group 1, no patients in group 2, and 2 patients (13%) in group 3.

Adolescent↗

Effects of atrial pacing site on atrial and atrioventricular nodal function.

The effects of the site used for atrial pacing on atrial and atrioventricular nodal conduction were assesed in 16 patients. In 13 patients, three atrial pacing sites were used: high right atrium, low lateral right atrium, and midcoronary sinus. Two recording sites were used: low septal right atrium, including His electrogram, and high right atrium. Stimulus (S) to high right atrium interval was longest with coronary sinus pacing (76 plus or minus 7 ms) (P less than 0.001), and shortes with high right atrial pacing (41 plus or minus 3 ms) (P less than 0.05). There was no significant difference in stimulus to low septal right atrium from all three pacing sites. Atrial functional and effective refractory periods were not significantly different. Mean low septal right atrium to His was significantly shorter from the coronary sinus (93 plus or minus 8 ms) (P less than 0.001), as compared to high right atrium (139 plus or minus 16 ms), and low lateral right atrium (129 plus or minus 13 ms) pacing. AV nodal functional and effective refractory periods, and the paced rate producing AV nodal Wenckebach were not significantly different when comparing the three sites. Left atrial appendage and high right atrium were similarly compared in three additional patients, and no significant differences were found in conduction times and refractory periods.

Adult↗

Return of normal conduction after paroxysmal heart block. Report of a case with major discordance of electrophysiological and pathological findings.

This report describes a 52-year-old male with paroxysmal heart block as well as left and right bundle branch block, resulting in Stokes-Adams attacks. The patient experienced a return to 1:1 atrioventricular (A-V) conduction with narrow QRS within 48 hours of the attacks and heart block never recurred. Electrophysiological studies three weeks later revealed a narrow QRS, a normal H-V interval (36 msec), 1:1 A-V conduction up to an atrial paced rate of 210 beats/min, and normal refractory periods with atrial extrastimulus techniques (His-Purkinje system refractory periods less than 370 msec). The patient died from a cerebral embolus incurred during diagnostic left heart catheterization two days after electrophysiological studies. Postmortem examination revealed calcific aortic stenosis with calcific impingement upon the pars membranacea resulting in compression of the distal His bundle and marked disruption of the proximal portions of both bundle branches. This report documents a major limitation of electrophysiological studies, this limitation being that these studies may be totally normal on one occasion in a patient with pathologically significant chronic conduction disease, which may become clinically manifest on another occasion.

Adams-Stokes Syndrome↗

Demonstration of sustained sinus and atrial re-entry as a mechanism of paroxysmal supraventricular tachycardia.

Electrophysiological studies in five patients with documented (4) or suspected (1) paroxysmal supraventricular tachycardia (PSVT), suggested sinus or atrial reentrance (SR or AR). Two of the patients had preexcitation, three had evidence of atrial enlargement, and all had organic heart disease. The following observations supported a diagnosis of SR and AR; 1) induction of sustained PSVT with atrial extrastimulus technique allowing definition of an echo zone; 2) induction of sustained PSVT during constant rapid atrial pacing at a rate less than that producing A-V nodal Wenckebach periods, or producing normalization of QRS complex in patients with pre-excitation: 3) P waves preceding each QRS during PSVT with an A-H interval appropriate for the rate of the PSVT; 4) antegrade P wave morphology during PSVT, a normal high to low sequence of right atrial activation (SR), or P wave morphology and atrial activation sequence different from sinus (AR); 5) lack of correlation of PSVT induction with critical A-H interval. The rates of induced sustained PSVT ranged from 114 to 143 beats/min, and were similar to those observed during spontaneous episodes of PSVT in the four patients. PSVT could be terminated with critically timed extra-stimuli or carotid massage. In conclusion, SR and AR appear to be mechanisms of spontaneous PSVT in man. Rates of SR and AR PSVT tend to be relatively slow.

Adolescent↗

Eectrophysiological observations in pateints with rate dependent bundle branch block.

Electrophysiological studies were conducted in 15 patients with tachycardic rate dependent bundle branch block (RDBBB): ten with left, and five with right. No bradycardic RDBBB was observed, despite occurrence of cycle lengths (CL) longer than 1200 msec in over half the patients studied. Onset of RDBBB was abrupt in 13 patients, and gradual in two. In three patients, the CL allowing reversion to normal conduction (once RDBBB was initiated) was 50, 55, and 190 msec longer, respectively, than the CL inducing RDBBB. Bundle brance refractory periods (RP) were measured with atrial extrastimulus technique in five patients. All RP (except one) were prolonged at all tested CL when compared to patients without conduction disease. The expected decrease in RP with shortening of CL did not occur in four of the five patients. The electrophysiological abnormality in patients with DBBB thus appeared to be an increase in refractoriness in the affected bundle branch, along with a loss of the normal decrease in refractoriness with decrease in CL. Similar findings might be demonstrable in patients with early bundle branch disease.

Adult↗

Comparison of cardiac refractory periods in children and adults.

Atrial (A) and A-V nodal (AVN) effective and functional refractory periods (ERP & FRP) were determined by atrial extrastimulus technique in 40 children, aged 7 months to 16 years, with normal P-R intervals and QRS durations. These data were compared to adult data at longest cycle lengths (CL) assuring atrial capture. All values are listed in msec as means plus or minus standard errors of the means. CL was 566 plus or minus 15 in children and 699 plus or minus 29 in adults (P less than .001). Refractory periods (RP) in children and adults were, respectively: AERP 196 plus or minus 9 and 239 plus or minus 13 (P less than .01), AFRP 225 plus or minus 8 and 284 plus or minus 11 (P less than .001), AVNERP 239 plus or minus 11 and 293 plus or minus 7 (P smaller than .001), AVNFRP 360 plus or minus 13 and 403 plus or minus 7 (P smaller than .005). RP were then compared at three equivalent CL ranges: CL1, 850-600; CL2 599-460; CL3 459-280. The following RP were significantly shorter in children (P smaller than .05-.001): AERP, AFRP, AVENERP and AVNFRP at CL2 and CL3. RP of the bundle branches were compared and tended to be shorter in children. In conclusion, atrial and A-V nodal ERP and FRP are shorter in children than adults. This shortening is only partially related to the shorter CL in children. These data are germane to understanding the maturation of the conduction system in man.

Adolescent↗

"Supernormal conduction" of a premature impulse utilizing the fast pathway in a patient with dual atrioventricular nodal pathways.

Electrophysiological studies with atrial extrastimulus technique suggested the presence of dual atrioventricular (A-V) nodal pathways in a patient with hypothyroidism, as evidenced by a sudden increase of H1-H2 intervals at critical A1-A2 coupling intervals. Following the atrial extrastimulus (A2), a third impulse (A3) occurred spontaneously. During slow pathway conduction of A2, and A3, appearing at a critically timed interval allowed fast pathway conduction, resulting in an earlier than expected QRS (a form of supernormal conduction). This demonstration of fast pathway conduction during slow pathway conduction adds strong evidence for the existence of dual A-V nodal pathways.

Aged↗

The effects of ouabain on induction of atrioventricular nodal re-entrant paroxysmal supraventricular tachycardia.

Electrophysiological studies utilizing His bundle recordings and atrial extra-stimulus technique were performed in 17 patients (pts) with documented paroxysmal supraventricular tachycardia (PSVT) before and after 0.01 mg/kg, i.v., ouabain. Before ouabaine, echozones(EZ) were demonstrated in 11 patients. After ouabain, EZ were abolished in two, decreased in five, unchanged in three, and increased in one. In one patient, EZ was demonstrated only after ouabain. Eleven patients could sustain PSVT before ouabain; after ouabain, only six patients could sustain PSVT. Analysis of A1-A2, H1-H2 curves revealed 11 patients with discontinous (dual pathway) and six patients with smooth conduction curves. In dual pathway patients, both the fast and slow pathway curves were shifted rightward and upward after ouabain. The changes in EZ were dependent upon the relative rightward shifts of the two pathways. In patients with smooth curves, EZ tended to shift rightward with a critical A-H being achieved at longer A1-A2 intervals after ouabain. In conclusion, the effects of ouabain on PSVT were variable. Beneficial effects included abolition or decrease of EZ and loss of the ability to sustain PSVT. Potentially deleterious effects included widening or new de-elopment of EZ.

Adult↗

Demonstration of dual atrioventricular nodal pathways utilizing a ventricular extrastimulus in patients with atrioventricular nodal re-entrant paroxysmal supraventricular tachycardia.

In patients with atrioventricular (A-V) nodal re-entrant paroxysmal supraventricular tachycardia (PSVT), atrial extrastimulus technique frequently reveals discontinuous A1-A2, H1-H2 curves suggestive of dual A-V nodal pathways. To further test the hypothesis that these curves in fact reflect dual A-V nodal pathways, a ventricular extrastimulus (VS) was coupled either to A2 at a fixed A1-A2 interval which reliably produced an A-V nodal re-entrant atrial echo (E) with a constant A2-E interval in two patients, or to QRS complex (V) during sustained PSVT with a constant E-E interval in one patient. Three response zones were defined: at longer A2-VS or V-VS coupling interval, VS manifested no effect on the timing of E (Zone 1). At closer A2-VS or V-VS coupling interval, VS conducted to the atrium, shortening the apparent A2-E or E-E interval (Zone 2). At shortest A2-VS or V-VS coupling interval, VS was blocked retrogradely, and no E was induced (Zone 3). The ability of VS to preempt control of the atria (Zone 2 response) strongly suggests the presence of dual A-V nodal pathways in these PSVT patients. If only a single pathway were present, VS would of necessity collide with the antegrade impulse and could not reach the atria. The Zone 3 response occurs because of retrograde refractoriness of the fast pathway. Failure of the echo during Zone 3 probably reflects concealed conduction to the fast pathway, or possibly interference in the slow pathway.

Adult↗

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

Electrophysiological studies were performed in two patients with documented paroxysmal supraventricular tachycardia and dual atrioventricular (AV) nodal pathways as defined by the atrial extra-stimulus technique. Both patients manifested two ranges of A-H intervals (AV nodal conduction times) at critical cycle lengths, reflecting fast- and slow-pathway conduction. The occurrence of fast- and slow-pathway conduction at the same cycle length depended on a long fast-pathway effective refractory period relative to the spontaneous or driven cycle length. At critical cycle lengths with fast-pathway conduction, a shift to slow-pathway conduction could be induced by a premature atrial impulse falling within the effective refractory period of the fast pathway. Repetitive retrograde concealed conduction to the fast pathway then maintained antegrade slow-pathway conduction. Resumption of fast-pathway conduction was induced with premature atrial impulses falling within the effective refractory periods of both the fast and the slow pathways, allowing recovery of the fast pathway for antegrade conduction. Atrial echoes and AV nodal reentrant paroxysmal supraventricular tachycardia occurred when sufficient slow-pathway delay was achieved to allow recovery of the fast pathway for retrograde conduction.

Atrioventricular Node↗