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Biomedical subjects

C Wyndham

Publications and source records attributed to C Wyndham.

47 records · Page 3Linked to original sources
PubMed1975

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↗
PubMed1975

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↗
PubMed1975

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↗
PubMed1975

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↗
PubMed1975

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↗
PubMed1975

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↗
PubMed1975

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↗
PubMed1975

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↗
PubMed1975

The electrophysiological effects of ouabain on sinus node and atrium in man.

Electrophysiological studies were performed in 16 patients before and 30 min after intravenous administration of ouabain (0.1 mg/kg). P-A interval (mean+/-SEM) was 40+/-2.1 ms before and 44+/- 1.5 ms after ouabain (P less than 0.001). Atrial effective and functional refractory periods (ERP and FRP) were measured in all patients during sinus rhythm and during driving at equivalent paced rates in 12 patients. The mean atrial ERP and FRP during sinus rhythm were, respectively, 244+/-10.5 and 307+/-11.0 ms before and 253+/-9.7 and 318+/-11.4 ms after infusion of ouabain (NS). Mean atrial ERP and FRP during driving were, respectively, 231+/-15.3 and 264+/-14.9 ms before and 266+/-18.6 and 296+/-19.7 ms after ouabain (P less than 0.01 and P less than 0.01). Mean sinus cycle length and sinus recovery times were, respectively, 887+/-31.2 and 1,113+/-38.7 ms before and 905+/-38.2 and 1,008+/-30.7 ms after infusion of ouabain (NS and P less than 0.005). Calculated sinoatrial conduction times before and after ouabain were 90+/-6.8 and 110+/-8.5 ms, respectively (P less than 0.005). In summary, ouabain produced depression of intraatrial conduction as manifested by increase in P-A interval and atrial effective and functional refractory periods. Ouabain significantly increased calculated sinoatrial conduction time without significant effect on spontaneous sinus cycle length.

Adult↗