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Biomedical subjects

P Denes

Publications and source records attributed to P Denes.

At least 127 records · Page 7Linked to original sources

An unusual variety of atrioventricular nodal re-entry due to retrograde dual atrioventricular nodal pathways.

Three patients with paroxysmal supraventricular tachycardia (PSVT) had discontinuous ventriculo-artrial conduction curves (V1-V2, A1-A2), suggesting dual A-V nodal pathways. Ventricular echoes occurred simultaneously with sudden increase of V-A interval. These echoes were characterized by retrograde P waves occurring in front of QRS, suggesting utilization of a slow pathway for retrograde conduction and a fast pathway for antegrade conduction. In case one, atropine improved retrograde slow pathway and antegrade fast pathway conduction and made A-V nodal re-entry sustained, resulting in PSVT (with retrograde P in front of the QRS). In cases 2 and 3, atropine markedly shortened retrograde fast pathway refractory period and slightly improved antegrade slow pathway conduction. The discontinuous V1-V2, A1-A2 curves and echoes were no longer demonstrable. However, with improvement of retrograde fast pathway and antegrade slow pathway conduction, A-V nodal re-entrant echoes and PSVT were observed, utilizing the slow pathway for antegrade conduction and the fast pathway for retrograde conduction (P simultaneous with QRS).

Adult↗

The determinants of atrioventricular nodal re-entrance with premature atrial stimulation in patients with dual A-V nodal pathways.

In patients with dual atrioventricular (A-V) nodal pathways, atrial extrastimulus testing induces either no echoes, single atrial echoes (Ae), or repetitive re-entrance (repetitive atrial and ventricular beating). We examined the fast and slow pathways properties in 38 patients with dual pathways in order to delineate the determinants of re-entrance. Seventeen patients had no Ae. Of these, six had no V-A conduction and 11, intact V-A conduction. The mean paced ventricular cycle length producing retrograde V-A block (VABCL) in this group (a measure of retrograde fast pathway refractoriness) was 552 +/- 32 msec (mean +/- SEM; 10 pts). In contrast, all 21 patients with Ae had intact V-A conduction with mean VABCL of 382 +/- 21 msec (14 pts) (P less than 0.05). Repetitive re-entrance occurred only when Ae conducted to the ventricles. Seven patients had only single Ae. The mean paced atrial cycle length producing Wenckebach periodicity (CLAWP) in this group (a measure of antegrade slow pathway refractoriness) was 490 +/- 31 msec (5 pts). Fourteen patients had repetitive re-entrance. The mean CLAWP in this group was 399 +/- 18 msec (8 pts) (P less than 0.05). In conclusion, our results suggest that in patients with dual pathway, the occurrence of single or repetitive re-entry is dependent upon measurable slow and fast pathway properties.

Adolescent↗

Sites of conduction disease in aortic stenosis: significance of valve gradient and calcification.

Electrophysiologic studies were done in 32 patients with aortic stenosis. In 24 patients with intact A-V conduction, A-H intervals ranged from 55 to 145 msec and were prolonged in two. Two had split His bundle potentials. The H-V intervals ranged from 25 to 94 msec and were prolonged in 12. The mean H-V interval was 63 +/- 2.6 msec in 12 patients with calcific aortic stenosis compared with 50 +/- 4.9 msec in 12 without calcification (P less than 0.05). The mean H-V in 10 patients with aortic gradients greater than 40 mm Hg was 62 +/- 5.6 msec compared with 47 +/- 3.1 msec in nine with gradients less than 40 (P less than 0.05). In patients with aortic stenosis and A-V block, the site of the block was distal to the His bundle in three and within the His bundle in five. All eight had calcified valves. Aortic stenosis was commonly associated with latent and manifest conduction disease in the His bundle and the trifascicular conduction system. Conduction disease was more extensive with calcified valves and greater valve obstruction.

Adult↗

Familial atrial tachyarrhythmia with short PR interval.

A family had an unusual and perhaps unique familial dysrhythmia. The proband had a short PR interval with normal QRS and chronic recurrent paroxysmal atrial tachycardia (Lown-Ganong-Levine syndrome). The arrhythmia produced left ventricular dysfunction. Both paroxysmal atrial tachycardia (PAT) and left ventricular dysfunction were reversed with administration of digoxin and propranolol hydrochloride. Three family members had paroxysmal or chronic atrial fibrillation, first diagnosed at a relatively young age (23 years, 38 years, and early 40s, respectively). Five additional family members had short PR intervals with normal QRS, and eight other family members had borderline short PR intervals. The mode of inheritance appeared to be autosomal dominant with varying expressivity. We have described a familial syndrome characterized by PAT or atrial fibrillation in its advanced form with short PR interval as a possible identifying trait. The future course of members with isolated short PR is unknown.

Adult↗

Sudden death in patients with chronic bifascicular block.

Prospective follow-up studies of 277 patients with chronic bifascicular block showed that 30 patients developed sudden cardiac death (SCD). Cumulative one-, two-, and three-year SCD mortality was computed. The patients that developed SCD were compared with the remaining patients (209 alive and 38 dead). The groups were similar in regard to age, sex, AH, and HV intervals. The following were more frequent in the SCD group (P less than .05): angina, previous myocardial infarction, heart failure, cardiomegaly, left bundle-branch block, premature ventricular beats, and ventricular tachycardia. Ventricular fibrillation was the cause of death in four cases of SCD where terminal ECG documentation was available. We concluded that SCD is a major cause of mortality in patients with chronic bifascicular block. The association of SCD with coronary disease and ventricular dysrhythmia suggested ventricular fibrillation as a frequent mechanism.

Adult↗

Significance of A-H interval in patients with chronic bundle branch block. Clinical, electrophysiologic and follow-up observations.

His bundle electrograms were recorded in 308 adults with chronic bundle branch block. The A-H interval was normal in 249 patients and prolonged in 59. Comparison of patients with normal and prolonged A-H intervals revealed a greater incidence of demonstrable organic heart disease in the latter (P less than 0.01). Dyspnea, cardiomegaly and congestive heart failure were more frequent in patients with A-H prolongation. These patients also had longer P-R intervals and atrioventricular (A-V) nodal effective refractory periods, lower paced rates producing second degree A-V block proximal to the His bundle and a greater frequency of H-V prolongation. All patients were prospectively followed up in a conduction disease clinic with mean follow-up periods (+/- standard error of the mean) of 523 +/- 23 and 588 +/- 47 days in the patients with normal and prolonged A-H intervals, respectively. Seven (3 percent) of the patients with a normal A-H interval had A-V block with probable or definite site of block proximal to the His bundle in three and distal to the His bundle in four. In five of the six patients with a prolonged A-H interval who experienced A-V block (10 percent), the probable or definite site of block was proximal to the His bundle. Mortality (both sudden and nonsudden) was not significantly different in the patients with normal and prolonged A-H intervals. In summary, A-H prolongation was associated with increased incidence of organic heart disease and myocardial dysfunction. The risk of development of A-V nodal block was greater in patients with a prolonged A-H interval but appeared to be of minimal clinical significance.

Adolescent↗

Electrophysiologic effects of atropine on human sinus node and atrium.

Electrophysiologic studies were conducted in 17 patients without apparent sinus node disease before and after intravenous administration of 1 to 2 mg of atropine. Mean values in milliseconds (+/- standard error of the mean) before and after administration of atropine were as follows: sinus cycle length 846 +/- 26.4 versus 647 +/- 20.0 (P less than 0.001); sinus nodal recovery time 1,029 +/- 37 versus 774 +/- 36 (P less than 0.001); mean calculated sinoatrial (S-A) conduction time 103 +/- 5.7 versus 58 +/- 3.9 (P less than 0.001); mean P-A interval 34 +/- 1.5 msec versus 31 +/- 1.5 (P less than 0.05); mean atrial effective and functional refractory periods during sinus rhythm 285 +/- 11.3 versus 238 +/- 7.9 and 331 +/0 11.6 versus 280 +/- 8.6, respectively (P less than 0.001 for both); mean atrial effective and functional refractory periods measured at equivalent driven cycle length 239 +/- 7.7 versus 213 +/- 7.4 and 277 +/- 11.4 versus 245 +/- 9.5, respectively (P less than 0.001 for both). In conclusion, atropine shortened sinus cycle length, sinus nodal recovery time and calculated S-A conduction time. The shortening of atrial refractory periods with atropine implies that vagotonia prolongs atrial refractoriness in man.

Adult↗

Electrophysiologic demonstration of bilateral anomalous pathways in a patient with Wolff-Parkinson-White syndrome (type B preexcitation).

Pre- and postoperative electrophysiologic studies are described that were suggestive of two (right- and left-sided) anomalous atrioventricular (A-V) connections in a patient with type B Wolff-Parkinson-White syndrome and intractable arrhythmias, who underwent epicardial mapping and successful surgical ablation of the right-sided anomalous pathway. The presence of the right-sided anomalous pathway capable of both antegrade and retrograde conduction was suggested by the following observations: (1) Type B preexcitation on the surface electro-cardiogram; (2) maximal preexcitation and minimal stimulus-delta with low lateral right atrial pacing; (3) epicardial mapping of the atria and ventricles; and (4) disappearance of ventricular preexcitation after surgical ablation of the right-sided anomalous pathway. The presence of an additional left-sided anomalous pathway capable of only retrograde conduction (concealed on the surface electrocardiogram) was sugg-sted by the following observations: (1) Left to right retrograde atrial activation sequence during reentrant tachycardia and ventricular pacing at rapid rates and with coupled ventricular pacing postoperatively; (2) spontaneous conversion of wide ORS tachycardia utilizing the anomalous pathway for antegrade conduction to narrow QRS tachycardia with significant slowing in rate; and (3) smooth antegrade A-V nodal conduction curves with echo zone postoperatively. The demonstration of bilateral anomalous pathway in patients with preexcitation has important electrophysiologic and surgical implications.

Adolescent↗

Electrophysiologic effects of atropine on sinus node and atrium in patients with sinus nodal dysfunction.

Electrophysiologic studies were conducted in 21 patients with sinus nodal dysfunction before and after intravenous administration of 1 to 2 mg of atropine. The mean sinus cycle length (+/- standard error of the mean) was 1,171 +/- 35 msec before and 806 +/- 29 msec after administration of atropine (P less than 0.001). Mean sinus nodal recovery time determined at a aced rate of 130/min and maximal recovery time were, respectively, 1,426 +/- 75 and 1,690 +/- 100 msec before and 1,169 +/- 90 and 1,311 +/- 111 msec after atropine (P less than 0.001 and less than 0.001). Mean calculated sinoatrial conduction time, measured in 16 patients, was 113 +/- 8 msec before and 105 +/- 9.7 msec after atropine (difference not significant). Mean atrial effective refractory period, measured at an equivalent driven cycle length, was 262 +/- 11.1 msec before and 256 +/- 10.3 msec after atropine (not significant). Mean atrial functional refractory period was 302 +/- 12.5 msec before and 295 +/- 11.3 msec after atropine (not significant). The shortening of sinus cycle length and sinus recovery time with atropine was similar to that noted in patients without sinus nodal dysfunction. In contrast, atropine had insignificant effects on sinoatrial conduction and atrial refractoriness in this group whereas it shortens both in normal subjects. This finding may reflect altered perinodal and atrial electrophysiologic properties in patients with sinus node disease.

Adult↗

Catheter mapping of retrograde atrial activation. Observations during ventricular pacing and AV nodal re-entrant paroxysmal tachycardia.

A systematic study of retrograde atrial sequence at commonly used electrode catheter recording sites in 8 patients without, and in 4 patients with AV nodal re-entrant paroxysmal tachycardia was made. During right ventricular pacing, the retrograde atrial activation sequence was low septal right atrium--proximal coronary sinus--distal coronary sinus--high right atrium. During the episodes of paroxysmal tachycardia, a similar pattern was observed. This information should be helpful in the understanding of abnormal activation sequences in patients with paroxysmal supraventricular tachycardia in whom retrogradely conducting anomalous pathways are suspected.

Adult↗

Intractable paroxysmal tachycardia caused by a concealed retrogradely conducting Kent bundle. Demonstration by epicardial mapping and cure of tachycardias by surgical interruption of the His bundle.

Electrophysiological and epicardial mapping studies are described in a patient without pre-excitation who had intractable recurrent paroxysmal supraventricular tachycardia. Electrophysiological studies revealed fixed VA conduction times during both rapid ventricular pacing and coupled ventricular stimulation. Catheter mapping of atrial activation during retrograde conduction and during induced paroxysmal supraventricular tachycardia revealed early distal coronary sinus activation (posterior left atrium) relative to the low septal, low lateral, and high lateral right atrium. These studies suggested the presence of a concealed left-sided bypass tract. The patient underwent surgical interruption of the His bundle for control of paroxysmal supraventricular tachycardia. Epicardial mapping of the atria (during ventricular pacing) confirmed the presence of a concealed left-sided bypass tract. Surgery produced antegrade av block (while retrograde conduction was maintained) and total cure of paroxysmal supraventricular tachycardia. This is the first reported case of a concealed retrograde extranodal pathway documented by epicardial mapping.

Adult↗

A quantitative description of normal AV nodal conduction curve in man.

The AV nodal conduction curve generated by the atrial extrastimulus technique has been described only qualitatively in man, making clinical comparison of known normal curves with those of suspected AV nodal dysfunction difficult. Also, the effects of physiological and pharmacological interventions have not been quantifiable. In 50 patients with normal AV conduction as defined by normal AH (less than 130 ms), normal AV nodal effective and functional refractory periods (less than 380 and less than 500 ms), and absence of demonstrable dual AV nodal pathways, we found that conduction curves (at sinus rhythm or longest paced cycle length) can be described by an exponential equation of the form delta = Ae-Bx. In this equation, delta is the increase in AV nodal conduction time of an extrastimulus compared to that of a regular beat and x is extrastimulus interval. The natural logarithm of this equation is linear in the semilogarithmic plane, thus permitting the constants A and B to be easily determined by a least-squares regression analysis with a hand calculator.

Adult↗

Electrophysiological and clinical observations in patients with alternating bundle branch block.

Electrophysiological studies (His bundle recordings and atrial stimulation) were performed in nine patients who manifested periods of both right and left bundle branch block (RBBB and LBBB). In seven of the patients, alternating bundle branch block appeared to reflect intermittent or chronic bundle branch block superimposed on incomplete (but electrocardiographically complete) block of the contralateral bundle branch. In three of these seven, shift from one bundle branch block pattern to the other was associated with reproducible change in H-V (mean change 30 msec), and could be induced by alteration of cardiac rate with carotid massage, coupled atrial stimulation, and rapid atrial pacing. In one of the seven, RBBB with a P-R of 0.20 seconds preceded chronic LBBB with a P-R of 0.24 seconds, implying that RBBB had been incomplete. In three of the seven, although a definite mechanism of alternation could not be demonstrated, transient contralateral bundle branch block occurred superimposed on chronic ipsilateral bundle branch block, implying that the ipsilateral block was incomplete. Two patients manifested periods of narrow QRS, LBBB, RBBB, and paroxysmal A-V block. Based upon pathological data (one case), this pattern appeared to reflect a lesion involving the distal His bundle and proximal bundle branches. In the total group of patients, clinical course was primarily determined by the severity of heart disease and not by occurrence of A-V block. The conduction defect in the majority of patients was surprisingly benign.

Adult↗

Prospective observations in patients with chronic bundle branch block and marked H-V prolongation.

Eighteen of 388 patients with chronic bundle branch block, studied electrophysiologically and followed prospectively, had H-V intervals of 80 msec or greater. Five patients were functional class I, five class II, seven class III, and one class IV. Follow-up ranged from 103 to 1919 days (mean 711 +/- 118). Three patients needed permanent pacing for the following indications: sino-atrial block, sinus bradycardia post-cardiac surgery, and 2 degrees block distal to the His bundle. Six patients died, three suddenly, and three nonsudden. The five initially asymptomatic patients are alive and without pacemakers (mean follow-up 732 +/- 139 days). Although marked H-V prolongation was associated with high morbidity and mortality in this small series, this was only in patients with symptomatic heart disease. Asymptomatic patients (five patients) had a benign clinical course. Prophylactic pacing would probably not modify clinical course in the former group, and is probably not indicated in the latter group. Longer follow-up will be needed for definitive prognostication.

Adult↗