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Biomedical subjects

R C Dhingra

Publications and source records attributed to R C Dhingra.

At least 19 recordsLinked to original sources
PubMed1979

Incidence and site of atrioventricular block in patients with chronic bifascicular block.

Four hundred fifty-two patients with chronic bifascicular block and initially intact atrioventricular (AV) conduction were detected, studied, and prospectively followed between January 1970 and March 1978. There were 360 males and 92 females, ages 18--93 years (mean +/- SD, 62 +/- 15 years). Follow-up ranged from 29-2804 days (mean 1066 +/- 97 days). AV block (2 degrees or 3 degrees) developed in 29 patients, nine with apparent cause and spontaneously in 20. Cumulative annual incidence of all heart block for 1--5 years was, respectively, 4%, 5.9%, 8.7%, 10.1% and 11.3%, and for spontaneous block was 2%, 3.1%, 5.2%, 6.7%, and 7.1%. Sites of spontaneous block were probably or definitely AV nodal in ten, His bundle in one, and trifascicular in nine. Cumulative incidence of AV block in surviving bifascicular block patients is 11% at 5 years, with 7% reflecting spontaneous block. The probable or definite site of AV block varies and is trifascicular in less than half of the patients. The small incidence of trifascicular block probably explains the difficulty in predicting this complication with electrophysiological studies.

Adolescent↗
PubMed1979

Effects of atropine on induction and maintenance of atrioventricular nodal reentrant tachycardia.

The electrophysiologic effects of atropine were studied in 14 patients with dual atrioventricular (AV) nodal pathways and recurrent paroxysmal supraventricular tachycardia (PSVT). During PSVT, all patients used a slow pathway (SP) for antegrade and fast pathway (FP) for retrograde conduction. Atropine enhanced both SP antegrade and FP retrograde conduction, shown by a decrease in paced cycle lengths (atrial and ventricular) producing AV and ventriculoatrial block. Five patients had induction of sustained PSVT before and after atropine. Seven patients failed to induce or sustain PSVT before atropine, because of retrograde FP refractoriness. All seven had induction of sustained PSVT after atropine due to facilitation of FP retrograde conduction. Two patients had only single atrial echoes before atropine, reflecting SP antegrade refractoriness. After atropine, sustained PSVT was inducible in one, and nonsustained in the other, PSVT cycle length could be compared in seven patients before and after atropine and decreased from 383 +/- 25 to 336 +/- 17 (p less than 0.05). Thus, in patients with dual AV nodal pathways, atropine facilitated SP antegrade and FP retrograde conduction, shortened cycle length of PSVT and potentiated ability to sustain PSVT.

Adult↗
PubMed1979

Significance of chronic bifascicular block without apparent organic heart disease.

Eighty-six of 452 patients (19%) with chronic bifascicular block were found to have no clinically apparent associated organic heart disease (OHD) and were defined as having primary conduction disease (PCD). Comparison of patients with PCD and OHD revealed a significantly lower incidence of the following clinical variables in the PCD patients (p less than 0.001): exertional angina, dyspnea, congestive heart failure, cardiomegaly, functional class I (all by study design), left bundle branch block and premature ventricular contractions. Both mean AH and HV intervals were significantly shorter in patients with PCD (p less than 0.01). The incidence of HV prolongation was 21% in PCD and 41% in OHD patients (p less than 0.001). All patients were prospectively followed for 21-2998 days with a mean +/- SEM of 1209 +/- 66 days for PCD and 1172 +/- 36 days for OHD. Atrioventricular (AV) block developed in three patients from the PCD group and 26 from the OHD group (NS), with spontaneous block occurring in one (1%) PCD patient and 19 (5%) OHD patients (p less than 0.05). Annual mortality due to sudden death as well as total cardiovascular mortality (including sudden death) for the 5-year follow-up was significantly lower in patients with PCD. Patients with PCD have significantly lower incidence of electrophysiologic abnormalities and subsequent spontaneous AV block as well as cardiovascular and sudden death mortality. The diagnosis of PCD based on clinical criteria probably underestimates the presence of underlying OHD, as suggested by a small but definite risk of cardiovascular mortality.

Adult↗
PubMed1979

Concealed nonparoxysmal junctional tachycardia.

Electrophysiologic studies were performed in a patient who had an apparently uncomplicated complete trifascicular block. His bundle recordings revealed atrioventricular dissociation with: 1) an atrial rate of 58 beats/min, 2) an idioventricular escape rate of 45 beats/min, and 3) nonparoxysmal junctional tachycardia (His bundle rhythm) at a rate of 65--85 beats/min. The latter arrhythmia was electrocardiographically silent, influencing neither atrial nor ventricular events. The arrhythmia probably reflected digitalis intoxication (digoxin level of 3.3 ng/ml). A repeat electrophysiologic study 4 days after digoxin was discontinued revealed complete trifascicular block (distal to H) with intact conduction between the atrium and the His bundle (AH of 150 msec). Thus, electrophysiologic study demonstrated an electrocardiographically silent but clinically relevant arrhythmia, suggesting that His bundle recording should be part of diagnostic study during temporary pacemaker implantation in patients with atrioventricular block.

Aged↗
PubMed1979

Significance of block distal to the His bundle induced by atrial pacing in patients with chronic bifascicular block.

Twenty-one of 496 (4%) patients with chronic bifascicular block, studied and followed prospectively, had block distal to the His bundle (BDH) induced by atrial pacing during initial electrophysiologic studies. In six, BDH was noted during pacing-induced atrioventricular (AV) nodal Wenckebach periods (at paced rates of 150--190 beats/min), with BDH in the short HH cycles after the AV nodal blocked P (lond cycle). The AH interval was normal in all six patients and HV was normal in four. None of the six patients has developed AV block during a mean follow-up of 5.33 +/- 0.48 years. In 15 patients, pacing-induced BDH was noted during intact AV nodal conduction (paced rate of 80--200 beats/min). The AH interval was prolonged in one, and HV was prolonged in 10 of the 15 patients. During a mean follow-up of 3.4 +/- 0.59 years, seven of these patients developed AV block, one had treadmill-provoked AV block, and two died suddenly (major morbid event in 10 of 15 patients). In conclusion, BDH induced by atrial pacing is an infrequent finding in patients with bifascicular block, and can be a functional as well as a pathologic response. The latter is associated with a high risk of major morbid events (AV block and sudden death).

Adolescent↗
PubMed1979

Chronic nonparoxysmal sinus tachycardia in otherwise healthy persons.

Seven patients had chronic, unexplained, nonparoxysmal sinus tachycardia. The clinical, electrocardiographic, and electrophysiologic characteristics of these cases are described. In each case electrocardiographic and electrophysiologic observations suggested that tachycardia was nonparoxysmal and due to increased automaticity of the sinus node (or of an automatic atrial focus located very near the sinus node). The mechanisms of increased sinus node automaticity in these patients were explored using drugs affecting the autonomic nervous system. In each patient these studies suggested a defect in either sympathetic or vagal nerve control of resting heart rate, with or without an abnormality of intrinsic heart rate. Data are also presented on baroreceptor reflex arc function in these patients.

Adolescent↗
PubMed1978

Significance of left axis deviation in patients with chronic left bundle branch block.

Forty-nine patients with chronic left bundle branch block and a normal frontal axis were compared with 53 patients with left bundle branch block and left axis deviation. The following clinical variables were more frequent (P less than 0.05) in patients with left axis deviation: greater age, exertional angina, congestive heart failure, cardiomegaly, cardiac functional class II to IV, coronary artery disease and presence of organic heart disease. Absence of organic heart disease (primary conduction disease) was seen only in patients with a normal axis. Patients with left axis deviation had longer (P less than 0.05) mean P-R, A-H and H-V intervals and atrial and atrioventricular (A-V) nodal effective refractory periods. All patients were prospectifely followed up for 30 to 2,271 days with a mean +/- standard error of the mean follo-up period of 538 +/- 72 for the group with a normal axis and 604 +/- 72 days for the group with left axis deviation (difference not significant). A-V block developed in three patients (6 percent) with left axis deviation and in none of those with a normal axis. The cumulative 4 year mortality rate for the entire group approached 75 percent. The patients with left axis deviation had greater cardiovascular mortality (P less than 0.05). In conclusion, among patients with left bundle branch block, those with left axis deviation have a greater incidence of myocardial dysfunction, more advanced conduction desease and greater cardiovascular mortality than those with a normal axis.

Bundle-Branch Block↗
PubMed1978

Electrophysiologic observations in a patient with bradycardia-dependent atrioventricular block.

In a patient with atrioventricular (A-V) block distal to the His bundle (H), 1:1 A-V conduction with right bundle branch block and H-V interval of 70 msec was established with atrial pacing at rates of 120 to 150/min, suggesting that the A-V block was bradycardia-dependent. Advanced second degree A-V block distal to the H deflection occurred with atrial pacing at 160/min after completion of A-V nodal Wenckebach periodicity proximal to the H deflection because of the long H-H encompassing the blocked P wave. Atrial extrastimulus testing coupled with sinus rhythm (with A-V block) demonstrated that critical H1-H2 intervals of less than 545 msec allowed conduction to the ventricles. The H2-V2 interval shortened progressively from 290 to 70 msec with shortening of these critical H1-H2 intervals. Atrial extrastimulus testing coupled with an atrial driven cycle lenght of 500 mesc (with intact A-V conduction) revealed block of the H2 deflection with an H1-H2 interval longer than 540 msec. In conclusion, at critical diastolic intervals, impulses were blocked, creating a state of decreased responsiveness. If a cycle length of subsequent impulses was shorter than the critical diastolic blocking interval, membrane responsiveness gradually improved and conduction resumed. If a cycle length of subsequent impulses was longer than the critical blocking diastolic interval, A-V block was sustained. Blocked impulses continually penetrated to the site of block and reset the state of membrane responsiveness.

Atrioventricular Node↗
PubMed1978

Electrophysiologic effects of lidocaine on sinus node and atrium in patients with and without sinoatrial dysfunction.

Electrophysiological studies were conducted in 13 patients with normal sinus node function and 14 with sinus node dysfunction before and after intravenous lidocaine. Mean +/- SEM sinus cycle length significantly shortened from 810 +/- 34.3 to 774 +/- 34.3 msec in patients with normal sinus node (P less than 0.001) and from 1061 +/- 67.6 to 1016 +/- 64.5 msec in patients with sinus node dysfunction (P less than 0.025) after lidocaine. Mean sinus recovery time was 1027 +/- 49.4 before and 1026 +/- 52.5 msec after lidocaine in patients with normal sinus node (NS) and 1269 +/- 97.7 before and 1170 +/- 73.8 msec after lidocaine in patients with sinus node dysfunction (P less than 0.05). Mean calculated sinoatrial conduction time was 87 +/- 9.5 before and 90 +/- 9.2 msec after lidocaine in patients with normal sinus node (NS) and 80 +/- 10.3 before and 96 +/- 10.2 msec after lidocaine in patients with sinus node dysfunction (P less than 0.001). Mean atrial effective and functional refractory periods were not significantly changed with lidocaine. Thus lidocaine shortened sinus cycle length in both groups, without affecting atrial refractoriness. Lidocaine appeared to depress perinodal tissue only in patients with sinus node dysfunction. The abbreviation of sinus recovery time in patients with sinus node dysfunction could reflect increased sinus automaticity and/or increased perinodal refractoriness, allowing entrance block to occur. This mechanism may explain why sinus arrest has been noted in some patients during lidocaine administration.

Adult↗
PubMed1977

Conduction system in a patient with Prinzmetal's angina and transient atrioventricular block.

His bundle recordings obtained during and between attacks of Prinzmetal's variant angina and transient atrioventricular (A-V) block were followed by a comprehensive serial section study of the conduction system in a 33 year old woman. Recordings between attacks showed normal A-H and H-V intervals. During an attack there was block proximal to the His bundle recording site. Pathologic studies revealed severe narrowing of the right coronary artery. Arteriolosclerosis of the heart was diffuse. Insignificant changes were found in the approaches to the A-V node and the A-V node itself. Major changes found in the left bundle branch had no counterpart in the electrocardiogram; the discordance in these findings is discussed.

Adolescent↗
PubMed1977

Atrial pacing at multiple sites in the Wolff-Parkinson-White syndrome.

Atrial pacing at multiple sites was used in an attempt to predict the site of pre-excitation in 5 patients with Wolff-Parkinson-White syndrome with 5 different anomalous pathway locations (right anterior, right posterior, septal, left posterior, and left lateral). At least 3 atrial pacing sites were tested in each patient. Pacing sites tested included high right atrium, low lateral right atrium, low septal right atrium, proximal coronary sinus, and distal coronary sinus. Atrial stimulation sites with shortest and longest stimulus-delta intervals could be identified in each patient, the shortest stimulus-delta interval in each case ranging from 60 to 80 ms. The difference between the shortest and longest stimulus-delta interval in each case ranged from 60 to 110 ms. It was suggested that the site with the shortest stimulus-delta interval corresponded to a site close to the atrial insertion of the anomalous pathway. This hypothesis was confirmed in all cases (3 with epicardial mapping and 2 with retrograde atrial activation data). In conclusion, atrial pacing at multiple sites is helpful in predicting the site of anterogradely conducting anomalous pathways, and appears particularly useful for differentiation of right posterior, left posterior, and septal pre-excitation.

Adolescent↗