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Biomedical subjects

N Shantha

Publications and source records attributed to N Shantha.

7 recordsLinked to original sources
PubMed1984

Effects of amiodarone on supraventricular tachycardia involving bypass tracts.

This study evaluates whether the electrophysiologic effects of i.v. amiodarone in patients with reentrant supraventricular tachycardia (SVT) can predict the efficacy of long-term oral therapy with this drug. The effects of oral and i.v. amiodarone were studied in 27 patients with SVT. In 14 the SVT circuit involved a concealed atrioventricular bypass for retrograde conduction (Group I), and in 13 a concealed atrio-His bypass (Group II). Intravenous amiodarone induced significant prolongation of the AH interval, the refractory periods of the atrium, atrioventricular node, His-Purkinje system and ventricular myocardium. The ventriculoatrial interval was slightly prolonged in Group I patients and did not change in Group II patients after i.v. administration of the drug. In both groups, the effective refractory period (ERP) of the concealed bypass was prolonged by i.v. amiodarone. During control state, SVT could be induced in all patients; after i.v. administration of the drug, SVT was presented in 6 patients in Group I and in 8 patients in Group II. In all cases, in which i.v. amiodarone prolonged the ERP of the concealed bypass to more than 350 ms, the drug always prevented SVT even when given orally. All but 2 patients--1 from Group I and 1 from Group II--remained asymptomatic after oral amiodarone. In the patient from Group I, SVT had been prevented by i.v. amiodarone, whereas in the patient from Group II SVT could not be induced by ventricular stimulation during the control state, but appeared after i.v. administration of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Clinical effects of digoxin on sinus node and atrioventricular node function after pharmacologic autonomic blockade.

The effects of digoxin on sinus node and atrioventricular (AV) node function were studied in 18 patients (mean age 53.6 years) with normal intrinsic heart rates. Electrophysiologic testing was performed both during basal state and after autonomic blockade with propranolol and atropine. Full digitalization was achieved by intravenous administration of digoxin (0.02 mg/kg) given in three divided doses over a 24-hour period. The following day, after a basal recording, autonomic blockade was again induced and the study was repeated. During basal state, digoxin significantly prolonged the sinus cycle length (SCL) (p less than 0.01) and the AH interval (p less than 0.01). However, when the intrinsic sinus node functions were compared (i.e., the values obtained after autonomic blockade), digoxin did not produce significant changes in intrinsic SCL, corrected sinus node recovery time, and sinoatrial conduction time. No significant changes were noted even in the intrinsic AH interval and AV nodal refractory periods. These findings suggest that: (1) intravenous administration of digoxin in therapeutic doses does not produce any depression of the intrinsic functions of the sinus node and AV node; and (2) the depressant effects induced by digoxin during basal state appear to be mediated through the autonomic nervous system.

Adult↗
PubMed1979

Clinical electrophysiological effects of propranolol on normal sinus node function.

In 35 patients aged 18 to 69 years (mean 48) with clinical, electrocardiographic, or electrophysiological evidence of normal sinus node function, the effect of intravenous propranolol (0.1 mg/kg) was assessed on 3 indices of sinus node function. The drug significantly prolonged sinus node cycle length (12%), slightly prolonged the corrected sinus node recovery time (15%), and slightly but insignificantly lengthened sinuatrial conduction time. Propranolol may be administered safely in patients with normal sinus node function without the fear of producing severe sinus bradycardia, sinuatrial block, sinuatrial pauses, or prolonged sinus asystole, after spontaneous or stimulation-induced conversion of a tachycardia.

Adolescent↗
PubMed1978

A new method for measurement of sinoatrial conduction time.

This study describes a new method (NM) for estimation of sinoatrial conduction time (SACT), which utilizes constant atrial pacing (AP) instead of the premature atrial beats (PABs) used in the method reported in 1973 by Strauss et al. The SACTs were obtained by both methods in 20 patients. The SACT by the Strauss method (SM) was calculated as A2A3 minus A1A1. The NM consists of high right AP for a train of eight consecutive beats at rates less than or equal to 10 beats/min faster than the sinus rhythm. The interval between the last paced atrial electrogram (Ap) and the first escape atrial electrogram (A) of sinus origin (Ap-A) was measured along with several post pacing sinus cycles. The SACT by the NM was calculated as follows: SACT = Ap-A minus A1A1. The effect of AP at higher rates was also analyzed. In two patients, the SACT with the SM could not be defined, as all the A2A3 intervals were fully compensatory; with the NM the SACT was 217 and 320 msec. In the remaining 18 patients the SACT was obtainable by both methods. With SM, the SACT ranged 105--452 msec (mean 219 +/- 102 SD) and with the NM it was 85--492 msec (mean 201 +/- 112 SD), and the difference was statistically significant (P = 0.0162). The coefficient of correlation between the two methods was r = 0.97. During AP at faster rates, a rate related increment in Ap-A intervals and also post pacing sinus cycles was noted. This study describes a new and simple method for measurement of SACT in man.

Adult↗
PubMed1975

P-A interval: lack of clinical, electrocardiographic and electrophysiologic correlations.

P-A interval is measured from the onset of the P wave to the onset of the low right atrial electrogram during His bundle recording. The significance of this interval was evaluated in 214 patients with intact A-V conduction and bundle branch block. One hundred fifty-eight patients had normal P-A (NPA) 27 +/- 9, mean +/- SD, and 56 had prolonged P-A (PPA). The NPA and PPA patients were similar (P greater than .10) in regard to sex, age, cardiac functional class, and P-R. PPA patients had significantly (P less than .05) greater P duration (mean +/- SEM, PPA vs NPA) 106 +/- 2 msec vs 100 +/- 1 msec), slower heart rates (72 +/- 2 vs 79 +/- 1), and longer sinus recovery times (1104 +/- 44 msec vs 980 +/- 38 msec). A-H was slightly shorter in PPA than in NPA patients suggesting that a systematic error in measruement of PA due to a relatively distal recording site may have been responsible for PA prolongation in some patients. Patients were prospectively followed for 16-56 months (mean 21.9 +/- 0.8 months). PPA was associated with only minor increase in P wave duration and decrease in sinus automaticity. PPA did not predict future occurrence of significant atrial dysrhythmia.

Arrhythmias, Cardiac↗