Corrected Sinus Node Recovery Time Research Articles

Clinical efficacy and electrophysiology of oral propafenone for ventricular tachycardia

Sixteen patients with ventricular tachycardia (VT) or nonfatal cardiac arrest were treated with propafenone (P), 900 mg/day. Electrophysiologic studies were performed before and during therapy with P. All patients had inducible sustained VT at the baseline study. During P therapy, VT was not inducible in 1 patient, was unsustained in 1 and was harder to induce in 2 patients. P increased the cycle length of VT from 307 ± 67 to 382 ± 107 ms. Five patients began outpatient therapy with P, including 2 in whom VT was slowed to < 125 beats/min. Two are arrhythmia-free during follow-up of 2 and 8 P significantly increased intraatrial conauction time (from 44 ± 12 to 72 ± 22 ms), AH interval (from 115 ± 36 to 152 ± 45 ms), HV interval (from 55 ± 18 to 92 ± 42 ms), QRS duration (from 140 ± 36 to 180 ± 48 ms) and QT interval (from 402 ± 30 to 459 ± 60 ms). P increased atrial (from 247 ± 36 to 288 ± 38 ms) and ventricular (from 249 ± 20 to 277 ± 32 ms) effective refractory periods, Sinus cycle length did not change, but the corrected sinus node recovery time increased (from 162 ± 85 to 821 ± 1,607 ms). P aggravated arrhythmias in 4 patients. The plasma P concentration, measured either at the time of electrophysiologic studies or when therapy was discontinued, was 753 ± 428 ng/ml. P suppressed ventricular ectopic beats in 33 % and increased them in 1 patient. P has antimonths. arrhythmic activity against VT similar to that of other antiarrhythmic drugs and has potential for serious adverse effects in some patients.

Reproducibility of electrophysiological parameters of sinus node following autonomic blockade

We investigated the reproducibility of sinus node cycle length (SCL), corrected sinus node recovery time (CSRT) and sino-atrial conduction time (SACT) during the control state and following autonomic blockade in 25 patients (mean age: 56.9 ± 13.8 years). Autonomic blockade was induced by i.v. administration of propranolol (0.2 mg/kg) and atropine (0.04 mg/kg). The electrophysiological study was repeated after 24 hr and the results were compared. The patients were divided into two groups: Group 1 (15) with normal and Group 2 (10) with abnormal intrinsic sinus node function. Following autonomic blockade in Group 1 the daily variations in SCL, CSRT and SACT were very slight whereas in Group 2 there was far greater variability in these parameters. However, in the latter group there were no patients who changed their status from prolonged to normal intrinsic CSRT on the second study, whereas SACT changed its status in 2 patients. In Group 1 the daily variations in sinus node parameters were much slighter following autonomic blockade than during the control state. In Group 2 the variations were very similar during control and following autonomic blockade. These data suggest that: (1) following autonomic blockade the reproducibility of sinus node parameters is very good in Group 1, whereas in Group 2 several patients show marked daily variations in sinus node parameters; (2) following autonomic blockade the sinus node electrophysiological parameters are meaningful in diagnosing an involvement of intrinsic sinus node function; and (3) in patients with abnormal sinus node parameters during control state, but with normal intrinsic sinus node function, the daily variations are mainly due to change in autonomic tone, whereas when the intrinsic sinus node function is abnormal, the day to day variations during control state appear due predominantly to intrinsic sinus node abnormalities.

Electrophysiological effects of prenalterol on the cardiac conduction system.

The electrophysiological effects of prenalterol, a new beta-receptor agonist, in a dose of 100 micrograms/kg body weight given intravenously for 5 min, were studied in 13 patients with signs of sinus node dysfunction and/or conduction defects within or distal to the atrioventricular (AV) node. In nine patients with signs of sinus node dysfunction a significant reduction was found in corrected sinus node recovery time, on an average by 1955 +/- 640 ms (-61%, P less than 0.05) and in atrial refractoriness, by 61 +/- 21 ms (-20%, P less than 0.05). Similar but insignificant changes were also seen in the four patients with normal sinus node function. In eight patients with AV nodal dysfunction, a significant increase was found in the Wenckebach point, by 51 +/- 10 b.p.m. (+52%. P less than 0.01) and a decrease in the AH interval, by 23 +/- 9 ms (-14%, P less than 0.05). AV nodal refractoriness tended to decrease by 115 +/- 58 ms (-24%, NS). Similar changes were found in the five patients with normal AV conduction. Heart rate increased in all 13 patients, on an average by 28 +/- 5 b.p.m. (+44%, P less than 0.001) and systolic blood pressure by 18 +/- 8 mmHg (+13% P less than 0.01). In conclusion, prenalterol increased sinus node automaticity and atrial and AV nodal conductivity, but did not improve infranodal conduction. Thus, the drug might be useful in the treatment of patients with sinus node dysfunction as well as in patients with spontaneous or induced atrioventricular conduction abnormalities.

Persistent sinus nodal electrograms during abnormally prolonged postpacing atrial pauses in sick sinus syndrome in humans: sinoatrial block vs overdrive suppression.

A transvenous electrode catheter technique was used for direct recording of bipolar sinus node electrograms during postpacing atrial pauses. Multiple repetitive local sinus node electrograms during atrial quiescence validate sinus node electrograms. Such atrial pauses with sinus node electrograms are due to sinoatrial block; atrial pauses without sinus node electrograms are due to overdrive suppression or improper recording. Eight consecutive patients were prospectively selected on the basis of a corrected sinus node recovery time greater than 1500 msec during diagnostic electrophysiologic evaluation. Six patients had atrial pauses with sinus node electrograms; three patterns of sinus node electrograms during atrial pauses were observed. We conclude that (1) sinus node electrogram recording is of value in understanding the mechanism underlying postpacing atrial pauses; (2) atrial pauses are usually (6/8) caused by sinoatrial block; (3) three patterns of sinus node electrograms are observed, thus making indirect interpretation unreliable.

Electrophysiologic and antiarrhythmic effects of oral flecainide in patients with inducible ventricular tachycardia

Flecainide has demonstrated unsurpassed antiarrhythmic activity in patients with stable ventricular arrhythmias, but its effects in those with ventricular tachycardia or fibrillation have not been evaluated. Electrophysiologic and hospital evaluation of oral flecainide therapy (150 to 200 mg every 12 hours for 4 to 6 days) was performed in 15 patients with clinically documented ventricular tachyarrhythmias treated unsuccessfully with an average of 3.7 (range 1 to 10) antiarrhythmic drugs. Plasma flecainide concentrations averaged 769 ng/ml (range 377 to 1,152). Cardiac conduction times increased; AH interval changed by + 29%, HV interval by +42%, PR interval by +25%, QRS duration by +14% (all p < 0.01). Ventricular refractory period increased by 10% (p < 0.01) and corrected sinus node recovery time lengthened by 153 ms (p < 0.02). During baseline programmed stimulation, sustained ventricular tachycardia was induced in six patients and nonsustained tachycardia (from 6 beats to 30 seconds' duration) in nine patients using up to three premature ventricular stimuli. Flecainide prevented tachycardia induction in 9 (60%) of 15 patients and improved response (marked increase in cycle length or difficulty of induction) in 2 (13%) of 15, for a 73% overall response. Cycle length of induced rhythms increased by 141 ms after drug administration in those with inducible responses. Antiarrhythmic response rate was higher in patients without coronary artery disease. Outpatient experience in 10 patients has been generally concordant with in-hospital evaluation at a median of 6.5 months. Flecainide has been well tolerated. Unexpected arrhythmias have included exercise-initiated tachycardia in one patient and slow, hemodynamically stable tachycardia (110 beats/min) in another patient. Oral flecainide is an important antiarrhythmic agent for the management of inducible ventricular tachyarrhythmias. Cardiac conduction times and ventricular refractoriness increase; favorable responses to programmed stimulation are frequent and generally predict outpatient safety and efficacy.

Electrophysiologic effects of intravenous timolol

We evaluated the electrophysiologic effects and dose response of the long-acting beta-blocking drug timolol given intravenously to 12 patients during intracardiac electrophysiologic study. Electrophysiologic parameters were measured during control and immediately, 30 minutes, and 48 hours following infusion. Significant changes in electrophysiologic parameters were only observed in the five patients (Group B) who received 0.05 mg/kg and not in the seven patients who received 0.02 mg/kg (Group A). In Group B patients immediately after timolol infusion sinus cycle length increased from 840 ± 254 msec to 1048 ± 63 msec ( P<0.01), A-H interval during normal sinus rhythm increased from 94 ± 42 msec to 101 ± 45 msec ( P<0.05), paced cycle length to A-V nodal Wenckebach increased from 370 ± 45 msec to 430 ± 76 msec ( P<0.05), and A-V nodal effective refractory period increased from 284 ± 63 msec to 360 ± 83 msec ( P<0.01). Significant increases in these electrophysiologic parameters were also noted at 30 minutes following timolol infusion. Other conduction times, atrial and ventricular refractory periods, and corrected sinus node recovery time were unaltered by timolol. All electrophysiologic parameters returned to control in 48 hours. No adverse effects were observed. We conclude that intravenous timolol in doses of 0.05 mg/kg significantly increases sinus cycle length and prolongs A-V nodal conduction and refractoriness, demonstrates peak effects immediately after intravenous administration, and is well tolerated.

Temporary atrial electrodes for diagnosis &amp; treatment of post operative arrhythmias

In a prospective study, the utility of atrial epicardial wire electrodes in the diagnosis and treatment of postoperative cardiac arrhythmias was evaluated. Atrial electrograms were recorded in 50 patients who underwent open heart surgery. In 9 patients, the atrial electrograms provided diagnostic information during 19 episodes of arrhythmias where the surface electrocardiogram was inconclusive. In 11 patients atrial electrograms provided accurate confirmation of the nature of the arrhythmia as suggested by the surface electrograms during 17 episodes of arrhythmias. Atrial pacing was used to effectively treat abnormalities of rhythm or conduction on 23 occasions. The epicardial wire electrodes were also utilised to evaluate sinus node functions at the bed side. Six patients had prolonged sinus and corrected sinus node recovery times (snrt, csnrt). Three of these also had prolongation of sinoatrial conduction time (sact). These parameters normalised in all within 2–3 weeks. Five of the six patients with sinus node dysfunction experienced significant post-operative arrhythmias. Their post-operative stay was also significantly prolonged till their sinus node function normalised. Thus atrial epicardial wires provide a simple, safe bedside technique for the accurate diagnosis and successful management of early postoperative arrhythmias following open heart surgery and also aid in the prognostic evaluation of patients susceptible to arrhythmias based on electrophysiologic evaluation of their sinus node functions.

Indications for Permanent Pacemakers in Young Adults

The sick sinus syndrome has become the most common indication for permanent pacemaker implantation. 1 In a recent review of 50 patients with the sick sinus syndrome treated with pacemaker insertion, the mean age of the group was 71 years. 2 There are occasional reports of the sick sinus syndrome in young adults. However, many of the reported cases involve postoperative congenital heart disease.3,4 Recently Kay and his group5reported a series of 18 cases of young adults who required pacemakers. Twelve had the sick sinus syndrome and served as the basis of their report. Electrophysiologic studies were performed in only 5 of their 12 cases, and the authors stressed that the corrected sinus node recovery time was normal in their 5 patients. We routinely perform electrophysiologic studies in all patients being considered for pacemaker implantations. We therefore reviewed our experience over 8 years with young adults who required permanent pacemaker insertions.

Diurnal changes and reproducibility of corrected sinus node recovery time.

Corrected sinus node recovery time (CSRT) has been found unreliable in identifying all cases of sick sinus syndrome. Since other factors than sinus node dysfunction might add to the pathologic significance of the CSRT, we assessed it in 15 patients (nine group I patients with "prolonged" CSRT max = 3,196 + 2,740 msec and six group II patients with "short" CSRT max = 367 + 79 msec) at 0800, 1100, 1400, 1700, 2000, and 2300 hours with atrial overdrive stimulation rates (AST) of 90, 110, 140, 170, and 200 bpm on three consecutive days using a loop-mounted stable atrial electrode. Only with AST greater than or equal to 140 beats per minute (bpm) did all CSRTI values prove prolonged (greater than or equal to 560 msec). CSRTI values at corresponding time intervals were reproducible with AST greater than or equal to 140 bpm (day 1 vs 2 vs 3, P greater than .05), but not at AST 90 bpm and 110 bpm (P less than .05); CSRTII results, however, varied from day to day (less than .05) due to less scatter of single results. CSRTI results increased progressively with AST 90, 110, and 140 bpm from 301 + 256 msec by 60% for each pacing rate up to 785 + 848 msec. With AST greater than or equal to 140 bpm, the pattern of CSRT changes was inconsistent; this was also reflected by the distribution of the mean maxima of CSRTI: For 0800 hours at AST 140 bpm = 822 + 937 msec; for 1100 hours at AST 200 bpm = 824 + 1446 msec; for 1400 hours at AST 140 bpm = 780 + 814 msec; for 1700 hours at AST 170 bpm = 1,099 + 1,008 msec; for 2000 hours at AST 200 bpm = 1,156 + 1,280 msec; and for 2300 hours at AST 170 bpm = 1,021 + 1,102 msec. We conclude therefore that the optimal diagnostic yield for sick sinus syndrome testing is influenced by the time of the day and the AST used for CSRT testing.

Effects of intravenous diltiazem on sinus node function and atrioventricular conduction in patients.

We studied the electrophysiologic effects of injectable diltiazem (dosage: bolus of 0.15 mg/kg, maintenance infusion of 0.3 mg/kg/h for 20 min) on sinus node function and atrioventricular function in 33 patients (22 men and 11 women, mean age 63.6 +/- 15.8 years). Seventeen patients had an electrophysiological exploration considered as normal, eight had sinus node dysfunction (corrected sinus recovery time greater than 525 ms), and eight had AV nodal block (PH greater than 160 ms and/or a Wenckebach point less than 125/min). Effects of the drug were assessed 20 min after the beginning of the infusion, which was continued until the end of examination. In normal subjects diltiazem lengthened corrected sinus node recovery time (305 +/- 115 ms leads to 451 +/- 283 ms) and slightly depressed AV nodal conduction (Wenckebach point: 163 +/- 23 leads to 147 +/- 25). In patients with sinus node dysfunction diltiazem provoked a bradycardia without significant changes in corrected sinus node recovery time or in estimated atrio-sino-atrial conduction time. In patients with AV nodal block diltiazem provoked a lowering of the Wenckebach point (137 +/- 47 leads to 122 +/- 38). There was no effect on hissian or infrahissian conduction, even when this was abnormal in the basal state. These data suggest that diltiazem must be utilized with caution in patients with sinus node dysfunction and AV nodal block.

The direct electrophysiologic effects of disopyramide phosphate in the transplanted human heart.

To evaluate the direct electrophysiologic effects of i.v. disopyramide phosphate and to differentiate these effects from its autonomically mediated actions, we administered the drug (2 mg/kg over 5 minutes) during electrophysiologic study to eight cardiac transplant recipients who had documented functional cardiac denervation. After disopyramide, the cycle length of the denervated donor right atrium increased from 626 +/- 129 to 716 +/- 148 msec (mean +/- SD, p less than 0.001), whereas that of the innervated recipient atrium decreased from 846 +/- 195 to 659 +/- 99 msec (p less than 0.02). There were small increases in both the sinus node recovery time (1128 +/- 616 to 1198 +/- 592 msec, p less than 0.05) and corrected sinus node recovery time (440 +/- 418 to 489 +/- 409 msec, p less than 0.02) of the donor atrium, whereas the recovery times of the recipient atrium shortened (sinus node recovery time, 1298 +/- 218 to 1218 +/- 196 msec; corrected sinus node recovery time, 464 +/- 108 to 410 +/- 115 msec). Disopyramide markedly prolonged all conduction intervals. The PA interval increased from 47 +/- 16 to 54 +/- 17 msec (p less than 0.01), the AH interval from 55 +/- 12 to 78 +/- 12 msec (p less than 0.001), the HV interval from 38 +/- 9 to 58 +/- 13 msec (p less than 0.001), the QRS duration from 93 +/- 18 to 129 +/- 34 msec (p less than 0.001) and the QT interval from 339 +/- 23 to 403 +/- 39 msec (p less than 0.001). There was no significant change in the effective refractory period of the atrium, ventricular or atrioventricular node. The functional refractory period of the atrioventricular node increased from 369 +/- 34 to 395 +/- 31 msec (p less than 0.001). The electrophysiologic effects of disopyramide in the denervated heart are markedly depressant. In the innervated normal heart, the majority of these effects are counteracted by the drug's autonomically mediated anticholinergic actions.

Postoperative hemodynamic and electrophysiological evaluation of the Senning procedure.

To determine efficacy of the Senning procedure for correction of transposition of the great arteries we performed detailed hemodynamic and electrophysiological studies in 6 consecutive children operated upon at 5-18 months of age. Cardiac catheterizations were performed 10-19 months following surgery. All patients were asymptomatic on no medication. Hemodynamic studies demonstrated no evidence of pulmonary venous obstruction, pulmonary hypertension, or left ventricular outflow tract obstruction. 1 patient had mild upper baffle limb obstruction. Angiography demonstrated tricuspid insufficiency in 2 patients and a small atrial level shunt in 1. Ambulatory electrocardiographic monitoring in 5 of 6 patients revealed multiple premature ventricular contractions in 1. Invasive electrophysiological studies for sinus node function were normal. Corrected sinus node recovery time was 36-348 ms while total sinoatrial conduction time, determined in 4 patients, ranged between 83 and 128 ms. At our institution the Senning procedure has a low incidence of residual hemodynamic or electrophysiological abnormalities. Detailed postoperative evaluation is necessary to determine extent of residual problems.

Sinus node function in first three weeks after cardiac transplantation.

Donor sinus node function was studied in 10 patients from day 4 to day 24 after cardiac transplantation. Cycle length, atrial arrhythmias, corrected sinus node recovery time, and estimated sinoatrial conduction time were recorded daily. Five patients had at least two sets of results suggesting sinus node dysfunction (group A) while five patients had no such abnormalities (group B). The prognosis in group A was poor, with four of the five patients dying within four months of the operation; one unexpected death from arrhythmias was recorded by ambulatory electrocardiographic monitoring. All five patients in group B survived for at least eight months. In nine patients sinus node function varied from day to day, with corrected sinus node recovery time reaching a peak at 11 to 18 days after operation. The longest corrected sinus node recovery time was 11 160 ms. Neither the differences between the patients, nor the day to day variation, could be explained solely by the degree of rejection as assessed by biopsy or by the ischaemia time of the heart during procurement. Sinus node dysfunction soon after transplantation is associated with a poorer prognosis and might be the terminal event in some cases.

The cellular electrophysiologic mechanism of the dual actions of disopyramide on rabbit sinus node function.

To determine the contribution of disopyramide's suggested opposing direct depressant and indirect acceleratory actions on sinus node function, we studied the effects of disopyramide, 1 x 10(-7) to 1 x 10(-4) M, on isolated rabbit sinus node preparations using standard microelectrode techniques. Transmembrane potentials were recorded simultaneously from the sinus node and adjoining crista terminalis area. Disopyramide, as much as 1 x 10(-5) M, had no effects on the sinus cycle length. At a concentration of 1 x 10(-4) M, sinus cycle length was significantly prolonged due to prolongation of the sinus nodal action potential duration. During cholinergic blockade with atropine, 1 x 10(-6) M, disopyramide, 1 x 10(-7) to 1 x 10(-4) M, significantly prolonged sinus cycle length as a result of a prolongation of the sinus nodal action potential duration and a decrease of the slope of phase 4 depolarization. During cholinergic stimulation with carbamyl choline, 1 x 10(-9) M, disopyramide, 1 x 10(-7) to 1 x 10(-6) M, tended to reverse carbamyl choline-induced prolongation of the sinus cycle length (NS). This acceleratory action of disopyramide was caused by a significant increase of the slope of phase 4 depolarization. Disopyramide, 1 x 10(-7) to 1 x 10(-4) M, had no significant effects on corrected sinus node recovery time or on sinoatrial conduction time under any conditions studied. We conclude that disopyramide has a direct depressant action on normal sinus node cells at the upper therapeutic and toxic levels, which is enhanced during cholinergic blockade, and that disopyramide's acceleratory action appears only at much lower concentrations and only during cholinergic stimulation.

Electrophysiologic effects of flecainide acetate in patients with sinus nodal dysfunction

Flecainide acetate (R818) is a new antiarrhythmic agent for oral and intravenous use; it has predominantly class I properties and a long plasma half-life. Electrophysiologic effects were evaluated in 11 patients with sinus nodal dysfunction before administration of flecainide acetate and 15 to 60 minutes after intravenous administration of 1.5 mg/kg body weight of flecainide acetate given over 15 minutes. In 8 of 11 patients the maximal sinus nodal recovery time increased after flecainide acetate. However, the mean maximal sinus nodal recovery time was not statistically significantly increased from 1,929 ± 184 (mean ± standard error of the mean [SEM]) to 2,770 ± 500 ms (p <0.10). The corrected sinus nodal recovery time increased from 875 ± 181 before to 1,727 ± 507 ms after administration of flecainide acetate (p <0.05). The sinus cycle length and sinoatrial conduction time were not significantly changed. Flecainide acetate induced a marked prolongation of the H-V interval (from 41 ± 3 to 52 ± 4 ms [p <0.01]) as well as a significant increase in the A-H interval, QRS duration, and QT 100 interval. The effective and functional refractory periods of the atria increased by 12% (p <0.01) and 11% (p <0.01), respectively. The atrioventricular (AV) nodal functional refractory period increased significantly by 7% (p <0.01), whereas the 9% prolongation of the effective refractory period was not statistically significant. No side effects were observed. It is concluded that flecainide acetate prolongs atrial and ventricular conduction and refractoriness, and thus appears to be a potent antiarrhythmic agent. However, the sinus nodal function is depressed, and thus caution is advised in the use of flecainide acetate in patients with sinus nodal dysfunction.

Serial Electrophysiologic Effects of Bretylium in Man and Their Correlation with Plasma Concentrations

The serial electrophysiologic effects of bretylium were studied in 10 patients undergoing cardiac catheterization before giving the drug, at the end of bretylium tosylate-loading infusion (5 mg/kg/15 min), and after 1 h of intravenous drug maintenance (1.5 mg/min). Mean blood pressure increased during drug loading from 93.6 +/- 10.9 mm Hg to 121.1 +/- 16.2 mm Hg (p less than 0.01, t = 15 min) but returned toward control (100.9 +/- 18.7 mm Hg, p = NS) during drug maintenance (t = 75 min). Small changes in PR, QRS, QTc, AH, and HV intervals during spontaneous and paced rhythms were not significant. Comparison of the control electrophysiologic study with early and late postdrug studies showed no significant changes in corrected sinus node recovery times and in Wenckebach cycle lengths, but small decreases in refractory periods occurred. After drug loading, decreases in mean effective refractory periods of atrium, AV node, and right ventricle of 12, 2, and 16 ms, respectively, occurred (p = NS); during drug maintenance (t = 75 min), these refractory periods had decreased with respect to control by 21, 36, and 13 ms, respectively (p less than 0.05, 0.05, and 0.01). Functional refractory period of the AV node decreased at 75 min by 31 ms (p less than 0.01). The observed shortening of refractory periods contrasts with the direct effects of bretylium in isolated ventricular muscle and Purkinje fibers, which consist of prolongation of effective refractory periods and action potential duration. Thus, indirect (adrenergic) effects may be more important to overall clinical electrophysiologic actions not only acutely during loading but also during at least the first 60-90 min of maintenance therapy, which spans the expected time of initial clinical antifibrillatory response.

Electrophysiologic effects of chronic amiodarone therapy in patients with ventricular arrhythmias

Detailed electrophysiologic studies were performed in nine patients with chronic refractory ventricular arrhythmias before and after 7 to 20 weeks (mean 11 weeks) of amiodarone therapy. The amiodarone dose at the time of the repeat study ranged from 400 to 800 mg/day. The drug reduced the sinus rate ( p < 0.001) and prolonged the sinoatrial conduction time ( p < 0.05) with some prolongation of the corrected sinus node recovery time. Intra-atrial conduction was slightly prolonged both in sinus rhythm and during atrial pacing. Anterograde conduction through the AV node was significantly prolonged both in sinus rhythm ( p = 0.001) and during atrial pacing ( p < 0.005), and Wenckebach AV block was seen at significantly lower atrial pacing rates after the drug ( p < 0.005). The HV interval was prolonged both in sinus rhythm ( p < 0.05) and during atrial pacing ( p = 0.001), and so was the QRS width during atrial pacing ( p < 0.05) and the QT interval in sinus rhythm ( p < 0.005) and during atrial pacing ( p < 0.005). Significant prolongation of the refractory periods in the atrium, AV node, and ventricular muscle were also seen following the drug. We concluded that the significant electrophysiologic effects of this drug throughout the heart during chronic oral use attest to its clinical effectiveness in patients with atrial and ventricular arrhythmias. With due care and despite its effects on the HV interval and QRS width, it can be used in patients with intraventricular conduction defects complicating severe organic heart disease.

Electrophysiological effects of glucose-insulin-potassium on sinus node function in patients with and without sinus node dysfunction.

The electrophysiological effects of glucose (100 g)-insulin (20 U)-potassium (10 mmol X litre-1) infusion (GIK) on three parameters of sinus node function were studied in 14 control subjects (mean age 53 +/- 14 yr) and 11 patients (mean age 50 +/- 17 yr) with sinus node dysfunction (SND). In a first series of experiments the response to GIK was examined in nine control and 11 SND patients. Following GIK, the mean spontaneous cycle length decreased by 17% (671 to 560 ms; P less than 0.01) in the control group and by 33% (1066 to 715 ms; P less than 0.001) in the SND patients; this difference between both groups was statistically significant (P less than 0.01). In the control group mean corrected sinus node recovery time (CRST) and calculated sinoatrial conduction time (SACT; n = 6) were not significantly altered after GIK. In SND patients GIK decreased the mean value of CSRT by 40% (693 to 416 ms; P less than 0.05) and of calculated SACT (n = 6) by 27% (130 to 95 ms; P less than 0.05); prolonged secondary pauses following termination of rapid atrial pacing in SND patients were also shortened. In a second series of experiments, mannitol (100 g, iv) was administered in five control patients but had no significant effect on the electrophysiological parameters tested. Plasma levels of glucose were significantly increased, by 500% (P less than 0.01), after GIK; plasma potassium and sodium concentrations decreased by 7 and 5% (P less than 0.05). The results indicate that GIK had a beneficial effect on sinus node dysfunction.

Electrophysiologic effects of propranolol on sinus node function in children

Little is known regarding the effects of propranolol (P) on sinus node function in children. In this study, corrected sinus node recovery time (CSNRT) and estimated sinoartial conduction time (SACT) were measured in 10 children (ages 3 to 16 years; mean 8.3 years) without clinical evidence of sinus node dysfunction before and after intravenous P. The spontaneous sinus cycle length (SCL) increased after P(0.1 mg/kg) in all patients. Mean SCL increased 13.4% from 635 ± 200 msec (± SD) to 720 ± 202 msec ( p < 0.01). Maximum CSNRT increased in nine patients after P and mean CSNRT increased 63% from 203 ± 61 msec to 330 ± 190 msec ( p < 0.05). SACT changed in a random fashion after P. Mean SACT did not change significantly. We conclude that P significantly suppresses sinus node automaticity in children with normal sinus node function but has little or no effect on sinoatrial conduction.

Comparative electrophysiologic effects of digoxin in the nonsedated chronically instrumented puppy

The electrophysiologic effects of acute but not chronic administration of cardiac glycosides have been studied. Nineteen chronically instrumented beagle puppies underwent 2-week courses of parenteral digoxin in three dosage regimens: six received digoxin, 0.04 mg/kg/day; seven received 0.03 mg/kg/day; and 11 received 0.02 mg/kg/day. Mean serum concentrations were 3.2 ng/ml, 1.3 ng/ml, and 1.0 ng/ml, respectively. Significant electrophysiologic effects on sinus node function were produced only by the highest dose. Atrioventricular node conduction was significantly delayed among animals receiving both high and middle dosages. All three regimens significantly effected atrioventricular specialized conduction system functional refractory periods. Atropine decreased digoxin-induced effects on all measured parameters but totally eliminated the digoxin effect on the corrected sinus node recovery time.