Overdrive Stimulation Research Articles

Determinants of Subsidiary Ventricular Pacemaker Suppression in Man

To investigate the relative contribution of the duration and rate of overdrive to subsidiary ventricular pacemaker suppression, in six patients with complete heart block after His-bundle ablation, ventricular overdrive stimulation studies were performed. The studies, which were spread over a mean follow-up period of 745 days, were carried out invasively with a temporary lead (one patient) as well as noninvasively with the implanted pacemakers and chest wall inhibition (five patients). The overdrive pacing rate was increased in steps of 10 beats/min, and the pacing duration was 15, 30, 60, 90, and 120 seconds at each level. A recovery period of 2 minutes was allowed after each overdrive stimulation. Incremental ventricular overdrive stimulation at increasing pacing durations consistently caused progressive suppression of ventricular impulse formation. Nonparametric variance analysis demonstrated a significant (P less than 0.0001) influence of both the pacing rate and duration on ventricular recovery time. Nonlinear regression showed an exponential increase in recovery time with incremental pacing rate and a biphasic increase in recovery time with incremental pacing duration. Beyond a pacing duration of 60 seconds ventricular impulse suppression was primarily dependent upon the pacing rate. A nonlinear regression model was applied to predict the number of beats required for return of the escape rhythm toward prepacing control values. The predicted maximum mean number of beats was 15.4 +/- 5.9 and independent of the rate and duration of pacing, although, the initial temporary instability of the escape rhythm was directly related to the degree of overdrive.

Trimetazidine inhibits Na +,K +-ATPase activity, and overdrive hyperpolarization in guinea-pig ventricular muscles

The effect of trimetazidine on Na +,K +ATPase activity or the Na +,K + pump was studied in guinea pig ventricular muscles with the use of biochemical and electrophysiological methods. The effect of trimetazidine on enzyme activity was compared with that in liver, jejunum and kidney obtained from the same species. Na +,K +-ATPase activity in the heart and liver was significantly and concentration dependently decreased by trimetazidine (above 1.5 × 10 −5 M). Even the highest concentration (1.5 × 10 −4 M) of trimetazidine failed to decrease the Na +,K +-ATPase activity in the jejunum and kidney. The membrane potential was recorded in the ventricular muscle with a microelectrode. The hyperpolarization which followed 1-min overdrive stimulation (3.3 Hz) was decreased by trimetazidine (1.5 × 10 −4 M). but the depolarization during the stimulation was not affected by this drug. Ouabain. a potent Na +,K + pump inhibitor, markedly decreased the overdrive hyperpolarization and increased the depolarization during the stimulation (10 −7, 5×10 −7, 10 −6 M). Therefore, the effect of trimetazidine and ouabain on the Na +,K + pump-mediated alteration in the resting potential is different, suggesting that trimetazidine has additional direct membrane effects, e.g. a decrease in K + conductance. In conclusion, trimetazidine inhibits Na +,K +-ATPase activity and thus the Na +,K + pump in the ventricular muscles but with an inhibitory effect about 300 times less than that of ouabain. Trimetazidine inhibited the Na +,K +-ATPase in the liver as well. but not that in jejunum and kidney.

The Effect of an Entrainment Protocol on Ouabain‐Induced Ventricular Tachycardia

Overdrive stimulation of reentrant ventricular tachycardias (VT) may result in entrainment and/or termination of these arrhythmias. We investigated whether surface ECG criteria of entrainment can also be observed in nonreentrant VT. For this purpose ouabain-induced tachycardias were used that are considered to be based on delayed afterdepolarizations. In nine conscious dogs, having surgically induced complete AV block, pacing was performed using trains of 20 stimuli from a site distant to the origin of the VT. The pacing intervals were shortened in steps of 5-10 msec, until complete capture from the pacing site or termination of the VT was obtained. During stimulation variable fusion was seen and complete capture of the ventricles from the pacing site occurred just after a slight decrease in pacing cycle length (20 +/- 10 msec). Overdrive stimulation resulted only in 1 out of 58 stimulation trains in termination of VT. Following stimulation it was observed that: (1) The length of the first postpacing interval was significantly longer (P less than 0.001) than both the mean prepacing VT cycle length and interstimulus interval; (2) A change in QRS configuration occurred after 57% of the stimulation trains; (3) The VT accelerated slightly in comparison to the prepacing rate (P less than 0.05); and (4) The length of the first postpacing interval and the mean R-R interval of the VT postpacing were directly related to the interstimulus interval (r = 0.82 and 0.97, respectively). In conclusion, overdrive stimulation of ouabain-induced arrhythmias did not result in entrainment or in termination of the tachycardia. Instead, other responses were seen that may be of help in differentiating between arrhythmias caused by delayed afterdepolarizations and reentry.

Treatment of Ventricular and Supraventricular Tachyarrhythmias by Transcutaneous Cardiac Pacing

The efficacy of noninvasive transcutaneous cardiac pacing (TCP) in the treatment of tachyarrhythmic events was tested in 24 patient: 14 with ventricular tachycardia, seven with supraventricular tachycardia and three with atrial flutter. Six (42.9%) ventricular tachycardias were interrupted: in two of the ten patients on whom underdrive pacing was attempted and in all four cases in which overdrive stimulation was possible. Five of the six supraventricular tachycardias utilizing an atrioventricular bypass tract were interrupted, while the TCP was unsuccessful on the only patient with atrioventricular nodal reentrant tachycardia. TCP failed to interrupt the arrhythmia in the three cases of atrial flutter. No clinically significant untoward effects (in particular tachycardia acceleration or ventricular fibrillation) were observed, except for a tolerable thumping sensation on the chest during pacing. In four patients, TCP effects on cardiac activation was evaluated by endocavitary recording: while the mean ventricular threshold was 70 mA, atrial capture was possible on only two patients at a current intensity of 140 and 150 mA. We consider our preliminary experience with TCP in the treatment of tachycardias encouraging. The technique was easily and rapidly usable and it was immediately successful in the majority of atrioventricular reentrant tachycardias and in a relevant percentage of ventricular tachycardias. In this latter setting TCP was mostly effective in the slower tachycardias where overdrive pacing was possible. A further experience with devices provided by higher pacing rates is warranted.

Suggestive evidence for inhibitory action of amiodarone on Na +, K +-pump activity in guinea pig heart

1. 1. Effects of amiodarone, a powerful antiarrhythmic agent, on Na +, K +-pump activity were examined on ventricular papillary muscle of guinea pig, by means of conventional microelectrode technique. 2. 2. The activity of Na +, K +-pump was measured by two methods. One of them was to measure the amplitudes of depolarization observed during overdrive stimulation (3.3 Hz) and of hyperpolarization observed after the overdrive stimulation (post-overdrive hyperpolarization), and the other, to measure the hyperpolarization observed following introduction of 10 mM K +, after exposure to K + free solution for a certain duration. 3. 3. Amiodarone significantly decreased the amplitude of depolarization during overdrive stimulation and the amplitude of post-overdrive hyperpolarization. 4. 4. In the latter method, the deactivation process of hyperpolarization recorded by the introduction of 10 mM K + following K + depletion slowed down by amiodarone. 5. 5. These findings suggest that amiodarone may inhibit, at least in part, the Na +, K +-pump activity in the ventricular muscle of guinea pig.

Transesophageal Programmed Atrial Pacing as a Method of Selecting Patients with Sick Sinus Syndrome for Permanent Atrial Pacing

Many recent studies have shown transesophageal programmed atrial pacing (TP) as a very practical, safe and convenient way for assessment of sinus node function and AV conduction. On the other hand, permanent atrial pacing is known to be superior to ventricular pacing due to arrhythmogenic and hemodynamic reasons. This is the reason why we decided to use TP as a method of choosing patients with sick sinus syndrome (SSS) for permanent atrial pacing. Sixty-three patients with symptomatic (58) and asymptomatic (5) SSS in a variety of clinical situations were examined in this way. The following electrophysiological features were examined: sinus cycle length, sinus node recovery time as well as corrected time, secondary pause after overdrive stimulation, sinoatrial conduction time, Wenckebach point, induction of supraventricular arrhythmias by S1, S2, S3 programmed stimulation and burst pacing. Patients with abnormal parameters were examined once more after intravenous atropine 0.2 mg/kg to evaluate parasympathetic component. Standard 12-lead ECG was performed in all, and Holter monitoring in most of patients. Twenty-six patients were candidates for permanent AAI pacing. Failures occurred in eight patients usually due to low P wave amplitude and electrode instability. Eighteen patients received AAI pacing systems: eight with brady-tachycardia syndrome, nine with bradyarrhythmia and one with sinoatrial block. In the follow-up of 5-28 months in one patient occurred high degree AV block (II degree) during digitalis therapy. Reduction of doses made this block disappear. Examination of Wenckebach point and possibility of inducation of supraventricular tachyarrhythmias in cases of atrial overexcitability are particularly useful in selecting patients for AAI pacing.

Subsidiary pacemaker function in complete heart block after His-bundle ablation.

To investigate the electrophysiological properties of ventricular impulse formation after His-bundle ablation in 11 patients, incremental ventricular overdrive stimulation studies were performed. The studies, which were spread over a follow-up period of up to 601 days, were carried out invasively with temporary leads as well as noninvasively with the implanted pacemakers and chest wall inhibition. The overdrive pacing rate was increased in steps of 10 beats/min, and the pacing duration was 2 minutes at each level. Ten out of 11 patients had a reliable ventricular escape rhythm; in the remaining patient, consistently no subsidiary pacemaker function was observed up to 10 seconds. In 83% of the studies, incremental ventricular overdrive stimulation caused progressive suppression of ventricular impulse formation with exponential increase in ventricular recovery time and progressive postrecovery subsidiary pacemaker depression. In the remaining 17%, ventricular recovery time showed a heterogeneous response to overdrive stimulation--as possible cause alterations in the sympathetic tone and limitations attributable to the method used are discussed. The results of this study demonstrate a rate-dependent overdrive suppression of subsidiary ventricular pacemaker tissue. This can be of clinical importance in patients with complete heart block and rate-adaptive pacemakers because sudden pacemaker failure or temporary pacemaker inhibition at high stimulation rates may cause Stokes-Adams attacks not reproducible at lower pacing rates.

Rate Dependent Depression of Subsidiary Ventricular Impulse Formation—Cause of Stokes‐Adams Attacks in a Patient with Rate Modulated Pacing

Following His bundle ablation and implantation of a rate adaptive pacemaker (Vitatron TX 911) a 52-year-old gentleman experienced several presyncopal attacks while driving a car. On examination pectoralis muscle contraction caused temporary pacemaker inhibition. Incremental overdrive stimulation demonstrated progressive depression idioventricular automaticity and was associated with similar symptoms following overdrive at high pacing rates. Following appropriate pacemaker programming the patient remained symptom free.

Transient increase in release of adenosine during rapid cardiac pacing; transient effects on overdrive suppression of ventricular automaticity.

A study was designed to test the hypothesis that endogenous adenosine concentration may increase during episodes of rapid ventricular pacing and, by virtue of its negative chronotropic effects, contribute to the transient suppression of automaticity that follows the period of overdrive. Isolated, perfused, rat ventricular preparations were subjected to periods of 6.0 Hz overdrive stimulation while adenosine release, oxygen consumption, and subsequent suppression of automaticity were measured. At the end of a 1 min episode of overdrive oxygen consumption and adenosine release were significantly increased, and the initial beating rate after 1 min overdrive was suppressed. At the end of 10 min overdrive oxygen consumption was still increased but adenosine release had returned to control values. Suppression of automaticity after 10 min overdrive was similar to that after 1 min overdrive. The relative magnitude of suppression after 1 min overdrive was decreased by theophylline (10(-4) mol.litre-1), and increased by the adenosine deaminase inhibitor, EHNA (10(-5) mol.litre-1). Neither theophylline nor EHNA had any discernible influence on suppression after 10 min overdrive. It its therefore concluded that endogenous adenosine may contribute to the suppression of ventricular automaticity that follows a 1 min episode of overdrive, but because of the transient nature of the increase in adenosine during overdrive endogenous adenosine does not contribute to the suppression that follows prolonged overdrive.

Atrial reentry around an anatomic barrier with a partially refractory excitable gap. A canine model of atrial flutter.

We have characterized, in dogs, a model of inducible regular atrial tachycardia that resembles atrial flutter. The model involves creating a Y-shaped lesion comprised of an intercaval incision and a connected incision across the right atrium. It is suitable for serial studies of the effects of pacing or antiarrhythmic drugs in chronically instrumented animals studied in the awake state for at least several months. The postoperative cycle length of the induced tachycardia varies from 143 to 188 msec, depending on the size of the dog. The tachycardia cycle length was consistent for each dog, and the rhythm--once induced--was very stable until terminated by pacing. The mechanism of the tachycardia was reentry due to circus movement based on the ability to induce and terminate it by premature impulses or overdrive, the ability to reset the tachycardia by single premature stimuli, the pattern of entrainment during overdrive stimulation, and the ability to terminate the tachycardia by interrupting the conduction pathway. The window of reset determined by the range of coupling intervals of premature stimuli that were able to enter and reset the tachycardia ranged from 56 to 82 msec. There appears to be incomplete recovery of excitability by the end of the excitable gap as evidenced by the fact that even late premature impulses that enter the reentrant circuit conduct more slowly than the tachycardia impulse, and because stimulation of muscarinic receptors that shortens the duration of the action potential and refractoriness also reduces the cycle length of the tachycardia. Epicardial and endocardial activation mapping during tachycardia showed the reentrant pathway does not merely encircle the lesion, particularly over the left atrial epicardium near the intercaval lesion. Rather, the impulse appears to travel around the atrial tissue just above the tricuspid ring, including a portion that travels through the right side of the lower intraatrial septum. Thus, the model involves circus movement around an anatomic barrier through normal tissue that contains no depressed segments. During the circus movement, there is a relatively long excitable gap during which there is incomplete recovery of excitability. This model should be useful for studies of the mechanism of antiarrhythmic drug action and the responses to premature stimulation in this particular subclass of reentrant rhythms, and for comparison with the behavior and responses of other forms of reentry.

Termination of atrial flutter during DDD pacing by rapid overdrive stimulation using the implanted pacemaker lead system

DDD pacing is not suitable in the presence of chronic atrial flutter or fibrillation. 1 However, patients with the bradycardia-tachycardia syndrome who mostly are in sinus rhythm may be considered for DDD pacing, although bradycardia control does not completely prevent further paroxysms of atrial tachyarrhythmia. 2 Even in patients without a history of attacks, future episodes of atrial flutter or fibrillation cannot be excluded at the time of implantation. 3,4 Atrial flutter may then be terminated by rapid overdrive stimulation, 5 which usually has to be performed through an additional temporary transvenous electrode catheter. However, in some dual chamber pacemakers the atrial and ventricular asynchronous modes (AOO and VOO) can be programmed to very high rates on a temporary basis “for use in clinical diagnostic settings to control and terminate episodes of tachycardia.” 6 This approach may also be suitable for converting atrial flutter to sinus rhythm without the need for additional transvenous lead insertion.

Rate Reduction by Overdrive Stimulation at the Origin of an Ectopic Ventricular Tachycardia in the Intact Pig Heart‐Evidence of Vagal Activation

Overdrive stimulation is used in the treatment of tachycardias. In this study, the effect of overdrive stimulation on a focal ventricular tachycardia was investigated. In 12 landrace pigs thoracotomy was performed. Stable ectopic ventricular tachycardias with a rate of 120–170/min were induced by subepicardial infusion of a solution of norepinephrine (10−4 M). Unipolar cathodal stimulation was carried out by an epicardial screw‐in electrode. During tachycardia, overdrive stimulation was undertaken in different distances to the ectopic focus, with different stimulus amplitude and duration. A significant rate reduction of the ventricular tachycardia was observed after stimulation. When stimulated directly at the focus the extent of rate reduction was larger than after stimulation in a distance of 10–40 mm. At the infusion site the rate of the tachycardia was lowered in direct relation to the stimulation amplitude and stimulus width. The marked reduction in rate after overdrive stimulation (18%) was nearly completely antagonized by atropine. This indicates that rate reduction caused by local overdrive stimulation is due to local acetylcholine liberation caused by vagal stimulation in the ventricular working myocardium in this experimental model.

Runaway Pacemaker Inhibited by External Overdrive Stimulation: A Case Report

A case is described of runaway pacemaker ( Stimulith ) which could be inhibited by external chest-wall overdrive. This pulse generator had been implanted for four years before runaway occurred; the runaway rate was 140/min with capture of the ventricles. Using external chest-wall stimulation at a rate of 170/min, we were able to achieve almost complete inhibition of the faulty generator, while preparing for emergency replacement.

Studies on overdrive stimulation of canine cardiac purkinje fibers: Maximal diastolic potential as a determinant of the response

The effects of overdrive stimulation were studied on preparations of isolated canine cardiac Purkinje fibers using standard microelectrode techniques. Preparations were made from false tendons, the subendocardial right bundle branch and 24 hour infarct zone Purkinje fibers. Three types of automaticity were recognized: high potential automaticity occurred in fibers with maximal diastolic potentials greater than -70 mV, intermediate potential automaticity occurred in fibers with maximal diastolic potentials between -61 and -70 mV and low potential automaticity occurred in fibers with maximal diastolic potentials less than -60 mV. Short periods of overdrive (15 seconds or 30 beats) resulted in marked suppression of high potential automaticity, slight suppression of intermediate potential automaticity and little or no suppression of low potential automaticity. The extent of postoverdrive suppression of intermediate potential automaticity was related to the rate and duration of the overdrive train and the amount of hyperpolarization that occurred in the pacemaker fiber. Finally, in three experiments on Purkinje fibers from 24 hour infarct zones, delayed afterdepolarizations occurred. In two of these preparations, overdrive stimulation resulted in biphasic responses (postoverdrive enhancement followed by postoverdrive suppression). The results of this study suggest that it may be possible to design simple electrophysiologic tests to determine whether an automatic arrhythmia is being caused by normal or partially depolarized ectopic pacemakers.

Na, K-ATPase activity, ATP and Pi concentrations in various regions of monkey heart and their relation to post-overdrive hyperpolarization.

The relationship among Na, K-ATPase activity, ATP and inorganic phosphate (Pi) concentrations in functionally different regions of cardiac and skeletal muscles were studied in the Japanese monkey (Macaca fuscata). The activity of Na, K-ATPase was determined by the method of FIske and SubbaRow, and the concentrations of ATP and Pi, by isotachophoresis. The ATP concentrations in several regions of cardiac and skeletal muscles correlated positively with the Na, K-ATPase activities and Pi concentrations, whereas there was no significant correlation between the Na, K-ATPase activities and the Pi concentrations. Therefore, the ATP concentrations in functionally different regions of the tissues seemed to be a feasible measure of Pi concentrations and the Na, K-ATPase activities. The Na, K-ATPase activity was significantly higher in the epicardium than in the endocardium of the ventricle. The post-overdrive hyperpolarization was compared in these two tissues, using microelectrode methods. The hyperpolarization which followed overdrive stimulation (3.3-3.8 Hz) in the epicardium exceeded that in the endocardium, and was attributed to the difference in Na, K-ATPase activity. Our findings suggest that tissues with a higher Na, K-ATPase activity may have a more potent Na, K-pump activity, in association with higher tissue concentrations of ATP and Pi.

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 ouabain and vagal stimulation on sinus nodal function in conscious dogs.

We studied the effects of intravenous ouabain administration (15 micrograms/kg) and vagal stimulation on instrumented conscious dogs. In these dogs, a special electrode was implanted on the epicardial surface over the sinus node and plaque electrodes were placed on the superior vena cava and left atrial appendage. Unipolar sinus electrograms were recorded through the terminals of the sinus electrode paired with the superior vena caval electrode. An electrode also was implanted around the desheathed cervical vagosympathetic trunk, and a coiled polyethylene tube with side holes was implanted cranial to it. Ouabain administration resulted in: (1) an increase in the sinus cycle lengths and sinoatrial intervals and increase in beat-to-beat variation of the sinus cycles and sinoatrial intervals, and (2) periods of sinus pacemaker shift, sinus arrest and sinoatrial block that occurred spontaneously or after atrial overdrive stimulation delivered through the electrode on the left atrial appendage. These effects of ouabain were abolished by intravenous administration of atropine (2 mg). Prior to vagal stimulation, intravenous propranolol (0.5 mg/kg) was administered to block sympathetic responses and 0.75% bupivacaine was injected through the polyethylene tube to block afferent transmission. Vagal stimulation in conscious dogs resulted in two types of responses: (1) slowing of sinus pacemaker rate accompanied by a decrease in diastolic slope and followed by sinus pacemaker shifts, and (2) gradual prolongation of the sinoatrial intervals followed by failure of sinoatrial conduction. An intravenous bolus of acetylcholine (0.1 mg) resulted in a response of type 2 in dogs in which vagal stimulation produced a response of type 1. The marked similarity between the effects of ouabain and vagal stimulation on sinus function and the abolition of the effects of ouabain by atropine suggest that the ouabain effects are vagally mediated.

Preferential sensitivity of the left canine purkinje system to cardiac glycosides.

Previous studies have shown that the toxic effects of cardiac glycosides are not manifested uniformly throughout the myocardium. The purpose of our study was to determine whether cardiac glycosides exert different effects on the right vs. left peripheral Purkinje systems and to ascertain mechanisms involved. Control in vitro measurements of paired right and left canine Purkinje fibers showed higher spontaneous rates in left (24.2 +/- 1.75 beats/min) than in right (11.6 +/- 1.55 beats/min, P less than 0.01, n = 81) Purkinje fiber bundles. Following overdrive stimulation, left Purkinje fiber bundles also showed earlier escape beats. After ouabain exposure (2 X 10-7 M), left Purkinje fiber bundles showed earlier signs of toxicity in 20 of 28 experiments, as determined by changes in the maximum diastolic potential, the degree of diastolic depolarization, spontaneous escape intervals, and the magnitude of delayed after-depolarizations. The enhanced sensitivity of left Purkinje fiber bundles was independent of the extracellular potassium concentration and glycoside polarity, and was also observed in situ. We conclude that distal Purkinje fibers are functionally dissimilar and that the left Purkinje system shows greater sensitivity to cardiac glycosides than the right Purkinje system. These data also support the observation that digitalis-induced dysrhythmias arise in the left ventricle.

Differences in automaticity between Purkinje strands from right and left dog ventricle.

Previous in situ studies have implicated differences in the pacemaker rates between the left and right ventricular conduction system. Our studies were conducted to characterize automaticity in peripheral right and left canine Purkinje fibers in vitro. Standard microelectrode techniques were utilized. In paired right (RPF) and left (LPF) canine Purkinje fibers, control intrinsic rate (IR) was found to be higher in LPF (24.8 +/- 1.7 beats/min) than in RPF (11.5 +/- 1.5 beats/min, P less than 0.01). Following overdrive stimulation at various cycle lengths, LPF consistently showed earlier escape beats. In low K0+ (1.35 mM), IR increased comparably in both RPF and LPF. However, high K0+ (5.4 mM) resulted in a greater reducton of the IR in RPF (-78%) than in LPF (-58%). After epinephrine (10(-6) M) the IR of LPF > RPF although the chronotropic response was more pronounced in RPF. Adrenergic stimulation preceded by beta-adrenergic blockade did not produce significant differences in the intrinsic rate between RPF and LPF. These findings indicate that automaticity in right and left Purkinje strands is functionally dissimilar.

Electrophysiological and clinical study of sick sinus syndrome using the overdrive suppression test.

1) Right atrial pacing was performed at rates of 80 to 200 beats/min for 30 seconds. The pacing rate was increased by an increment of 10 beats/min, with a 30 second rest period after each atrial pacing. One hundred three patients with sick sinus syndrome (SSS) and 25 normal subjects were studied. Recovery time (RT) was defined as the longest R-R interval of the five subsequent beats after cessation of overdrive stimulation at each rate, and was expressed as the ratio of RT to resting R-R interval (%RT). Accordding to the origin of the beat following the longest pause, RT was divided into sinus node recovery time (SNRT) and A-V junctional recovery time (JRT). The longest RT in all pacing rates was defined as the maximum recovery time (max RT). 2) In normal subjects, the ratio of SNRT to the resting R-R interval (%SNRT) was only slightly affected by the pacing rate, though showed a two-phase phenomenon. Among cases with SSS, in patients with a maximum %SNRT of more than 200%, %SNRT progressively increased as the pacing rate increased. In patients with a maximum %SNRT less than 200%, however, %SNRT remained essentially constant over a wide range of pacing rates. JRT in cases with SSS showed a two-phase pattern with a maximum pause at a pacing rate of 260-280% with reference to the resting heart rate. 3) Patients with SSS were classified into three different response groups according to the above values and patterns of %RT against the pacing rate, with each group showing different clinical and electrocardiographic features. In the 43-case low-rate response group (%RT already more than 200% below a pacing rate of 200%), sinus arrest was detected in 65% of the cases and paroxysmal tachycardia and syncopal attack in about half. In the 31-case high-rate response group (%RT smaller than 200% at a pacing rate lower than 200% but %RT over 200% at a pacing rate more than 200%), SA block was found in 74% of the cases, paroxysmal tachycardia in 8 l% and syncopal attack in 81%. Maximum suppression of sinus node automaticity occurred at a higher pacing rate of 300-400% in some cases. In the 29-case normal response group (%RT smaller than 200% at all pacing rates and little affected by the pacing rate), sinus bradycardia was found in 72% of the cases, but syncopal attack in 24% of the cases despite occurrence of paroxysmal tachycardia in about half of the cases. The importance of pacing rate effect on RT should be stressed in the overdrive suppression test. Hence, our classification was thought to be useful in unmasking the presence of sinus node dysfunction and in confirming its severity in patients with SSS.