Is the Ventricular Effective Refractory Period Different When Determined by Incremental Versus Decremental Scanning?: The Effect of Pacing Cycle Length,d-Sotalol,and Levcromakalim

In tbe clinical setting, the ventricular effective refractory period (VERP) is determined by an 8-beat drive train (S1S1), followed by a premature stimulus (S2), which is decremented in subsequent drive trains until capture is lost. Variation in intertrain pauses and capturing extra stimuli disturb steady-state conditions and reduce reproducibility of values found for the VERP. To increase reproducibility, a protocol without intertrain pause and incremental scanning (IS) of S2 was developed. In anesthetized dogs with chronic AV block, determination of the VERP using IS and decremental scanning (DS) without intertrain pause was compared at 800 and 350 msec pacing cycle length (PCL). The measurements were repeated after the administration of d-sotalol to lengthen the VERP and levcromakalim to shorten the VERP. The results showed no difference between IS and DS at both PCLs with or without medication. Recurrent and abrupt rate changes were avoided daring IS, making this the protocol of choice when induction of arrhythmias is to be avoided.     

Steady-State and Dynamic Behavior of Ventricular Repolarization and Refractoriness in the Dog: The Effect of Multiple Cycle Length Changes and d-Sotalol Administration

In anesthetized dogs with chronic, complete AV block we studied the characteristics of ventricular repolar-ization and refractoriness. Therefore, we determined: (1) steady-state values of ventricular effective refractory period (VERP), action potential duration (APD), and stimulus T interval (STI) before and after d-sotalol treatment at various pacing cycle lengths (PCLs); and (2) the dynamics of VERP, APD, and STI before and after d-sotalol treatment after the abrupt PCL decreases. VEHP, APD, and STI showed a normal frequency dependency. All three parameters increased significantly after d-sotalol administration. During steady-state and dynamic measurements, STI was always longer than APD and APD was always longer than VERP in an individual animal, irrespective of PCL and conditions. Standard deviations of steady-state and dynamic values indicated a considerable interindividual variation. However, the dynamics of VERP, APD, and STI after an abrupt decrease in PCL were highly correlated (linear regression analysis: r²± 0.93). The best mathematical model to describe these dynamics was a bi-exponential model (r²± 0.98) with a very short first and a much longer second time constant. We found that there was a very consistent relation between VERP, APD, and STI, not only during steady-state but also in the dynamic situation after various abrupt PCL decreases. This relation does not change after the administration ofd-so-talol. Therefore, STI could be used to predict steady-state and dynamic values of VERP and APD. Since STI can be made available online in implantable pacing systems this could lead to the development of new features in these devices.     

Rate dependent effects of procainamide on the threshold current for pacing in the setting of postrepolarization refractoriness in dogs

Normally, ventricular APD exceeds the VERP. However, under specific circumstances this relation may change and can become inverse. This phenomenon of postrepolarization refractoriness may be caused by a decrease in excitability. The threshold current (TC) for pacing has never been quantified as a possible explanation for these observations. Using a MAP pacing catheter in the right ventricular apex, the rate dependent behavior of TC, VERP, and APD before and after procainamide (dose 20 mg/kg in 10 min + 5 mg/min infusion) was determined in 17 dogs with chronic complete AV block. Initially, TC was determined with 0.1 mA accuracy. Using a pacing current of at least twice TC, VERP and APD showed a similar, rate dependent shortening for PCLs 800, 575, and 350 ms. Procainamide treatment led to an equal, rate independent VERP and APD increase: no post repolarization refractoriness. Subsequently, accuracy for TC determination was increased to 0.01 mA. Comparing PCLs 800 and 250 ms, TC doubled from 0.05 +/- 0.01 to 0.10 +/- 0.09 mA during control and almost tripled from 0.06 +/- 0.02 to 0.17 +/- 0.10 mA (P < 0.05) after procainamide. Using a fixed pacing current of exactly twice TC found at 800 ms PCL during control, VERP exceeded APD after procainamide treatment at 300 and 250 ms PCL: postrepolarization refractoriness. Increasing the pacing current to twice the rate dependent TC, the relation between VERP and APD normalized: no postrepolarization refractoriness. We conclude that after procainamide, rate dependent TC increase is of major importance for the phenomenon of postrepolarization refractoriness.     

Comparison of Ventricular Refractory Periods Determined by Incremental and Decremental Scanning of an Extrastimulus

This study compared the ventricular effective refractory periods measured by scanning diastole with an extrastimulus in incremental and decrementaJ steps of 5 msec. The subjects of the study were 80 patients undergoing a clinically indicated electrophysiological test. Eight beat basic drive trains at a cycle length of 600 msec and an intertrain pause of 4 seconds were used to measure the ventricular effective refractory period (VERP). In the incremetal method, the extrastimulus initially was positioned at a coupling interval shorter than the VERP and the coupling interval then was progressively increased until ventricular capture occurred. In the decremental method, the initial extrastimulus coupling interval was longer than the VERP and the coupling interval was progressively shortened until ventricular capture was lost. In 50 subjects, the mean VERP determined by the incremental method, 252 ± 18 (± standard deviation), was significantly longer than the mean VERP determined in the same patients by the decremental method, 248 ± 18 msec (P < 0.0001). In ten subjects, a subthreshold stimulus (S') positioned 10 msec earlier than the VERP had an inhibitory effect that lengthened the VERP by an average of 7 msec; however, when S' was positioned after the seventh beat of an eight heat drive train, no inhibitory effect could be demonstrated. In 20 subjects, VERP's were determined by the incremental and decremental methods using intertrain pauses of 1, 4, 8, 12, and 20 seconds. The mean VERP measured by the incremental method was significantly less than the mean VERP measured by the decremental method when the intertrain pause was 1,4, or 8 seconds, but not when the pause was 12 or 20 seconds. The results of this study demonstrate that incremental scanning of an extrastimulus with eight beat basic drive trains yields a longer VERP than when the extrastimulus is scanned in decremental fashion. The discrepancy between the two methods is not attributable to inhibition by noncapturing extrastimuli in the incremental method, but rather to a decrease in the VERP caused by an effect of extrastimuli that capture the ventricle in the decremental method. Therefore, when a conventional eight beat driye train and 4 second intertrain pause are used to measure ventricular refractoriness, incremental scanning of an extrastimulus yields a more accurate VERP than does decremental scanning.     

Detection of rapid changes in ventricular refractoriness in human studies

Conventional determination of the ventricular effective refractory period (VERP) is unsuitable for detection of rapid fluctuations in the effective refractory period (ERP). A programmed stimulation system was developed that adapts continuous atrioventricular sequential pacing, incremental extrastimulus interval (S1S2) scanning, and automatic detection of extrastimulus capture which is followed by shortening of S1S2 to execute repeated scanning. The accuracy of ERP determination was tested using variable incremental (2 and 4 ms) and decremental (4-16 ms) steps of the S1S2 interval. Based on a mean of 82 determinations in eight patients, the average VERP values stayed at 249.8-251.0 ms except during the highest capture frequency. Standard deviation of ERP values ranged from 1.1 to 2.5 ms on average at the tested incremental and decremental steps. One determination was accomplished within 7.8-15.6 seconds on average. The ability to track changes in ERP was tested by changing the drive cycle length. Time constants for the adaptation rate of VERP and ventricular monophasic action potential duration at a 90% level of repolarization were determined from each test, and were similar, 51 +/- 8 seconds (mean +/- SEM) for ERP and 51 +/- 6 seconds for the action potential duration. Thus, the developed method provides accurate ERP measurements during rapid variation in ventricular refractoriness. It allows studying the recovery of excitability and the action potential duration simultaneously, and would be valuable particularly in pathological conditions and pharmacologic interventions where these electrophysiological variables become dissociated.     

The Ventricular Excitability-Interval Relationship in Early Diastole in Humans: The Influence of the Electrode Configuration During Bipolar Stimulation

The purpose of this study was to determine the relationship between ventricular excitability and the extrastimulus (S2) coupling interval in early diastole in humans. The influence of the electrode configuration during bipolar stimulation was examined. Ventricular strength-interval curves were constructed using an eight beat drive train at a cycle length of 600 msec, 2-msec decrements in the S2 coupling interval, and 0.2-mA increments in the current intensity of S2 at each coupling interval. A transient dip in the excitation threshold was observed in early diastole during bipolar pacing when the distal electrode was the anode in six of 17 patients (35%). In contrast, this type of dip was not observed when the distal electrode was the cathode. The excitation threshold at the trough of the dip ranged from 1.0 to 2.2 mA. Unipolar strength-interval curves indicated that a dip occurred with anodal but not cathodal pacing. We postulated that the dip might interfere with the accurate determination of the ventricular effective refractory period by resulting in transient loss of ventricular capture during decremental scanning of diastole with S2. A gap in ventricular capture was produced in all six patients who demonstrated a dip in the bipolar strength-interval curve by selecting an S2 current intensity that fell within the dip. In conclusion, the bipolar strength-interval curve may display an early diastolic dip in the excitation threshold, depending on the electrode configuration.(ABSTRACT TRUNCATED AT 250 WORDS)     

The Effect of Rate on Prolongation of Ventricular Refractoriness by Quinidine in Humans

In this study, the rate dependent effect of quinidine on the ventricular elective refractory period (VERP) was evaluated in 30 patients undergoing electropharmacological testing with quinidine. The VERPs were measured in the baseline state and after at least 2 days of treatment with 1,458–2,044 mg/day of quinidine gluconate (mean plasma quinidine concentration 2.2 ± 0.7 mcg/mL). In 20 patients, the VERP was measured using conventional basic drive trains of 8 beats and basic drive cycle lengths of 600, 500, 400, and 350 msec. In another 10 patients, the VERP was measured after 3 minutes of continuous ventricular pacing at cycle lengths of 600 and 400 msec, and compared to the VERPs measured at the same basic drive cycle lengths using basic drive train durations of 2 and 8 beats. In the baseline state and after treatment with quinidine, the VERP shortened progressively as the basic drive train cycle length decreased and as the drive train duration increased to 3 minutes (P < 0.001). Quinidine consistently prolonged the VERP by 9%–11% (P < 0.001 J, regardless of the basic drive train cycle length. Quinidine's effect was also not affected by the basic drive train duration. In conclusion, the effect of quinidine on VERP in humans is independent of the rate of the basic drive train, both when measured using conventional 8-beat basic drive trains and when a three minute drive train duration is used in order to attain the maximum effect of the basic drive train cycle length on the VERP. Therefore, in contrast to quinidine's known rate dependent effect on conduction, it's effect on ventricular refractoriness at doses and basic drive train cycle lengths which are used clinically are not rate dependent.     

Applicability of the Stimulus-T Interval for Antitachycardia Pacing

At (he onset of tachycardia, the refractory period (RP) changes together with the tachycardia terminal ion window. We evaluated dogs with total atrioventricular (AV) block lo determine if stimulus-T interval (STJ) can be used to adjust the coupling interval(s) of an antitachycardia pacemaker in relation to changes in HP. Endocardial STI was recorded continuously together with six surface EGG leads. Steady-state (> 2 miii) RP was determined for drive cycle lengths (DCL) 400 msec and 900 msec. The test pulse (TP) coupling interval, with DGL 900 msec, was chosen to be equal to (he RP of DCL 400 msec, DCL was then changed to 400 msec until TP captured. STI of DCL of beat before capture was gained was measured. DCL was then changed back to 900 msec and the interval determined when capture was lost. TP was then lengthened In 5 msec and the procedure repeated until TP captured immediately upon changing to DCL 400 msec. Results: The difference between RP at onset of pacing at DGL of 400 msec and RP when capture n us achieved with the shortest coupling interval was 35–50 (mean 40) msec. This required 35–90 (mean 62) seconds. The correlation coefficient RP to STI was > 0.95. Conclusions: (1) RP changed by as much as 35–50 msec at the: onset of an abrupt increase in rate in a 35–90-second period; and (2) STI enables estimation of RP on a beat-to-beat basis. Capture can therefore be preditrd from the previous beat mid the coupling interval adjusted accordingly in an antitachycardia pacing mode.     

Summation of Excitation with a Single Conditioning Stimulus in the Canine Heart

A subthreshold stimulus was reported to become effective in producing a propagated ventricular response when preceded by another subthreshold stimulus or stimuli, a phenomenon that is known as summation of excitation but has not been studied systematically. Effect on summation of current intensity and coupling interval of a conditioning stimulus (Sc, protocol #1) and that of stimulation site of Sc (protocol #2) were determined in anesthetized, open-chest dogs. Effective refractory period (ERP) was determined with an extrastimulus (S2) at a ventricular pacing cycle length (S1S1) of 500 msec. Pulse width of S1, S2 and Sc was 2 msec. For pacing protocol #1 (12 dogs), current intensity of S1 and S2 was equal (twice diastolic threshold, 2, 5, or 15 mA), and that of Sc was equal to or lower than that of S1. S1S2 interval was fixed 1 msec shorter than ERP, and Sc was delivered 5 msec prior to S2. The S1Sc interval was shortened in 2 msec steps. Summation was present if Sc plus S2 evoked a propagated response. Prevalence of summation increased along with an increase in current intensity of Sc (P less than 0.01). For pacing protocol #2 (7 dogs), current intensity of S1, S2 and Sc was equal (twice diastolic threshold, 5 or 10 mA). As the distance between site of Sc and that of S2 increased, prevalence of summation decreased (P less than 0.01). Summation did not occur when Sc was delivered at a site only 5 mm away from the site of S2. In conclusion, summation of excitation with a single conditioning stimulus was both time and strength dependent, and limited in development spatially.     

Effect of the Intertrain Pause on the Ventricular Effective Refractory Period Measured by the Extrastimulus Technique

This study determined the effect of the duration of the intertrain pause on the ventricular effective refractory period (VERP) measured by the extrastimulus technique using conventional eight-beat basic drive trains. In 50 subjects, the VERP was measured using a basic drive train cycle length of 500 msec, 2-msec steps in the extrastimulus coupling interval, and intertrain pauses of 0, 1, 4, 8, 20, 40, 60, or 180 seconds. The VERP increased significantly with each stepwise increment in the intertrain pause up to 20 seconds, then reached a plateau. The VERP measured with an intertrain pause of 20 seconds was a mean of 13 msec longer than when measured with a conventional 4-second pause. The results of this study demonstrate a direct relationship between the VERP and the duration of the pause separating the eight-beat basic drive trains used to measure the VERP. When the cycle length of the basic drive train is 500 msec, the VERP lengthens as the duration of the intertrain pause increases from 1 to 20 seconds, demonstrating that the basic drive trains exert a cumulative effect on the VERP when the intertrain pause is shorter than 20 seconds. A cumulative effect of the basic drive trains on the VERP is lost when the intertrain pause is 20 seconds or more.     

Rate and Time Dependent Effects of D-Sotalol on the Monophasic Action Potential After Sudden Increase of the Heart Rate

Experimental and clinical data suggests that almost all Class III antiarrhythmic agents diminish their ability to prolong cardiac repolarization at fast heart rates. However, only limited data exists about the time course of efficacy decay of Class III agents after sudden increase of the heart rate. In the present study, we assessed both rate and time dependent changes of the efficacy of d-sotalol in higher stimulation frequencies following an abrupt increase in heart rate. This might imitate the situation seen in the development of paroxysmal tachycardias. Monophasic action potentials were recorded from the right ventricular apex during sinus rhythm and constant stimulation with the paced cycle length (PCL) of 550 ms, 400 ms, and 330 ms in the baseline and 20 minutes after intravenous administration of d-sotalol (2.5 mg/kg) in seven patients with documented life-threatening ventricular tachyarrhythmias. D-sotalol significantly prolonged monophasic action potential duration at different steady-state heart rates (sinus rhythm: 21.1%± 3.6%; PCL 550 ms: 16.6%± 4.3%, 400 ms: 11.2%± 2.7%, 330 ms: 5.8%± 2.1%). The prolongation is significantly shorter in higher steady-state pacing, confirming a pronounced reverse-use dependent decrease of the efficacy of d-sotalol at faster stimulation frequencies. After the abrupt increase in heart rate, the beat-to-beat adaptation of the postdrug action potential prolongation exhibits only slight reverse-use dependent shortening. The decrease of the efficacy of d-sotalol is insignificant for the first 20 consecutive beats at the stimulation frequency of the PCL of 400 msec (from 16.6% at PCL of 550 ms to 14.6% at the 20th beat of the PCL of 400 ms), and for the first ten consecutive beats at the stimulation frequency of the PCL of 330 ms (from 16.8% at PCL of 550 ms to 12.3% at the 10th beat of the PCL of 330 ms). This slow decay of action potential prolongation after an abrupt increase in heart rate might contribute to the antiarrhythmic action of d-sotalol in cardiac tachyarrhythmias.     

Changes in Ventricular Effective Refractory Periods After Two Extrastimuli and Ventricular Electrical Instability

Using programmed stimulation with one and three extrastimuli delivered in the right ventricular apex, we compared the effective refractory period (ERP) during sinus rhythm (ERP-SR) and during the third extrastimulus (EHP-S₃) in patients without ventricular tachycardias (control group, n = 87) and in patients with documented ventricular tachycardia (VT group, n = 76). The protocol was not completed to determine ERP-S₃ in one patient in the control group and in 15 patients in the VT group. We observed a significantly greater change (i.e., shortening) in ERP after two extrastimuli in the VT group compared with patients without VT (ΔERP = 45 ± 20 msec in the control group and 70 ± 16 msec in the VT group, P < 0.001), This electrophysiological phenomenon, along with conduction delay, may play an important role in VT induction.     

Frequency Dependent Effects of d-Sotalol and Amiodarone on the Action Potential Duration of the Human Right Ventricle

Frequency dependent effects of d-Sotalol (2.0 mg/kg IV, n = 6) and amiodarone (400 mg/day for 3 months, n = 9) were studied on the action potential duration (APD) in 14 patients who underwent electrophysiological testing. Monophasic action potentials were recorded from the right ventricle at five different steady-state paced cycle lengths (700 msec, 600 msec, 500 msec, 400 msec, and 350 msec), and during ventricular extra stimuli with coupling intervals between 300 msec and 1000 msec, before and after d-sotalol and amiodarone, respectively. D-sotalol caused a prolongation of the APD at slow steady-state stimulation rates (11 ± 5% at cycle length of 700 msec), which became attenuated at faster cycle lengths (5 ± 3% at cycle length of 350 msec). Prolongation of APD after amiodarone was independent of pacing rate, e.g., 12 ± 9% at cycle length of 700 msec, and 11 ± 6% at cycle length of 350 msec. Similar frequency dependent prolongation of the APD was observed during abrupt changes of cycle lengths after d-sotalol, whereas amiodarone caused uniform prolongation of the APD at different extrasfimulus intervals. Thus, d-sotalol, a nonselective potassium channel blacker, has reverse use-dependent effects on the human ventricular APD, while amiodarone with greater potassium channel selectivity, has equal ability to prolong the ventricular APD at fast and slow heart rates.     

Partial Pacemaker Recycling of Implanted QRS-Inhibited Pulse Generators

In the evaluation of twenty-three patients with implanted QRS-inhibited lithium-powered pulse generators (Intermedics C-MOS-1 and ARCO L1-2D), we repeatedly observed the phenomenon of partial pacemaker recycling (PPR), in which the escape interval induced by a premature ventricular beat is shorter than the automatic interval (AI). In order to determine the sensing properties of these pulse generators, programmed chest wall stimulation (CWS) was systematically performed in all 23 patients and, in addition, intracardiac programmed ventricular stimulation (PVS) via temporary intravenous pacing catheters was performed in 9 of them. The AI of these pulse generators ranged from 820 to 860 msec and absolute refractory periods (ARP) from 220 to 330 msec. Precise correlation in determining pacemaker sensing properties could be demonstrated between CWS and PVS. The phenomenon of PPR occurred 110 to 240 msec following ARP with both CWS and PVW, and appeared to be time- rather than voltage-dependent. We conclude that: (1) CWS is a safe, simple and accurate method for studying pacemaker sensing properties, and (2) time-dependent PPR is a normal electrical feature of certain implanted QRS-inhibited lithium-powered pulse generators.     

Influence of Duration of Rapid Ventricular Pacing on Ventricular Refractoriness in the Presence of Propafenone and Lidocaine

Propafenone and lidocaine have a rate dependent negative dromotropic effect on intraventricular conduction. We investigated the use dependent actions of propafenone and lidocaine on intraventricular conduction in isolated guinea pig hearts perfused by the method of Langendorff. Of primary interest was how the number of stimuli of the conditioning train (S1) might influence the ventricular effective refractory period (VERP) when refractoriness is assessed at a high pacing rate. Propafenone (0.3 μM) and lidocaine (50 μM) caused a comparable prolongation of the intraventricular conduction time during sinus rhythm. During ventricular pacing in the presence of propafenone an abrupt decrease of the pacing cycle length (220 to 120 ms) resulted in an initial peak of rate dependent prolongation of the QRS interval that subsequently decreased to a stable steady-state level. Lidocaine also induced a rate dependent increase of the intraventricular conduction time up to a steadystate level. The time constant, characterizing the changes of the intraventricular conduction time after shortening the ventricular pacing cycle length from 220 to 120 ms was significantly (P < 0.01) longer in the presence of propafenone (τ= 31 ± 4 beats; mean ± SEM; n = 11) than for lidocaine (τ= 3 ± 1; n = 10). Both drugs caused the greatest increase of tbe VERP when the number of conditioning stimuli (S1, interstimulus interval = 120 ms) was in the range of their respective time constant. However, when the number of conditioning stimuli was further increased, VERP progressively diminished. These effects may be explained by a shortening of the action potential during high rates that results in a decreased binding of propafenone to Na⁺ channels and by the direct shortening of repolarization period by lidocaine (Class IB drug).     

Reappraisal of Inhibition and Summation with a Single Conditioning Stimulus in Man

A noncapturing conditioning stimulus is known to exert inhibitory effect on a subsequent suprathreshold stimulus, while summation occurs rarely in man. The present study was conducted to revaluate whether conditioning stimulus at a relatively low intensity produced inhibition and summation in man. Thirteen patients with various arrhythmias, 47 +/- 19 years old, were studied. Basic ventricular driving stimuli (S1S1 = 600 msec), a conditioning stimulus (Sc), and extrastimulus (S2) were introduced from a catheter electrode. Sc at an intensity of twice the late diastolic threshold inhibited suprathreshold S2 from evoking a response in all 13 patients. The ScS2 interval producing inhibition was from 11 +/- 4 to 38 +/- 26 msec. When Sc preceded S2 by 5 msec, effective refractory period was shortened by 16 +/- 7 msec in 7 of 13 patients, a phenomenon of summation. The present study demonstrates that inhibition and summation are common phenomena with a single conditioning stimulus at relatively low intensities.     

Lack of relation between the ventricular refractory period prolongation by amiodarone and the thyroid state in rats

We investigated the possibility that the prolongation of the ventricular effective refractory period (VERP) by amiodarone might be mediated, at least in part, by inhibition of thyroid influence on the heart. VERP values were measured in vitro in isolated septal preparations obtained from control, thyroidectomized and thyroxine (tetraiodothyronine; T4)- or triiodothyronine (T3)-treated rats. Differences in thyroid influence on the heart between these groups were assessed by changes in the myosin isozyme (V1, V2, V3) pattern. VERP measurements were also done in similar groups treated with amiodarone for 7 days (50 mg/kg/day i.p.). VERP tended to be increased by thyroidectomy and was significantly reduced by T4 or T3 treatment when compared with the control group. Amiodarone treatment significantly prolonged VERP in control (33.4 +/- 1.9 to 45.0 +/- 4.5 msec), thyroidectomized (39.9 +/- 1.7 to 48.3 +/- 2.8 msec), T4-treated (26.2 +/- 1.0 to 37.4 +/- 1.3 msec) and T3-treated rats (25.6 +/- 1.1 to 34.3 +/- 1.3 msec). However, the magnitudes of the VERP prolongation by amiodarone were not significantly different among the four groups. The action of amiodarone on action potential duration was similar to its action on VERP. The myocardial concentrations of amiodarone and desethylamiodarone were not significantly different among the four groups. Amiodarone treatment produced a significant reduction of serum T3 levels in the control and in the T4-treated groups and an increase in reverse T3 levels. Thus, the class III action of amiodarone was not affected, in the present model, by experimental modification of thyroid influence on the heart.     

Assessment of Long-Term Stability of Chronic Ventricular Pacing Thresholds in Steroid-Eluting Electrodes

Sixteen patients with Medtronic 4003 steroid-eluting electrodes implanted in the ventricular position were followed over 5 years. In each patient a special type of Medtronic 2443 pacemaker was implanted to allow programming of output at 1.35 V. Chronic threshold values in these patients measured at an output of 1,35 V were stable over the first 18 months of follow-up. Mean values were: 0.06 ± 0.03 msec at 6 months and 0.08 ± 0.02 msec at 18 months; these did not differ from each other significantly. However, during the period from 18 to 36 months postimplantation, a significant increase in mean pacing threshold was observed: 0.08 ± 0.02 msec at 18 months postimplantation versus 0.14 ± 0.05 msec at 36 months (P < 0.01), After 36 months, the chronic pacing threshold remained stable until the end of the 5-year follow-up period. Further long-term study of chronic threshold behavior of steroid-eluting electrodes measured at low amplitudes is warranted.     

Randomized Cross-Over Evaluation of Two Adaptive Pacing Algorithms for the Termination of Ventricular Tachycardia

Objective: In a randomized, cross-over study we evaluated the efficacy of rate adaptive constant cycle length (BURST)and autodecremental (RAMP)pacing for termination of sustained monomorphic ventricular tachycardia. Methods: An external device capable of delivering the same types ofantitachycardia pacing as the newer generation implantable cardioverter defibrillators wos used. Thirty-one patients with ischemic and nonischemic cardiomyopathy and documented clinical ventricular tachycardia or ventricularfibrillation were examined during routine invasive electrophysiological studies. RAMP and BURST pacing were each attempted in 54 matched pairs of induced ventricular tachycardia. After a therapy was applied, the tachycardia was reinitiated and the other therapy applied during the second episode so that a total of 108 ventricular tachycardia episodes were studied. Results: Overoll efficacy of ventricular tachycardia pace termination was 69% and the time required to stop ventricular tachycardia was 14.1 ± 11.3 seconds. The ability to terminate ventricular tachycardia by RAMP (72%)or BURST (65%)pacing was not significantly different. However, time to terminate ventricular tachycardia by HAMP (It.8 ± 8.5 sec)was significantly shorter than by BURST (16.4 ± 13.5), P < 0.001. Acceleration of ventricular tachycardia was uncommon with both pacing modes, 7/108 (7%). The ability to pace terminate ventricular tachycardia was cycle length dependant. The highest success was with ventricular tachycardia cycle length between 300 and 350 msec. The success rate decreased with faster and also slower ventricular tachycardia. Conclusions: 1. Rate adaptive pacing methods for ventricular tachycardia termination are effective and safe. 2. Autodecremental fiAMP pacing afford quicker ventricular tachycardia termination than constant cycle length BURST pacing. 3. The ability to terminate ventricalar tachycardia is cycle length dependent with cycle length range of 300–350 msec being most responsive to pace termination