QT Interval and QT Dispersion Measured with the Threshold Method Depend on Threshold Level

Various computerized methods with multiple parameter options for measurements of the QT interval now are available. The optimum parameter setting for most algorithms is not known. This study evaluated the influence of the threshold level applied on the T wave differential on the QT interval and its dispersion measured in normal and abnormal electrocardiograms (ECGs). Seven hundred sixty ECGs recorded in 76 normal subjects and 630 in 63 patients with hypertrophic cardiomyopathy (HCM) (10 consecutive recordings in each individual) were analyzed. In each lead of each ECG, the QT interval was measured by the threshold method applied to the first differential of the T wave. The threshold level was varied between 5% and 30% of the T wave maximum in 1% steps, resulting in 26 different choices of QT measurements. With each choice the maximum QTc and the QT dispersion (QTd, standard deviation of the QT in all 12 leads) were obtained for each recording. The maximum QTc was significantly longer in HCM patients than in normal subjects (P < 0.001) at all threshold levels except between 5% and 7%. The QTd was significantly greater in HCM patients at all threshold levels. The QTc and QTd changed significantly with the threshold level. The maximum QTc varied up to 60 ms in normal subjects and up to 70 ms in HCM patients, depending on the threshold level. Thus, the QT intervai and its dispersion measured with the threshold method applied to the first T wave differential depended significantly on the threshold level in both normal and diseased hearts. All programmable options of available automatic instruments should be examined carefully before any study, and all algorithmic details should be systematically presented.     

Intrapatient Comparison of Atrial and Ventricular Sensing, Pacing Threshold, and Impedance: Benefits with Steroid-Eluting Leads

We compared the atrial and ventricular bioelectrical effects relating to pacing threshold, pacing impedance, and pacing energy in each of 58 patients to determine the importance of pacing impedance in safe low energy stimulations. The study was conducted during 4 years of follow-up. Of the 58 patients in our study, 31 were stimulated in both chambers with steroid-eluting leads (Capsure 4503 and 4003) and 27 with platinum electrode catheters (Target Tip 4511 and 4011). The two groups were homogeneous in sex, age, cardiopathy, and reason for implant. At 6 months, the mean impedance values for the Target Tip were: 358 ± 72 Ω for the atrium and 443 ± 87 Ω for the ventricle (P < 0.00002): after 1 year, atrium = 386 ± 77 Ω, ventricle = 439 ± 42 Ω (P < 0.04); at 2 years, atrium = 409 ± 86 Ω, ventricle = 510 ± 94 Ω (P < 0.0001); at 3 years, atrium = 428 ± 81 Ω, ventricle = 494 ± 67 Ω (P < 0.02); and at 4 years, atrium = 424 ± 71 Ω and ventricle = 501 ± 69 Ω (P < 0.003). The mean impedance value (for the Capsure) was: atrium = 351 ± 43 Ω, ventricle = 431 ± 81 Ω at 6 months (P < 0.03); at 1 year, atrium = 359 ± 38 Ω, ventricle = 446 ± 83 Ω (P < 0.01); at 2 years, atrium = 304 ± 124 Ω, ventricle = 459 + 108 Ω (P <0.0003); at 3 years, atrium = 359 ± 108 Ω, ventricle = 461 ± 89 Ω (P < 0.02); and at 4 years, atrium = 419 ± 133 Ω and ventricle = 515 ± 75 Ω (P < 0.03;. In view of the chronic threshold, low energy stimulation was used at follow-up. The mean low energy stimulation values programmed for Target Tip were: atrium = 2.5 V/0.35 ms, ventricle = 2.5 V/0.30 ms; for Capsure, atrium = 2.5 V/0.25 ms, ventricle = 2.5 V/0.25 ms. The mean stimulation energy value was 31% higher in the atrium than in the ventricle with Capsure leads, and 39% higher with Target Tip. Pacing impedance was lower in the atrium than in the ventricle with both leads. Energy consumption in the atrium is significantly greater than in the ventricle with both leads, particularly with Target Tip.     

Rate-Dependent Threshold Changes During Atrial Pacing: Clinical and Experimental Studies

In 36 patients undergoing a permanent right atrial pacing for the treatment of sick sinus syndrome and/or atrioventricular block, the stimulation threshold was determined at a wide range of pacing rates (60 to 120 beats/min) 7 to 10 days after the lead implantation. Twenty-nine (80%) of these cases showed rate-dependent threshold changes, with significantly lower thresholds at higher than lower pacing rates (e.g., 2.91 +/- 1.01 mA at 70 beats/min and 2.32 +/- 0.75 mA at 120 beats/min, P less than 0.01). Thus, with a fixed, smaller current strength, the stimuli often failed to capture the right atrium at lower rates, but caused a 1:1 capture at higher rates. In an echocardiographic study in another series of eight patients, the end-diastolic diameter of the left atrium was decreased from 3.2 +/- 0.9 to 2.7 +/- 0.8 cm (P less than 0.01) when the pacing rate was increased from 60-70 beats/min to 100-120 beats/min. In experiments using two anesthetized, open-chest dogs, a rapid withdrawal of 500 mL of arterial blood reduced the right atrial dimension. This was accompanied by an increased amplitude of the right atrial endocardial electrogram, and the initially subthreshold stimuli became effective in capturing the atria. It was concluded that (1) rate-dependent threshold changes were commonly observed in the early stage of atrial pacing, and (2) fluctuations in the electrode contact with the endocardium appeared responsible for such threshold changes.     

Measurement of Pacing Threshold

Thresholds in constant current and constant voltage are reported for 405 CPI 4118 (Cardiac Pacemakers, Inc.) tined leads. In 98% of the cases, the constant current threshold was equal to or lower than 0.6 mA. A constant voltage threshold was equal to or lower than 0.5 V in 96% of the cases. Three external pacemakers and two pacing system analyzers were evaluated as threshold testing devices. For analyzing the waveforms of current and voltage stimuli, a calibrated isolation amplifier was used. We could not find a definite difference between the value, at which pacing is lost with reduction of the pulse generator output, and the value at which increase reestablishes pacing.     

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.     

Moricizine Induced Increase in Pacing Threshold

GIROD, J.P., et al. : Moricizine Induced Increase in Pacing Threshold. A 72-year-old woman who was experiencing incessant ventricular tachycardia and recurrent automatic implantable cardioverter defibrillator (AICD) firing despite amiodarone therapy was referred to the Cleveland Clinic Foundation. Myocardial ischemia and infarction were ruled out by standard means. Several antiarrhythmic medications were tried previously without success. Moricizine, 200 mg three times daily, was initiated and controlled the ventricular tachycardia. However, after the dose of moricizine was titrated upward, the patient became symptomatically bradycardic and the ECG exhibited 2:1 block of her paced rhythm and an increased ventricular pacing threshold. (PACE 2003; 26[Pt. I]:110–111)     

Short-Term Threshold Behavior of Human Ventricular Pacing Electrodes: Noninvasive Monitoring with a Multiprogrammable Pacing System

Twenty-two patients were studied for 8 to 12 weeks following pacemaker implantation. A unipolar multiprogrammable pacing system was used to assess and compensate for early post-implant changes in pulse width threshold (PWT). Changes in PWT were estimated by noninvasive measurements of the lowest pulse width required for 100% capture at constant voltage. All patients showed an early increase in PWT. The magnitude of this change was unpredictable and ranged from 2- to 10-fold. For pacing, we selected an appropriate margin of safety to be a pulse width three times the PWT. During the study period, 4 patients showed critical increases in PWT, requiring reprogramming to an increased pulse width as above, whereas only one patient required lead repositioning. The majority of patients achieved a stable low PWT and were reprogrammed to a reduced pulse width. The programmable pacing system provides a safe accurate technique for monitoring early changes in PWT, defines the need for appropriate alterations in programmable functions, decreases the risk of early pacemaker failure, and offers promise for improved pacemaker longevity in many patients.     

Pacing Threshold Spikes Months and Years After Implant

To determine patterns of variation in chronic pacing thresholds, we made 4,942 threshold measurements in 257 patients with 312 leads, at times from implant to 295 months (median 17 months) including 1,053 determinations in 46 children < 12 years old. Motivation was late sudden death in two single-ventricle pacemaker-dependent children with multiple possible death causes. At stimulus duration 0.5 ± 0.04 msec, mean of the thresholds, measured 1 month or more after implant, was 1.3 ± 0.66 volts (V) for endocardial electrodes and 2.8 ± 1.39 V for epicardially applied electrodes. Highest mean thresholds were in the 6 to 12-year-old age group. In 34 leads studied at implant, again within a month and for at least three years thereafter, time of maximum threshold occurred after one month in 59%, independent of lead type or patient age. Of 107 leads with five or more measurements after 3 months use, gradual increase in threshold continued after 3 months in 24%. An additional 21% had at least one threshold that exceeded the post-three-months individual patient lead mean by three standard deviations. Most striking was the occurrence of transient several-volt increases and decreases in threshold as late as 8 years after lead implantation in at least three children. These temporary changes were detected initially transtelephonically by the vario method of threshold measurement. They occurred during minor illnesses such as summer colds, yet similar illnesses also occurred without threshold elevation. We suggest further study of pacing threshold variations in highly pacemaker-dependent children whose cardiac anatomy makes use of epicardial electrodes necessary.     

Effects of Oral Propafenone Therapy on Chronic Myocardial Pacing Threshold

The effects of oral propafenone therapy on pacing threshold were studied in 36 patients chronically paced for sick sinus syndrome or AV block. The pacemakers, all unipolar models and with noninvasive threshold measurement facilities, were: 9 VVI, 15 AAI, and 12 DDD. Each patient received an initial propafenone dose of 450 mg/day, that in 18 cases was increased to 900 mg/day. Threshold was tested at baseline and at each dosage after 7 days of therapy. With the lower propafenone dosage the threshold, measured at 2.5 V, rose from 0.14 +/- 0.10 to 0.21 +/- 0.16 msec (+55%) in the atrium (P less than 0.0001) and from 0.10 +/- 0.08 to 0.15 +/- 0.09 msec (+63%) in the ventricle (P less than 0.0001). In the 18 patients who received both dosages, the mean atrial and ventricular threshold increased from 0.12 +/- 0.10 to 0.17 +/- 0.14 msec with the lower dose and to 0.27 +/- 0.22 msec (+125%) with the higher dose (P less than 0.0001 for both increments). With the 900 mg/day dose, a threshold increment greater than or equal to 300% was observed in 15% of the stimulated chambers. A good linear correlation (r = 0.76) was found between the ventricular threshold increment and the drug induced QRS widening. In conclusion, treatment with oral propafenone increases atrial and ventricular stimulation threshold in pacemaker patients. Threshold increment is dose dependent and proportional to the drug induced QRS widening. In the majority of the cases the threshold increment is not clinically significant, but caution must be used in prescribing high doses of the drug to patients with high baseline threshold.     

Chronic Ventricular Pacing Using an Output Amplitude of 1.0 Volt

Thirty-seven patients (21 male, 16 female, mean age 71 years) received identical DDD pacemakers. They also received the same bipolar ventricular passive fixation electrode, which has a microporous tip of platinum-iridium, a surface area of 5.8 mm², and steroid elution. Eighteen months after implantation the ventricular charge threshold [μC] was measured telemetrically at 0.5, 1.0, and 2.0 V, respectively. For the 1.0 and 2.0 V amplitudes the pulse duration was increased until the charge per pulse [μC] was twice the threshold value, thus giving a 100% safety margin in terms of charge ("safety charge"). Patients who had ventricular capture at 0.5 V were permanently programmed to 1.0 V (30/37 patients), while those who did not capture at 0.5 V were set to 2.0 V (7/37 patients). In both cases, the pulse duration was programmed according to the rationale of "safety charge." During a routine follow-up period of 6 months, no complications were observed and none of the patients suffered from symptoms indicating loss of ventricular capture. Twenty-four-hour Holter recordings, obtained from all patients at the end of the follow-up with the output parameters unchanged, revealed constant ventricular capture. In patients with chronic stable pacing thresholds and steroid-eluting low threshold leads who have capture at 0.5 V, chronic ventricular pacing at an output amplitude of 1.0 V is feasible, and it seems to be safe if the pacing threshold is measured as charge delivered per pulse and a 100% safety margin in terms of charge is programmed. Reducing the output amplitude to well below the battery voltage may increase pacemaker longevity.     

Acute and Chronic Cycle Length Dependent Increase in Ventricular Pacing Threshold

Several factors have been shown to influence ventricuJar pacing threshold in humans, including pacing lead location (endocardial vs epicardial), lead maturation, and antiarrhythmic agents. To determine whether ventricuJar pacing rate has a significant influence on acute and chronic pacing thresholds, we measured pacing thresholds in 16 patients receiving an implantafaleantitachycardia pacemaker cardioverter defibrillator (Cadence?). Ventricular pacing thresholds were determined using the device programmer at cycle lengths of GOO, 400, and 300 msec at the time of implantation; prior to hospital discharge at 3-14 days; and during follow-up outpatient visits at 6-8 weeks, 3 months, and 6 months to 1 year. Eleven patients had an epicardial lead system and five an endocardial lead system. Eleven patients were being treated with antiarrhythmic drug therapy. Device output ranged from 1-10 V and was adjustable in 1-V increments (pulse width was held constant at 1 msec). A cycle length dependent increase in pacing threshold (defined as a ≤ 1-V increase in threshold at 400 or 300 msec relative to 600 msecj was observed in 10/16 patients during 12/72 pacing trials at 400 msec, and in 15/16 patients during 31/67 trials at 300 msec. In trials in which an increase in pacing threshold occurred, the magnitude of the increase at 400 msec relative to 600 msec was only 1 V in all 12 trials, but at 300 msec the increase ranged from 4–9 V in 7/31 (23%) trials. There was an equal percentage (67%) of patients demonstrating a cycle length dependent increase in threshold with measurements made at the time of device implantation and at the 6 month to 1 year follow-up period. Two-way analysis of variance showed a significant effect of cycle length and time from implantation on mean pacing thresholds at the three cycle lengths. In conclusion, a cycle length dependent increase in pacing threshold occurred in virtually all patients during follow-up of up to 12 months and, thus, its presence was independent of lead location, presence of antiarrhythmic agents, and the state of lead maturation. These findings suggest that pacing thresholds measured at rates just above the sinus rate may not always apply to the faster rates utilized for antitachycardia pacing and indicates the need for threshold measurement at the designed pacing rate.     

Circadian Variations of Heart Rate and STIMT Interval: Adaptation for Nighttime Pacing

In order to determine the optimal pacing rate for pacemaker patients at night, 150 normal subjects with regular sinus rhythm and free of manifest heart disease, were studied using 24-hour Holter monitoring. Minimum and average heart rates were analyzed on an hourly basis. The study group was divided into six age groups, 25 subjects each, ranging from 20-29 years to 60-69 years. The minimum heart rate during the night was found to be lower than 65 ppm for all groups. The youngest subjects showed the largest variation in the minimum heart rate. The results suggest that an automatic lowering of the pacing rate during the night would allow for longer periods of sinus rhythm, thereby improving hemodynamic performance and reducing pacemaker power consumption. Suitable sensors for automatic lowering of the pacing rate include inbuilt 24-hour clock systems and the QT interval that lengthens during sleep.     

Rapid Atrial Pacing Does Not Decrease the Atrial Defibrillation Threshold

The aim of the study was to evaluate the effect of preshock atrial pacing on the atrial defibrillation threshold (DFT) during internal cardioversion of AF. The implantable atrial defibrillator has been added to the therapeutic options for patients with recurrent episodes of persistent AF. Although the device is efficient in restoring sinus rhythm, patient discomfort is a limitation. Methods that lower the ADFT are needed. Eleven patients with AF underwent internal cardioversion. In a randomized, crossover design, ADFT testing was performed, applying a step-up protocol starting at 100 V. Rapid atrial pacing was performed with a right atrial catheter for 20 seconds at 90% of the average cycle length of the fibrillatory waves and was immediately followed by a biphasic defibrillation shock. At each energy level, pacing + shock was compared to shock only, until the level at which sinus rhythm was restored by both modes. The step-up protocol was thereafter repeated using the inverse sequence of the two modes. A total of 19 ADFTs were obtained. For 10 the ADFT was lower with pacing + shock, in 4 equal and in 5 higher, than with shock only. The ADFT (mean ± SD) with pacing + shock was   260 ± 84   V   (3.4 ± 2.9 J)   and did not differ from shock only:   268 ± 85   V   (3.8 ± 3.0 J) (P > 0.05)   . The coefficient of variation and the coefficient of reproducibility for pacing + shock was 16% and 60 V, respectively, and for shock only 17% and 61 V. Rapid atrial pacing did not influence the internal ADFT in AF. The randomized, crossover protocol used was reproducible between different modes, and seems useful when testing the impact of different interventions on the ADFT. (PACE 2003; 26[Pt. I]:1461–1466)     

Propafenone Induced Acute Variation of Chronic Atrial Pacing Threshold: A Case Report

A marked increase of chronic atrial pacing threshold resulting in loss of atrial capture, induced by propafenone, is reported in a patient with bradycardia-tachycardia syndrome. After atrial pacemaker implant, the atrial threshold had been measured repeatedly noninvasively and shown to be stable. The threshold rise and loss of atrial capture occurred after 7 days of treatment with propafenone at the dosage of 450 mg daily; drug withdrawal resulted in resumption of atrial capture and a return to prior pacing thresholds.     

Short AV Interval VDD Pacing Does Not Prevent Tilt Induced Vasovagal Syncope in Patients with Cardioinhihitory Vasovagal Syndrome

Eleven subjects (mean age 50 years, range 33–71 years), who had previously received permanent dual chamber pacemakers for cardioinhibitory vasovagal syncope, underwent paired Westminster protocol tilt tests, one with short AV delay VDD pacing and one without pacing, to test the hypothesis that continuous ventricular pacing would prevent the cardiac initiation of vasovagal syncope. Nine (82%) of the paced tilts produced positive vasovagal outcomes compared with seven (64%) of the unpaced tilts. No important differences in the heart rate or blood pressure behavior during tilt or the time to positive vasovagal outcomes were observed between the paired tilts. There was more accelerated syncope/presyncope once symptoms had developed during the paced tilts of subjects in whom both study tilts were positive, although this did not reach statistical significance (P = 0.054). This study shows that atrial synchronous ventricular pacing does not prevent the initiation, or progression, of tilt induced vasovagal syncope in predisposed subjects.     

Adaptive Rate Pacing Controlled by the Right Ventricular Preelection Interval: Clinical Experience With a Physiological Pacing System

In the Precept pacing system, the right ventricular intracardiac impedance waveform is used to evaluate either of two indicators of metabolic demand relative right ventricular stroke volume and preejection interval (PEI). PEI is known to reliably parallel contractility changes, which is reflective of physical and emotional stress. The stability and dynamic behavior of PEI were tested in ten patients with a Precept pacing system under various forms of exercise and during postural changes. Although significant patient-to-patient variability of the sensor values was observed, reflecting individual physiological differences, the chronic stability of PEI was excellent in the total device experience of 147 months. In all patients, PEI shortened significantly during bicycle ergometry from a mean value of 137.7 +/- 17.8 (range 96-162) to a mean value of 103.0 +/- 21.6 (range 92-109) (P less than 0.05). Low level bicycle exercise of short duration resulted in a prompt decrease in PEI and increase in pacing rate in all patients. There were no uniform postural responses overall, although some posture related rate changes were observed in two patients. We conclude that the first generation of a PEI based pacing system holds promise for adaptive rate pacing.     

Cardiac Stimulation Threshold in Familial Amyloidosis with Polyneuropathy

It has been suggested that a higher cardiac stimulation threshold reduces the applicabilty of pacemaker therapy in cardiac amyloidosis. We therefore reviewed threshold data in patients with familial amyloidosis with polyneuropathy (FAP), which is an inherited type of systemic amyloidosis, invariably involving the heart. Fourteen FAP patients treated with a pacemaker were studied. The mean (±SD) voltage stimulation threshold during implantation was 1.0 ± 0.5 V, and noninvasive follow-up 6 months later revealed a mean Vario threshold of 1.9 ± 0.5 V. Beyond this time, the threshold tended to be stable, and high threshold exit block did not occur in any patient. Several FAP patients did show a moderately elevated threshold, and a multiprogrammable pulse generator with a high output capability is recommended when pacemaker therapy is considered in these patients.     

Steroid-Eluting Electrodes Prevent Chronic Pacing Threshold Rise in the Atrial Chamher After Oral Propafenone Administration

The aim of the study was to evaluate chronic atrial pacing threshold increase after oral propafenone therapy. Fifty patients affected by advanced AV block and sick sinus syndrome were studied at least 6 months after pacemaker implantation, before and after oral propafenone therapy (450–900 mg/day based on body weight). The patients were subdivided into three groups as to the type of electrode implanted, all three unipolar: group I (20 patients) Medtronic CapSure 4003, group II (13 patients) Medtronic Target Tip 4011, group III (17 patients) Medtronic 4057 screw-in leads. In all cases, Medtronic unipolar pacemakers were implanted with the same noninvasive autothreshold measurement method. Propafenone and 5-OH-propafenone blood levels were measured 3–5 hours after drug administration. The pacing autothreshold was measured at 0.8, 1.6, and 2.5 V by reducing the pulse width. After propafenone. groups II and III showed a statistically significant threshold rise (P ranging from < 0.01 to <0.05), whereas no significant difference was found in group I. Propafenone and 5-OH-propafenone blood levels did not show any significant difference among the three groups. Strength-durution curves were drawn for the three groups before und after propafenone: at baseline the curves shifted to the left with the steep part above the knee, clearly favoring CapSure over the other two groups. After propafenone, the curves shifted to the right, with the flat part progressively more evident in groups II and III. In the atrial chamber, steroid-eluting leads prevented threshold increase after propafenone therapy, in contrast with a significant threshold rise with conventional porous and screw-in leads.     

Impedance Cardiography for Atrioventricular Interval Optimization During Permanent Left Ventricular Pacing

TSE, H-F., et al. : Impedance Cardiography for Atrioventricular Interval Optimization During Permanent Left Ventricular Pacing. Left ventricular (LV) pacing is increasingly used in the management of congestive heart failure. Optimization of the atrioventricular (AV) interval is essential to maximize the hemodynamic benefits of this therapy. Although Doppler echocardiography (echo) is the most widely used method, it is time-consuming, expensive, and operator-dependent. We examined the value of an impedance cardiography (IC)-based method of cardiac output (CO) measurement to optimize the AV interval in 5 men and 1 woman (mean age   = 72 ± 11   years) during permanent LV pacing with a 4.8 Fr unipolar coronary sinus pacing lead. Simultaneous measurements of CO by IC and echo were performed at AV intervals of 50, 80, 110, 150, 180, and 225 ms during DDD pacing at 85 beats/min. The optimal AV interval varied between 110 and 180 ms. In 5 of 6 patients (83%), the optimal AV interval by echo and IC was identical. While CO measurements were higher with IC than with echo (   6.1 ± 0.4 L/min   vs 4.7 ± 0.3 L/min, P < 0.05), CO measurements by IC and echo were closely correlated   r = 0.67   , P < 0.001). In conclusion, our initial experience suggests that IC is a reliable method of AV interval optimization during LV pacing. IC and echo measurements of CO during LV pacing were closely correlated. (PACE 2003; 26[Pt. II]:189–191)     

Relationship Between QT Interval Duration and Electrical Induction of Ventricular Tachycardia

The relation of inducible ventricular tachycardia (VT) to QT interval duration of ventricular paced rhythm has not been evaluated. To clarify this relation we measured corrected QT interval duration (QT_C) during sinus rhythm and QT interval duration during ventricular paced rhythm (QT-V) in patients with coronary artery disease without (non-VT group = group B) and with inducible VT (VT group = group A). Duration of QT-V was greater in the VT group (n = 20) compared with non-VT group (n = 20) during ventricular pacing at cycle lengths of 600 ms (424 ± 26 vs 396 ± 19 ms, P < 0.01), of 500 ms (407 ± 20 vs 383 ± 21 ms, P < 0.01), and of 400 ms (390 ± 21 vs 362 ± 17 ms, P < 0.001). During sinus rhythm the mean values of QT_C were similar in both groups (408 ± 25 vs 413 ± 20 ms, NSJ. During ventricular stimulation the percentage of patients with values of QT-V exceeding 380 ms was 35% in non-VT group and 95% in VT group (P <0.01) at cycle length of 500 ms and 5% versus 60%, respectively, (P < 0.01), at cycle length of 400 ms. Thus, a trend toward longer QT values of ventricular paced rhythm exists in patients with inducible VT.