Paced QRS Duration Research Articles

A comparison of standard and high-dose regimens for the initiation of amiodarone therapy

The effects of two regimens for the initiation of amiodarone therapy were compared in 92 patients with inducible sustained ventricular tachycardia (VT) at baseline electrophysiologic testing. Two groups of 46 patients each received a total of 16.8 gm of oral amiodarone before follow-up electrophysiologic testing. Group A (standard dose) received 1200 mg/day for 14 days, and group B (high dose) received 2400 mg/day for 7 days. Amiodarone suppressed the induction of sustained VT in six subjects (13%) in group A versus 10 (22%) in group B ( p = NS). In subjects who continued to have inducible VT after amiodarone loading, the mean increase in cycle length of induced VT was similar in group A (Δ = 85 ± 73 msec) and group B (Δ = 78 ± 59 sec). The mean increase in sinus cycle length, AH and HV intervals, paced QRS duration, and ventricular refractory periods was also not significantly different between the two groups. Side effects developed in 10 (22%) patients in group B but were serious only in one, and one patient required a reduction in dosage. Thus compared to the 14-day standard-dose regimen, the 7-day high-dose regimen was well tolerated and had similar effects on VT inducibility and electrophysiologic variables. Its use may significantly shorten the duration of hospitalization in patients with life-threatening inducible VT who are undergoing loading with amiodarone on an inpatient basis.

Clinical significance of QRS duration during ventricular pacing.

To clarify the clinical significance of an abnormally prolonged paced QRS duration, we studied 114 patients who had undergone pacing for atrioventricular block (AVB). Patients were divided into two groups: group I consisted of 29 patients with at least one paced QRS duration greater than or equal to 180 msec during the follow-up period; group II consisted of 85 patients with paced QRS durations less than 180 msec. The clinical background, QRS complexes before pacing, and the echocardiographic findings were assessed. Males (P less than 0.05), those with H-V block (P less than 0.05) and a wider QRS complex of conducted and escape beats (both P less than 0.01) were dominant in group I. The incidence of underlying heart disease was greater in group I than in group II (83% vs 32%, P less than 0.01). Reduced left ventricular ejection fraction (LVEF) and increased left ventricular end-diastolic dimension (LVDd) were more prominent in group I than in group II (LVEF 0.49 +/- 0.17 vs 0.68 +/- 0.10, P less than 0.01, LVDd 57.1 +/- 7.9 mm vs 48.5 +/- 5.6 mm, P less than 0.01). The paced QRS duration correlated with LVEF (r = -0.61) and LVDd (r = 0.81). A paced QRS duration greater than or equal to 180 msec was sensitive and specific for a LVEF less than 0.5 (83.3% and 85.2%) and LVDd greater than or equal to 60 mm (100% and 81.4%). We conclude that patients with a prolonged paced QRS duration have more serious heart disease, and the paced QRS duration can be a useful indicator of impaired LV function.

Rate-dependent failure of ventricular capture in patients treated with oral propafenone.

The effects of propafenone on ventricular excitability were studied in 18 patients after 9 +/- 6 days on oral propafenone (900 mg/day). Late diastolic double threshold right ventricular stimulation was performed at variable rates. In five patients (28%, group I) an intermittent, rate-dependent failure of ventricular capture was reproducibly observed during stimulation at rates above the sinus rhythm but not exceeding 150 beats min-1. In four patients loss of capture was preceded by gradual prolongation of the interval between the stimulus artifact and the local right ventricular bipolar electrogram. Such findings were not observed in the remaining 13 patients (group II) on propafenone nor in 28 studies in the same patients on different antiarrhythmic agents. Group I vs group II patients were older (72 +/- 4 vs 53 +/- 18 years, P = 0.002), had longer right ventricular effective refractory periods on the baseline (P = 0.004) and on propafenone (P = 0.0003), and had longer QRS duration on propafenone. The increase produced by propafenone in sinus rhythm QRS duration, paced QRS duration and ventricular effective refractory period was greater in group I than in group II: 42 +/- 36 vs 14 +/- 12 ms, P = 0.01, 94 +/- 43 vs 34 +/- 26 ms, P = 0.0002, 88 +/- 64 vs 22 +/- 37 ms, P = 0.025, respectively. Thus propafenone can produce rate-dependent failure of ventricular capture which is associated with marked prolongation of refractoriness and QRS duration suggesting a marked use-dependent drug effect in selected patients.

Effects of Pirmenol on Electrical Induction of Sustained Ventricular Tachycardia in a Seven-Day-Old Canine Myocardial Infarction

Effects of pirmenol on electrical induction of sustained ventricular tachycardia (VT) were examined in 14 dogs with 7-day-old myocardial infarctions. Before administration of the drug, sustained VT was induced in 8 of 14 dogs. After administration of 3 mg/kg pirmenol, induction of VT was suppressed in 2 dogs but remained inducible in 6 dogs. After cumulative administration of 5 mg/kg pirmenol, VT was no longer inducible in 3 dogs but in the other 3 dogs VTs were still inducible at increased cycle lengths. After 7 mg/kg pirmenol, VT was not inducible in the remaining three dogs. Arrhythmias could not be provoked in any postinfarction dogs after pirmenol administration. Plasma concentrations after sequential and cumulative administration of 3, 5, and 7 mg/kg pirmenol averaged 0.43, 0.65, and 1.15 micrograms/ml, respectively. Administration of pirmenol increased the effective refractory period (ERP) and paced QRS duration in both the normal and infarcted ventricular myocardium. In the infarcted myocardium, prolongation of the ERP for the second and third extrastimuli was greater than for the first one (p less than 0.05). Results indicate that pirmenol is effective for prevention of sustained VT owing to prolongation of both the ERP and conduction time in recent myocardial infarction.

Efficacy of propafenone in preventing ventricular tachycardia: Inverse correlation with rate-related prolongation of conduction time

The efficacy of propafenone in preventing induction of ventricular tachycardia was evaluated in 25 consecutive patients (mean age 62 ± 8 years) with remote myocardial infarction who underwent programmed electrical stimulation for ventricular arrhythmia using up to three extrastimuli after basic drive at the right ventricular apex. In nine patients (Group A), propafenone prevented induction of sustained ventricular tachycardia (noninducible in four, nonsustained [<30 s] in five). In the other 16 patients (Group B), sustained ventricular tachycardia was still inducible; in 11 of the 16, the tachycardia configuration was unchanged but the cycle length was significantly longer (431 ± 99 versus 284 ± 44 ms, p < 0.001).Propafenone did not significantly affect either sinus cycle length or AH and HV intervals. However, it prolonged QRS duration during sinus rhythm equally in both groups of patients. With ventricular pacing, propafenone also prolonged right ventricular effective and functional refractory periods and surface QRS duration. There was greater lengthening of the paced surface QRS duration when drug therapy was ineffective (for example, +35 ± 12 ms in Group A versus +69 ± 23 ms in Group B at a basic drive of 400 ms, p < 0.01). Drag-induced prolongation of a paced QRS complex >40 ms had a 94% positive predictive value for drug failure to prevent induction of ventricular tachycardia. Drug-induced percent prolongation of ventricular tachycardia cycle length in Group B did not correlate well with percent QRS prolongation. Rather, the best correlation was with percent prolongation of right ventricular effective (r = 0.72, p < 0.02) and functional (r = 0.73, p < 0.02) refractory periods at a basic drive of 400 ms.These observations suggest that excessive prolongation of conduction time in presumably normal tissue reduces the ability of propafenone to prevent ventricular tachycardia induction. It is speculated that effects of a drug on conduction time in partially refractory abnormal tissue forming the reentrant circuit may play a role in determining the tachycardia cycle length in the presence of that drug.

Efficacy of procainamide on ventricular tachycardia: Relation to prolongation of refractoriness and slowing of conduction

The effect of procainamide on intraventricular conduction and refractoriness, and the prevention of induction of ventricular tachycardia (VT) were studied in 29 patients who had remote myocardial infarction and inducible sustained monomorphic VT. After intravenous administration of 15 mg/kg procainamide, induction of VT was suppressed in seven (24%) patients (responders), while in 22 (76%) VT was still inducible (nonresponders). The percent change in paced QRS duration at a cycle length (CL) of 400 msec produced by procainamide was significantly less in responders than in nonresponders: 29.8 ± 3.9% versus 38.9 ± 10.8% ( p = 0.0020). The percent change in the right ventricular effective refractory period (ERP) at CLs of 600 and 400 msec was significantly greater in responders than in nonresponders: 14.6 ± 6.9% versus 7.9 ± 7.3% ( p = 0.0414) for ERP at a CL of 600 msec and 15.1 ± 7.0% versus 8.0 ± 7.4% ( p = 0.0386) for ERP at a CL of 400 msec. Stepwise discriminant analysis showed that greater percent increase in ERP at a CL of 400 msec and lesser percent increase in paced QRS duration at a CL of 400 msec were significant independent markers for the responders. These findings suggest that lesser slowing of conduction and greater prolongation of refractoriness by procainamide tend to abolish reentry within the reentrant circuit. Greater slowing of conduction and lesser prolongation of refractoriness tend to stabilize a reentrant circuit, and promote the continued induction of VT.

Predicting ventricular tachycardia cycle length after procainamide by assessing cycle length-dependent changes in paced QRS duration.

To determine if paced cycle length-dependent changes in the QRS duration correlate with the change in ventricular tachycardia (VT) cycle length after procainamide, we measured the QRS duration during sinus rhythm and during right ventricular pacing before and after procainamide (mean concentration, 9.9 micrograms/ml) in 18 patients with morphologically identical VT induced at both study periods. Pacing was performed at 600 msec or the longest cycle length that allowed for uninterrupted capture and at a cycle length that was within 50 msec of the VT cycle length observed during the control study (mean, 313 +/- 51 msec). After procainamide, the VT cycle length increased from 285 +/- 62 to 368 +/- 70 msec (percent change, 30 +/- 13%). The QRS duration during sinus rhythm increased from 125 +/- 25 to 145 +/- 29 msec (percent change, 16%). The QRS duration at both paced cycle lengths was the same in the baseline state (191 +/- 26 msec). However, the change in QRS duration after procainamide at the shorter paced cycle length compared to a 39 +/- 13 msec (18%) increase at the longer paced cycle, p less than 0.001. There was a significant correlation between the percent change in QRS duration at the shorter paced cycle length and the percent change in VT cycle length (r = 0.84, p less than 0.001) with the relation expressed by the regression equation: percent change in VT cycle length = -2.8 + 1.16 x percent change in QRS duration.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of lidocaine and procainamide on normal and abnormal intraventricular electrograms during sinus rhythm.

The effect of lidocaine (n = 6) and procainamide (n = 12) on electrogram characteristics from electrically normal right ventricular and electrically abnormal left ventricular endocardial sites was determined in 18 patients with prior myocardial infarction. Bipolar electrograms were recorded during sinus rhythm with No. 6F catheters positioned at a left ventricular abnormal site (electrograms fulfilling two of the following criteria: amplitude less than 3 mV, duration greater than 70 msec, or an amplitude to duration ratio less than .046) and normal sites at the right ventricular apex (RVA) and right ventricular outflow tract (RVOT). All electrograms were recorded from the same location before and after intravenous lidocaine or procainamide administered to obtain mean serum concentrations of 4.2 +/- 0.6 and 9.42 +/- 2 micrograms/ml respectively. Lidocaine and procainamide had no significant effect on sinus cycle length or electrogram amplitude. After lidocaine, no significant change in QRS width (112 +/- 23 vs 114 +/- 24 msec), left ventricular electrogram duration (76 +/- 21 vs 78 +/- 15 msec), or right ventricular electrogram duration (RVA 33 +/- 9 vs 33 +/- 10 msec, RVOT 31 +/- 9 vs 33 +/- 11 msec) was noted during sinus rhythm. At a paced cycle length of 600 msec, there was also no change in the paced QRS duration (197 vs 198 msec), the RVA electrogram duration (30 vs 32 msec), the RVOT electrogram duration (49 vs 52 msec), or the left ventricular electrogram duration (102 vs 108 msec).(ABSTRACT TRUNCATED AT 250 WORDS)