Shortening of ventriculoatrial intervals with left bundle branch block during orthodromic reciprocating tachycardia in three patients with a right-sided accessory atrioventricular pathway.

Previous studies of the effects of bundle branch block on ventriculoatrial (VA) intervals during orthodromic reciprocating tachycardia have focused on the timing of the atrial electrograms. However, left bundle branch block importantly affects the timing of initial ventricular activation, and this effect would also be expected to affect VA intervals during orthodromic reciprocating tachycardia. Presented here are three patients with a single right-sided accessory atrioventricular pathway exhibiting left bundle branch block during orthodromic reciprocating tachycardia. Each had shortening of the VA interval by 10 to 30 ms during left bundle branch block beats. This shortening was accompanied by a nearly equal increase in the HV interval, with the His bundle to atrial interval remaining constant. It is concluded that the timing of ventricular as well as atrial electrograms impacts on the VA intervals with left bundle branch block beats during orthodromic reciprocating tachycardia. With left bundle branch block, delay in initial left septal activation results in later onset of the QRS complex and, with right ventricular activation occurring normally, shortening of the VA interval occurs in patients with a right-sided pathway.

Rate-dependent effects of intravenous lidocaine, procainamide and amiodarone on intraventricular conduction.

In this study, the duration of the QRS complex during ventricular pacing was used as an index of intraventricular conduction to quantitate the rate-dependent effects of intravenous lidocaine, procainamide and amiodarone. Right ventricular apical pacing (15 to 20 beats) was performed at cycle lengths of 600, 500, 400, 350, 300, 275 and 250 ms, before and 5 minutes after the intravenous administration of lidocaine in 11 patients (serum level 3.2 +/- 0.8 micrograms/ml [mean +/- SD] ), procainamide in 14 patients (serum level 8.2 +/- 1.9 micrograms/ml) and amiodarone in 12 patients (serum level 3.9 +/- 1.2 micrograms/ml). Electrocardiographic recordings were made at a paper speed of 150 mm/s. QRS duration was measured in a blinded fashion, with reproducibility within 5%. In the control state, QRS duration was the same at all paced cycle lengths. After lidocaine, procainamide and amiodarone administration, the shortest paced cycle length with complete ventricular capture was 250 +/- 0, 275 +/- 38 and 264 +/- 20 ms, respectively. At a paced cycle length of 600 ms, the increase in QRS duration compared with the control state was 1 +/- 2% with lidocaine (p greater than 0.05), 21 +/- 7% with procainamide (p less than 0.001) and 6 +/- 6% with amiodarone (p less than 0.05). At the shortest paced cycle length with complete capture, the increase in QRS duration compared with the control state was 20 +/- 6% with lidocaine (p less than 0.001), 42 +/- 11% with procainamide (p less than 0.001) and 26 +/- 4% with amiodarone (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Ventricular response to atrial fibrillation: role of atrioventricular conduction pathways.

Irregularity of the ventricular rhythm is a hallmark of patients with atrial fibrillation, yet the genesis of the irregularity is not yet fully understood. The role of the atrioventricular (AV) node in determining the irregularity of the ventricular response to atrial fibrillation was investigated by comparing the frequency distributions of the atrial (AA) and the ventricular (RR) intervals. Atrial electrograms and surface electrocardiographic leads were recorded during sustained atrial fibrillation in 12 patients with conduction over the AV node. The scaling factor (mean RR interval/mean AA interval) quantified the ability of the conduction pathway to scale the atrial input to a slower ventricular response and ranged from 2.55 to 5.92 (mean +/- SD 3.77 +/- 0.92). The coefficient of variation (SD/mean) measured the relative variability of the AA and RR interval distributions. The atrial and ventricular coefficients of variation were not significantly different (0.20 +/- 0.04 versus 0.21 +/- 0.03, p greater than 0.27). Similar recordings were analyzed in six patients with conduction over a accessory AV pathway. The scaling factor ranged from 1.54 to 2.46 (2.02 +/- 0.39) and, as was the case for patients with conduction over the AV node, the atrial and ventricular coefficients of variation did not significantly differ (0.24 +/- 0.08 versus 0.27 +/- 0.10, p greater than 0.6). For both groups of patients, ventricular variability and the maximal RR intervals were predicted by the product of the scaling factor and either atrial variability or maximal AA intervals, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Detection of changes in atrial endocardial activation with use of an orthogonal catheter.

The ability of a catheter with an orthogonal electrode configuration to sense differences in the direction of local atrial endocardial activation was tested in 18 consecutive patients with intact retrograde conduction. In all 18, discrimination of anterograde from retrograde conduction at a single atrial site was examined; in 5 of the 18, multiple sites were examined to determine if the discriminatory ability of the catheter was site dependent. The catheter was specially designed with bipoles in the x, y and z directions. A vector was computed for each electrogram during anterograde and retrograde conduction. Electrogram amplitude along the standard bipole was also compared for anterograde and retrograde conduction. Mean electrogram amplitude for the standard bipole was significantly different for anterograde than for retrograde conduction in 17 of 18 patients (mean +/- SD 4 +/- 1.9 vs. 2.7 +/- 1.3 mV; p less than 0.005), with complete separation of amplitude distributions in 4 patients. The electrogram vector during anterograde conduction was significantly different from that during retrograde conduction in all 18 patients (p less than 0.0001), with complete separation of vector distributions in 14. In some patients with multiple site recordings, the choice of site greatly affected separation based on electrogram amplitude or vector, or both. The orthogonal catheter can be used to sense directional differences in local endocardial activation. The catheter shows promise for discriminating anterograde from retrograde conduction and examining the direction of endocardial activation in the heart during an electrophysiologic examination.

The plasma catecholamine response to ventricular tachycardia induction and external countershock during electrophysiologic testing.

Adrenergic activation during electrophysiologic study could potentially alter the electrophysiologic properties of the arrhythmia substrate. However, the catecholamine response to ventricular tachycardia induction and termination during electrophysiologic testing has to date not been quantitated. Therefore, in 13 patients undergoing electrophysiologic study, arterial plasma norepinephrine and epinephrine were measured before, during and 1, 3, 5, 10 and 15 minutes after ventricular tachycardia induced by programmed stimulation and terminated by a single 100 J external countershock. Sinus rate and the effective refractory period at the right ventricular apex at a basic drive cycle length of 400 ms were measured after the countershock at the same time intervals used for the catecholamine measurements. The mean ventricular tachycardia cycle length (+/- SD) was 187 +/- 30 ms, and the mean duration of ventricular tachycardia was 18 +/- 4 seconds. Plasma norepinephrine and epinephrine increased, respectively, from a baseline of 286 +/- 141 and 119 +/- 40 pg/ml to 770 +/- 330 (169%) and 597 +/- 467 pg/ml (402%), (p less than 0.01) at 1 minute after the countershock. The mean plasma norepinephrine and epinephrine levels during ventricular tachycardia and at times greater than 1 minute after the shock did not differ significantly from baseline levels. Sinus rate increased from a baseline of 74 +/- 13 to 103 +/- 26/min (39%) at 1 minute after the shock (p less than 0.05) and then returned to baseline.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute and chronic effects of amiodarone on ventricular refractoriness, intraventricular conduction and ventricular tachycardia induction.

In eight patients, the right ventricular effective refractory period, rate-dependent changes in intraventricular conduction (as reflected by QRS duration during ventricular paced cycle lengths of 600 to 250 ms) and results of programmed ventricular stimulation were determined in the control state, 5 minutes after the intravenous infusion of 10 mg/kg body weight of amiodarone and after 2 months of treatment with oral amiodarone. The right ventricular effective refractory period was 230 +/- 30 ms (mean +/- SD) in the control study, 248 +/- 27 ms after intravenous amiodarone (p less than 0.001) and 296 +/- 26 ms after oral amiodarone (p less than 0.001). In the control state, QRS duration was constant at all paced cycle lengths. Intravenous amiodarone resulted in a rate-dependent prolongation of QRS duration. This rate-dependent prolongation was markedly accentuated by oral amiodarone in six patients who had an elevated serum level of reverse triiodothyronine (T3) after 2 months of oral treatment, but it was not more pronounced than the effects of intravenous amiodarone in two patients with a normal reverse T3 serum level after oral therapy. Both intravenous and oral amiodarone either suppressed or modified the induction of ventricular tachycardia by programmed stimulation in some patients, but in a discordant fashion. The relative effects of intravenous and oral amiodarone on ventricular refractoriness and conduction and on ventricular tachycardia induction did not correlate with serum amiodarone levels. Chronic amiodarone therapy results in a marked prolongation in ventricular refractoriness compared with the relatively small but significant increase that occurs after intravenous amiodarone.(ABSTRACT TRUNCATED AT 250 WORDS)

Determinants of QRS alternans during narrow QRS tachycardia.

This study was designed to prospectively determine the incidence of QRS alternans during various types of narrow QRS tachycardia and to clarify the determinants of QRS alternans. An electrophysiologic study was performed in 28 consecutive patients with a narrow QRS tachycardia. Persistent QRS alternans was observed in 6 (43%) of 14 patients during orthodromic reciprocating tachycardia, 5 (71%) of 7 patients during atrial tachycardia and 3 (43%) of 7 patients during atrioventricular (AV) node reentrant tachycardia. Incremental atrial pacing during sinus rhythm resulted in QRS alternans in patients who had QRS alternans during tachycardia, unless the shortest pacing cycle length associated with 1:1 AV conduction exceeded the tachycardia cycle length. In patients without QRS alternans during narrow QRS tachycardia, incremental atrial pacing during sinus rhythm resulted in persistent QRS alternans in five patients in whom the shortest pacing cycle length associated with 1:1 AV conduction was 60 to 180 ms less than the tachycardia cycle length. In an additional 20 patients without a narrow QRS tachycardia, persistent QRS alternans was observed during incremental atrial pacing in 11 (55%) of the patients. In six of six patients who had QRS alternans during abrupt rapid atrial pacing, QRS alternans was not observed when the same pacing rates were achieved gradually. Among the patients with narrow QRS tachycardia, the mean tachycardia cycle length in those who had QRS alternans (mean +/- SD 288 +/- 44 ms) was significantly shorter than in those who did not (369 +/- 52 ms, p less than 0.001). The presence of QRS alternans was not related to the tachycardia mechanism, relative or functional refractory period of the His-Purkinje system (at a drive cycle length of 500 ms), age, presence of structural heart disease, direction of input into the AV node or concealed retrograde conduction in the His-Purkinje system. In conclusion, QRS alternans during narrow QRS tachycardias is a rate-related phenomenon that depends on an abrupt increase to a critical rate and is independent of the tachycardia mechanism.

Concealed anterograde accessory pathway conduction during the induction of orthodromic reciprocating tachycardia.

The purpose of this study was to determine whether concealed anterograde accessory pathway conduction occurs during the induction of orthodromic tachycardia by an atrial extrastimulus (S2). Sixteen patients with an overt (n = 9) or concealed (n = 7) accessory pathway had inducible orthodromic tachycardia by S2 during an atrial drive (S1) cycle length of 500 to 650 ms. A ventricular extrastimulus (S3) was introduced coincident with the His depolarization resulting from S2 during the longest S1S2 interval that reproducibly induced orthodromic tachycardia. The S1S3 interval was decreased in 10 ms steps until S3 reached ventricular refractoriness. Retrograde accessory pathway conduction of S3 in the presence and absence of S2 was compared at the same S1S3 intervals. In the absence of S2 there was retrograde accessory pathway conduction after S3 in each patient. In the presence of S2, in patients with overt pre-excitation, retrograde accessory pathway conduction after S3 was absent in one patient, prolonged in four patients and present only after long S1S3 intervals in three patients. Only one patient had unchanged retrograde conduction regardless of the presence or absence of S2. In patients with a concealed accessory pathway, retrograde accessory pathway conduction after S3 was absent in five patients and was prolonged in two. Thus, concealed anterograde accessory pathway conduction was present in 15 of 16 patients at the time of orthodromic tachycardia induction. In conclusion, concealed anterograde accessory pathway conduction occurs in a majority of patients with an overt or a concealed accessory pathway during induction of orthodromic tachycardia by an atrial extrastimulus.(ABSTRACT TRUNCATED AT 250 WORDS)

Coexistent posteroseptal and right-sided atrioventricular bypass tracts.

Twelve patients with a posteroseptal accessory pathway underwent complete electrophysiologic studies, and four were found to have a second atrioventricular (AV) bypass tract that was right anterior, right anteromedial or right anterolateral in location. In two of these four patients, the presence of the right-sided AV bypass tract was confirmed by intraoperative epicardial mapping or after catheter-induced abolition of retrograde conduction through the posteroseptal bypass tract. In three of the four patients with a dual AV bypass tract, the delta wave pattern was clearly atypical of the pattern seen with an isolated posteroseptal accessory pathway. Instead of a transition from an isoelectric or slightly positive delta wave in lead V1 to markedly positive delta waves in leads V2 to V6, the delta waves were negative or only slightly positive in leads V2 to V5. However, in a fourth patient with dual AV bypass tracts, the only atypical electrocardiographic finding was an intermittently positive delta wave in lead II; at times this patient's electrocardiogram was consistent with an isolated posteroseptal bypass tract, with negative delta waves in the inferior leads. There appears to be an association between posteroseptal and right-sided accessory pathways. In patients with a posteroseptal accessory pathway who are candidates for catheter or surgical bypass tract ablation, a complete mapping study of the tricuspid anulus is mandatory, even when the electrocardiogram is typical of an isolated posteroseptal bypass tract.

Role of myocardial ischemia during programmed stimulation in survivors of cardiac arrest with coronary artery disease.

The role of ischemia in the induction of ventricular tachycardia during programmed stimulation was studied in 19 patients who survived a cardiac arrest and were found to have a significant stenosis in at least one branch of the left coronary artery. The arterial-coronary sinus lactate difference was measured during electrophysiologic testing, before the induction of ventricular tachycardia. Ventricular tachycardia was induced in 15 patients; it was sustained and unimorphic in 6 patients and polymorphic in 9. Myocardial ischemia, as reflected by net myocardial lactate production, was present within 60 seconds before the induction of ventricular tachycardia in 8 of the 15 patients with inducible ventricular tachycardia. In 9 of the 15 patients, programmed stimulation was repeated after a 15 minute rest period, with the same coupling intervals that had induced ventricular tachycardia previously. Net myocardial lactate production was not present in any patient during this repeat attempt. In three patients without evidence of ischemia during the first induction of ventricular tachycardia, the arrhythmia was induced again by the specific coupling intervals that had induced it previously. However, in five of six patients with net myocardial lactate production during the first induction of ventricular tachycardia, the same coupling intervals that had induced the arrhythmia in the presence of ischemia no longer induced it in the absence of ischemia. The results of this study suggest that myocardial ischemia may be a requirement for the induction of ventricular tachycardia in some patients with coronary artery disease who survive a cardiac arrest.

Electrophysiologic testing in patients with unexplained syncope: clinical and noninvasive predictors of outcome.

To assess whether the level of risk of having significant electrophysiologic abnormalities can be determined, 29 clinical variables were analyzed in 104 patients with unexplained syncope who underwent electrophysiologic testing. A positive electrophysiologic study was defined as: a sinus node recovery time greater than or equal to 3 seconds; HV interval greater than or equal to 100 ms; infranodal block during atrial pacing; unimorphic ventricular tachycardia; and supraventricular tachycardia associated with hypotension. Thirty-one patients had a positive study, with inducible ventricular tachycardia being the most common finding (71% of positive studies). A left ventricular ejection fraction less than or equal to 0.40 was the most powerful predictor of a positive electrophysiologic study (p less than 0.00001), followed by the presence of bundle branch block (p less than 0.00003), coronary artery disease (p less than 0.0003), remote myocardial infarction (p less than 0.00006), use of type 1 antiarrhythmic drugs (p less than 0.00003), injury related to loss of consciousness (p less than 0.01) and male sex (p less than 0.01). A negative electrophysiologic study was associated with an ejection fraction greater than 0.40 (p less than 0.00001), the absence of structural heart disease (p less than 0.00001), a normal electrocardiogram (ECG) (p less than 0.0001) and normal ambulatory ECG monitoring (p less than 0.0001). The probability of a negative study increased as the number and duration of syncopal episodes increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of coupling intervals that induce clinical and nonclinical forms of ventricular tachycardia during programmed stimulation.

Coupling intervals of extrastimuli that induced 57 previously documented unimorphic ventricular tachycardias (VTs) were compared with coupling intervals that induced 57 episodes of polymorphic VT or ventricular fibrillation (VF) in patients without a documented or suspected history of polymorphic VT or VF. Programmed stimulation was performed with the patient in the drug-free state, with 1 to 3 extrastimuli and 2 basic drive cycle lengths (600 or 500 ms, and 400 ms) at 2 right ventricular sites; stimuli were twice diastolic threshold. The mean coupling intervals of the first, second and third extrastimuli that induced nonclinical VT/VF (241 +/- 19, 185 +/- 19 and 173 +/- 24 ms, respectively, mean +/- standard deviation) were significantly shorter than the corresponding coupling intervals that induced the clinical VTs (266 +/- 25, 228 +/- 32 and 214 +/- 27 ms, respectively, p less than 0.001 for each). Regardless of the basic drive cycle length, the shortest coupling interval required to induce a clinical VT was 180 ms. Depending on the drive cycle length, 29 to 70% of nonclinical VT/VF induced by 3 extrastimuli required a coupling interval of less than 180 ms to induce. Therefore, a lower limit of coupling intervals may be identified below which only nonclinical VT/VF is induced by programmed stimulation. Restriction of coupling intervals to this lower limit may allow for significant improvement in specificity without compromise in the sensitivity of programmed ventricular stimulation protocols.

Immediate reproducibility of clinical and nonclinical forms of induced ventricular tachycardia.

This prospective study assessed the immediate reproducibility of clinical and nonclinical forms of ventricular tachycardia (VT) induced by programmed ventricular stimulation. Twenty-three clinical VTs were unimorphic and previously documented and 22 nonclinical VTs (17 polymorphic and 5 unimorphic) were induced in patients with either no documented or suspected history of VT, or documented VT that had a configuration different from that of the induced VT. The stimulation protocol included 1 to 3 ventricular extrastimuli, 2 drive cycle lengths, and 2 right ventricular stimulation sites. Each VT was induced on the first attempt, then the stimulation protocol was repeated twice in the drug-free state. After the first VT induction, 21 of 23 clinical VTs (91%) and 17 of 22 nonclinical VTs (77%) were reinduced on the second attempt. After 2 VT inductions, 21 of 21 clinical VTs (100%) and 15 of 17 nonclinical VTs (88%) were reinduced on the third attempt. The reinduction rates of the clinical and nonclinical VTs were not significantly different. Among the clinical VTs, the reproducibility of the induction technique was 81% after 1 induction and 88% after 2 inductions with the same technique. These results imply that acute drug testing can be reliably performed after 2 inductions but not 1 induction of clinical VT; reproducibility is not helpful in determining whether an induced VT is clinical or nonclinical; and changes in induction technique during drug testing should be interpreted with caution because changes may occur in the absence of drugs.

Effects of high stimulation current on the induction of ventricular tachycardia.

Programmed stimulation at 2 right ventricular sites with 1 to 3 extrastimuli was performed at current strengths of twice diastolic threshold (1.0 +/- 0.2 mA, mean +/- standard deviation) and 10 mA in 41 patients undergoing an electrophysiologic study because of sustained ventricular tachycardia (VT) (11 patients), nonsustained VT (19 patients) or unexplained syncope (11 patients). In 26 patients, VT was not induced by programmed stimulation at twice diastolic threshold. Programmed stimulation at 10 mA induced VT or ventricular fibrillation in 16 of these 26 patients (62%). In 4 of 16 patients, the coupling intervals of the extrastimuli that induced VT/ventricular fibrillation at 10 mA were all equal to or longer than the shortest coupling intervals resulting in ventricular capture at twice diastolic threshold. Fifteen patients had inducible VT at twice diastolic threshold. Programmed stimulation at 10 mA induced a similar VT in 12 of these patients, but resulted in no VT induction in 3 of 15 patients (20%), despite ventricular capture at the same coupling intervals that had induced VT at twice diastolic threshold. This study shows that programmed stimulation at a high current strength may either facilitate or prevent induction of VT. Facilitation of VT induction usually is attributable to a shortening of ventricular refractoriness and the ability of extrastimuli at 10 mA to capture the ventricle at shorter coupling intervals than possible at twice diastolic threshold. However, in 25% of cases, the facilitation of VT induction by 10-mA stimuli is not explained by a shortening of ventricular refractoriness.(ABSTRACT TRUNCATED AT 250 WORDS)

Use of multiple patches during implantation of epicardial defibrillator systems.

During implantation of epicardial automatic defibrillator systems, occasional patients have difficulty in obtaining adequate defibrillation thresholds. Of 236 consecutive patients undergoing implantation of epicardial defibrillator systems, 18 patients received a 3-patch (n = 15) or 4-patch (n = 3) defibrillator system. Twelve patients who received a multiple-patch defibrillator system had a best 2-patch defibrillation energy requirement of > or = 30 J; in the remaining 6 patients less stringent clinical criteria were used in the decision to add a third defibrillator patch (defibrillation energy requirement > 18 J in 4 patients, and > 20 J in 2 patients). Technically, multiple-patch systems were made possible with either the use of Y-connectors or defibrillators allowing output to 3 patches. In 3 patients, addition of a third epicardial patch still resulted in a defibrillation energy requirement of > or = 30 J; in these 3 patients, addition of a fourth patch resulted in a defibrillation energy requirement of < or = 20 J. All patients receiving a multiple-patch defibrillator system had a reduction in defibrillation energy requirement, and 12 patients had a reduction in defibrillation energy requirement of > or = 10 J over the best 2-patch defibrillation energy requirement. In the patients who eventually had placement of a multiple-patch system, the best 2-patch defibrillation energy requirement was > 18 J in 4 patients, > 20 J in 2 patients, > or = 30 J in 9 patients, and > 40 J in 3 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Natural history and determinants of conduction defects following coronary artery bypass surgery.

Ninety-three consecutive patients undergoing coronary artery bypass grafting (CABG) were followed prospectively to ascertain the natural history and determinants of new postoperative conduction defects. Each patient was followed in the postoperative period with serial electrocardiograms and continuous monitoring. In the last 70 patients, a technetium pyrophosphate scan was obtained 48 to 72 hours after operation. Postoperatively, new bundle-branch or fascicular block developed in 42 patients (45%) and third-degree atrioventricular (AV) block, in 4 (4%). The occurrence was compared with patient age, preoperative bundle-branch block or fascicular block, number of diseased arteries, number of bypassed arteries, total time of cardiopulmonary bypass, aortic cross-clamping time, occurrence of a preoperative or perioperative myocardial infarction, and presence of disease in the left anterior descending or right coronary artery. Only the number of bypassed arteries, the total time of cardiopulmonary bypass, and the aortic cross-clamping time were related to the development of postoperative conduction defects (all, p less than .05). The conduction defect resolved partially or completely by the time of hospital discharge in 54% of patients. In the 4 patients with third-degree AV block, AV block resolved on postoperative day 2 in 1 patient and resolved transiently for up to 5 days or persisted in 3 patients. At two months of follow-up, all 3 patients discharged in third-degree AV block with a permanent pacemaker were no longer in AV block. In conclusion, following CABG, the occurrence of new AV conduction defects is related to the number of vessels bypassed, the cardiopulmonary bypass pump time, and the aortic cross-clamping time.(ABSTRACT TRUNCATED AT 250 WORDS)

Measuring the organization of cardiac rhythms using the magnitude-squared coherence function.

The application of the magnitude-squared coherence (MSC) spectrum as a measure of the degree of organization of the cardiac electrical activity is explored. The MSC spectrum is a frequency-domain measure of the linear relationship between two signals. In the work described the two signals are two bipolar electrograms from either acutely placed catheter(s) or automatic implantable cardioverter/defibrillator electrodes. It is shown that the MSC is a dimensionless (no units), real-valued spectrum that is always in the range of zero to unity. The case of zero is found at frequencies where there is no linear relationship between the signals, and the case of unity implies a linear, noise-free relationship. The way the MSC spectrum is normalized makes it insensitive to gain or gain differences between the two signals. Example MSC spectra are presented and discussed. Striking differences in the spectra for fibrillatory and nonfibrillatory rhythms are seen.

An analysis of post-pacing R-R intervals during atrial fibrillation.

Bursts of ventricular pacing at cycle lengths of 350-260 ms were introduced during atrial fibrillation in nine patients, and the post-pacing R-R intervals were compared to the R-R intervals of spontaneous QRS complexes. In eight of nine patients, the mean post-pacing R-R interval was 126-199 ms longer than the mean spontaneous R-R interval (p less than 0.005). Spontaneous runs of aberrantly conducted supraventricular complexes were recorded during atrial fibrillation in one patient. The mean R-R interval following the runs of aberrantly conducted supraventricular complexes was significantly longer than the mean R-R interval of spontaneous narrow QRS complexes (p less than 0.001), but not significantly different than the mean post-pacing R-R interval. The findings of this study suggest that the R-R interval that follows a wide-complex tachycardia during atrial fibrillation is unlikely to be of value in differentiating ventricular tachycardia from aberrantly conducted supraventricular complexes. Analysis of R-R intervals that follow bursts of ventricular pacing suggests that there is likely to be considerable overlap between the R-R intervals that follow runs of ventricular tachycardia and the spontaneous R-R intervals during atrial fibrillation. Furthermore, even when the post-tachycardia R-R interval clearly exceeds the longest spontaneous R-R interval during atrial fibrillation, this is still of little diagnostic value, because a long pause may occur after either a run of ventricular tachycardia or a run of aberrantly conducted QRS complexes of supraventricular origin.

Effect of propranolol on ventricular rate during atrial fibrillation in the Wolff-Parkinson-White syndrome.

Atrial fibrillation was induced during an electrophysiology study in 10 patients with the Wolff-Parkinson-White (WPW) syndrome, after determination of baseline properties of the accessory atrioventricular (AV) connection; intravenous propranolol (0.2 mg/kg) was then administered. Atrial fibrillation terminated during the drug infusion in three patients, allowing determination of propranolol's effects on conduction and refractoriness during sinus rhythm, before atrial fibrillation was reinduced. In these three patients propranolol had no effect on refractoriness or conduction properties of the accessory AV connection during sinus rhythm. The mean ventricular rate during atrial fibrillation was slowed by 15-56 beats/min in six patients, had no effect on the mean rate in three patients, and markedly increased the ventricular rate (203 to 267 beats/min) in one patient. In this patient, 54% of QRS complexes during atrial fibrillation were narrow, compared to 0-25% in the other patients. Propranolol reduced the percentage of QRS complexes that were narrow from 13 +/- 16% to 1 +/- 2% (mean +/- standard deviation, p less than 0.05). We conclude that propranolol may slow the ventricular rate during atrial fibrillation in some patients with the WPW syndrome, probably by blocking the effects of adrenergic activation. However, propranolol should not be used in patients with the WPW syndrome who have atrial fibrillation, if most QRS complexes during atrial fibrillation are preexcited. When a large percentage of QRS complexes are narrow, propranolol may increase the ventricular rate, probably by eliminating concealed retrograde conduction in the accessory AV connection.