Effect of Propranolol on Ventricular Rate During Atrial Fibrillation in the Wolff-Parkinson-White Syndrome

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/74695/1/j.1540-8159.1987.tb04511.x.pd

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

AbstractThe purpose of this study was to determine whether concealed anterograde accessory pathway conduction occurs during the induction of orthodromic tachycardia by an artrial extrastimulus (S2). Sixteen patients with an overt (n = 9) or concealed (n = 7) accessory pathway had inducible orthodromic tachycardia by S2during an atrial drive (S1) cycle length of 500 to 650 ms. A ventricular extrastimulus (S3) was introduced coincident with the His depolarization resulting from S2during the longest S1S2interval that reproducibly induced orthodromic tachycardia. The S1S3interval was decreased in 10 ms steps until S3reached ventricular refractoriness. Retrograde accessory pathway conduction of S3in the presence and absence of S2was compared at the same S1S3intervals.In the absence of S2there was retrograde accessory pathway conduction after S3in each patient. In the presence of S2, in patients with overt pre-excitation, retrograde accessory pathway conduction after S3was absent in one patient, prolonged in four patients and present only after long S1S3intervals 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 S3was 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. In some patients, the initiation of orthodromic tachycardia may depend on a critical interaction between the degree of concealed anterograde accessory pathway conduction and atrioventricular conduction delay after S2

An Analysis of Post-Pacing R-R Intervals During Atrial Fibrillation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/74691/1/j.1540-8159.1986.tb04496.x.pd

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 (1) acute drug testing can be reliably performed after 2 inductions but not 1 induction of clinical VT; (2) reproducibility is not helpful in determining whether an induced VT is clinical or nonclinical; and (3) changes in induction technique during drug testing should be interpreted with caution because changes may occur in the absence of drugs.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26088/1/0000164.pd

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. In these cases, and in the patients in whom 10-mA stimuli prevent the induction of VT that was inducible at twice diastolic threshold, the effects of high current strength appear to be mediated through some other mechanism. Other possible mechanisms include an effect on temporal dispersion of refractoriness or on the pattern or extent of ventricular activation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/25627/1/0000177.pd

The interplay between endogenous catecholamines and induced ventricular tachycardia during electrophysiologic testing

Plasma epinephrine and norepinephrine concentrations were measured before, during, and shortly after induced ventricular tachycardia (VT) in 22 selected patients. Sustained, unimorphic VT was induced by programmed ventricular stimulation and terminated after 45 to 384 seconds by overdrive pacing in all patients. In no patient did VT result in loss of consciousness. The baseline plasma catecholamine concentrations did not correlate with the baseline right ventricular effective refractory period, the cycle length of induced VT, or the number of extrastimuli required to induced VT. Induced VT was not associated with a significant increase in the mean plasma epinephrine concentration. In contrast, the plasma norepinephrine concentration increased from a mean baseline level of 317 +/- 136 pg/ml (mean +/- standard deviation) to 418 +/- 220 pg/ml during VT (p = 0.01) and increased further to 569 +/- 387 pg/ml shortly after VT (p p < 0.05 for each). In eight patients the same configuration of VT was induced on two sequential attempts; in five patients the same number of extrastimull were required for the second induction of VT as for the first, whereas in three patients fewer extrastiuli were required. Plasma cateholamine concentrations were not higher in patients requiring fewer extrastimuli to induce the second episode of VT, either shortly after the first episode of VT or shortly after the second episode of VT. In conclusion, plasma catecholamines do not influence baseline ventricular refractoriness, the cycle length of induced VT, or the VT induction technique. Induced VT, which does not require termination by direct-current countershock, is generally associated with little or no increase in plasma epinephrine and a variable increase in plasma norepinephrine concentration, depending on the severity and duration of hypotension during VT. The plasma catecholamine response to VT does not affect a second induction of VT. Therefore, endogenous catecholamines exert little influence on the results of electrophysiologic testing in patients with sustained VT which does not require termination by direct-current countershock.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26830/1/0000389.pd

Effects of chronic aminodarone therapy on ventricular tachycardia induced by programmed ventricular stimulation

Several studies have reported upon the inducibility of ventricular tachycardia (VT) with programmed ventricular stimulation (PVS) during chronic amiodarone therapy; however, few studies have systematically described and compared the morphology, duration, and cycle length of VT induced by PVS before and after amiodarone. In this study, 26 patients with symptomatic VT or ventricular fibrillation were evaluated by PVS by means of one to three extrastimuli (ES) before treatment and after 2 months of amiodarone therapy. Before amiodarone, sustained unimorphic VT was induced in 21 patients (group A) and symptomatic, nonsustained VT was induced in five patients (group B). After 65 +/- 8 days of amiodarone (total dose 64.5 +/- 8.9 gm, mean +/- S.D.), 15 of 21 patients (71%) in group A had sustained VT, five patients (24%) had nonsustained VT, and one patient had no VT induced. Four of five patients (80%) in group B had sustained VT and one patient had no VT induced. VT was induced by the same or by fewer number of ES in 79% of cases. When the morphologies of the VT induced before and after amiodarone were compared, the morphology of VT induced after amiodarone was the same in only 8 of 24 patients (33%), unimorphic but different in 14 patients (58%), and polymorphic in the remaining two patients. No correlation was found between the serum concentrations of amiodarone, desethylamiodarone, tetraiodothyronine, triiodothyronine, or reverse triiodothyroinine, and similarities or differences in VT morphology, VT cycle length, or the relative number of ES required to induce VT after treatment with amiodarone. Although VT is ofter still inducible after 2 months of amiodarone therapy, the VT induced is different from the baseline VT in the vast majority of patients.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26864/1/0000429.pd

Interrelationships between serum levels of amiodarone, desethylamiodarone, reverse T3 and the QT interval during long-term amiodarone treatment

The interrelationships between serum levels of amiodarone, desethylamiodarone, and reverse T3, and changes in the corrected QT interval ([Delta]QTc) were examined in 22 patients during long-term treatment with amiodarone. At 1, 3, and 6 months of follow-up, the correlation coefficient between serum levels of amiodarone or desethylamiodarone and reverse T3 ranged from 0.01 to -0.2 (p > 0.4). At the same time intervals, the correlation coefficient between both amiodarone and desethylamiodarone levels and [Delta]QTc ranged from 0.1 to -0.1 (p > 0.6), and the correlation coefficient between reverse T3 and [Delta]QTc also ranged between 0.1 to -0.1 (p> 0.5). Substituting percent [Delta]QTc for [Delta]QTc also did not reveal a significant correlation. These data demonstrate that serum levels of reverse T3 cannot be used as a substitute for serum levels of amiodarone in monitoring patients being treated with amiodarone. The absence of a correlation between serum reverse T3 levels and [Delta]QTc suggests that the delay in repolarization which occurs during amiodarone therapy is not secondary to an amiodarone-induced abnormality in thyroid hormone metabolism.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26433/1/0000521.pd

The hemodynamic effects of ventricular pacing with and without atrioventricular synchrony in patients with normal and diminished left ventricular function

The relative hemodynamic effects of heart rate, inotropic state, and atrioventricular (AV) synchrony during ventricular pacing were evaluated in 10 patients with normal left ventricular ejection fraction (LVEF) (0.66 +/- 0.07, mean S.D.) and in eight patients with a diminished LVEF (0.34 +/- 0.18). Hemodynamics were measured at AV intervals of 130, 0, and -130 msec during ventricular pacing at a baseline rate that was 10 pulses/min greater than the resting heart rate, at 130 pulses/min alone, and at 130 pulses/min during continuous intravenous infusion of dobutamine. During baseline ventricular pacing and during ventricular pacing at 130 pulses/min with and without dobutamine, both groups of patients had a significant decrease in cardiac index, stroke volume index, and stroke work index when the AV pacing interval was decreased from 130 to 0 msec. The observed decrease in these three hemodynamic variables was similar when patients with diminished LVEF were compared to patients with normal LVEF. No further significant decrease in cardiac index, stroke volume index, and stroke work index occurred in either group when the AV interval was changed from 0 to -130 msec during baseline ventricular pacing or during ventricular pacing at 130 with and without dobutamine. Beneficial hemodynamic effects occur during ventricular pacing when AV synchrony is maintained at resting heart rates and during increases in heart rate and inotropic state in patients with normal and diminished LVEF.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26988/1/0000555.pd