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

Supraventricular Tachycardia Induced by Swallowing: A Case Report and Review of the Literature

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71974/1/j.1540-8159.1987.tb05933.x.pd

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

Sequelae of nonsustained polymorphic ventricular tachycardia induced during programmed ventricular stimulation

The results of 206 programmed ventricular stimulation studies performed in 130 patients (100 men and 30 women, mean age 62 +/- 12 years, +/- standard deviation) were examined prospectively to determine the sequelae of nonsustained polymorphic ventricular tachycardia (VT) induced during programmed ventricular stimulation. The clinical indication for the electrophysiologic study was either documented monomorphic VT or unexplained syncope. The pacing protocol included 2 right ventricular pacing sites, 2 basic drive cycle lengths and up to 3 extrastimuli. In 111 studies, nonsustained polymorphic VT was induced and with continuation of the programmed stimulation protocol, sustained monomorphic VT was induced in 48 studies (43%) and polymorphic VT was induced in 13 studies (12%). Overall, sustained monomorphic VT was induced in 110 studies and sustained polymorphic VT in 18 studies. The incidence of nonsustained polymorphic VT preceding the induction of sustained polymorphic VT was significantly greater than the incidence of nonsustained polymorphic VT preceding the induction of sustained monomorphic VT (72 vs 44%, p < 0.05). Nonsustained polymorphic VT is not a useful predictor of the outcome of programmed ventricular stimulation. The use of nonsustained polymorphic VT as an endpoint for stimulation would be likely to improve the specificity of programmed ventricular stimulation by limiting the induction of sustained nonclinical arrhythmias that require countershock, but at the cost of significantly impairing the yield of monomorphic VT.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/27686/1/0000070.pd

Acute changes in pacing threshold and R- or P-wave amplitude during permanent pacemaker implantation

This study examines the changes in pacing threshold and R- or P-wave amplitude during the first 30 minutes after implantation of tined and screw-in leads. The leads examined were those of 1 manufacturer (Medtronic) and consisted of 3 ventricular pacing leads (model numbers 6957 unipolar screwin [11 patients], 6961 unipolar tined [12 patients] and 6962 bipolar tined [7 patients]) and 1 atrial lead (model number 6957J unipolar screw-in [10 patients]). After optimal lead position was obtained fluoroscopically in the right ventricular apex or right atrium, the pacing threshold and R- or P-wave amplitudes were measured at 5-minute intervals for 30 minutes.The acute ventricular pacing threshold with the screw-in lead was significantly higher than with the tined lead (0.84 +/- 0.17 vs 0.58 +/- 0.15 volts; p < 0.001). There was a significant (p < 0.001) acute decrease in the ventricular pacing threshold with both lead types, with the maximum decrease occurring 5 minutes after lead implantation. There was a significant acute increase in R-wave size with the ventricular screw-in lead that peaked 20 minutes after lead implantation (11.9 +/- 3.0 to 14.7 +/- 4.1 mV; p < 0.001). The atrial screw-in lead behaved in a manner identical to its counterpart in the ventricle. In conclusion, there are acute changes in the pacing threshold and R- or P-wave amplitude obtained with tined and screw-in pacing leads. In some patients, a pacing threshold or R- or P-wave amplitude that is initially unacceptable may improve to an acceptable level over 15 to 20 minutes without further lead manipulation, especially when an atrial screw-in lead is used.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/28618/1/0000430.pd

Electrophysiologic effects and efficacy of recainam for sustained ventricular tachycardia

Recainam is an investigational antiarrhythmic drug recently introduced into clinical testing. It is a phenylalkyl urea derivative that produces a concentrationdependent decrease in membrane responsiveness and maximal upstroke velocity.1 The reduction in maximal upstroke velocity displays use-dependence,1 similar to the class 1A drugs. However, unlike class 1A drugs, but similar to class 1B agents, recainam does not prolong action potential duration.1 Other studies demonstrated that recainam slows conduction with minimal effect on ventricular refractoriness,2 effects consistent with a class 1C antiarrhythmic action. Thus, these preliminary investigations suggested that recainam possesses a unique electrophysiologic profile with properties of each of the 3 class 1 subclasses. Other preclinical studies have demonstrated recainam's efficacy in suppressing ventricular arrhythmias in the postinfarction dog model3 and initial clinical studies have demonstrated that it is highly effective in suppressing ventricular premature complexes.4-6 However, no studies to date have reported the electrophysiologic effects of recainam in patients with sustained ventricular tachycardia (VT). Such is the purpose of this report.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/28136/1/0000587.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

Value of programmed ventricular stimulation in presumed carotid sinus syndrome

This study determines the results of programmed stimulation in patients with syncope or near-syncope presumed to have the carotid sinus syndrome based on the finding of carotid sinus hypersensitivity and the absence of any other apparent cause for syncope or near-syncope after clinical evaluation. Fourteen patients had coronary artery disease, 1 had dilated cardiomyopathy and 18 patients did not have structural heart disease. Programmed simulation was performed at 2 basic drive cycle lengths and 2 right ventricular sites with 1 to 3 extrastimuli. Sustained unimorphic ventricular tachycardia (VT) was induced in 5 of 15 patients who had structural heart disease, and in none of the 18 patients who did not (p 0.05). Patients who had inducible unimorphic VT were treated with antiarrhythmic drugs that suppressed the induction of VT, and 4 of 5 patients also received a pacemaker; no patient had a recurrence of syncope during followup. Patients who had inducible polymorphic VT and VF (n = 10) or no inducible VT (n = 18) received treatment directed at only carotid sinus syndrome. Two patients with inducible VT or VF and 1 patient without inducible VT had recurrent syncope during follow-up, but none had cardiac arrest or died suddenly. It is concluded that programmed stimulation should be performed in patients presumed to have carotid sinus syndrome who have structural heart disease; unimorphic VT may be induced in one-third of these patients, raising the possibility that VT is the cause of syncope. Antiarrhythmic drug therapy may be unnecessary if polymorphic VT or VF is induced. In patients without heart disease, programmed stimulation is highly unlikely to yield a clinically significant arrhythmia.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26529/1/0000068.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 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