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Biomedical subjects

L E Waspe

Publications and source records attributed to L E Waspe.

At least 19 recordsLinked to original sources
PubMed1997

Ultrarapid train stimulation versus conventional programmed electrical stimulation for induction of ventricular arrhythmias in patients with coronary artery disease.

Conventional programmed electrical stimulation (PES) of the ventricle is useful for establishing inducibility or noninducibility of clinical ventricular arrhythmias (VA) but is complex and time consuming. The present study was designed to compare a standard PES protocol with an alternative method using ultrarapid train stimulation in patients with VA and coronary artery disease (CAD). A prospective, randomized, crossover design was used. During each session in the electrophysiology laboratory, patients were studied using both the trains and PES protocols in randomized order. In 82 matched pairs of comparisons in 50 patients, results were concordant in 85% (p < 0.0001). There were no differences related to type of clinical arrhythmia or to the presence of antiarrhythmic drugs. There were no significant differences in the induction of nonclinical arrhythmias with the two methods (p < 0.0001 for concordance). There were no significant differences related to the cycle length of the trains (10, 20, or 30 ms, equivalent to 100, 50, or 33 Hz). The number of drive-extrastimuli sequences and the time required to complete the trains protocol was significantly shorter (p < 0.0001) using trains versus PES. Ultrarapid train stimulation provides results in CAD patients that are comparable with those of conventional PES protocols. There is a significant savings in time, adding practical value to intrinsic electrophysiologic interest. Trains may be useful when multiple inductions are desirable, for example, in the setting of antitachycardia pacing parameters in an implantable defibrillator (ICD), during ICD implantation, or in other circumstances where the main question is inducibility of ventricular arrhythmias.

Aged↗
PubMed1995

Accuracy and clinical utility of transtelephonic pacemaker follow-up.

The diagnostic accuracy of transtelephonic pacemaker monitoring (TTM) has been quantified in a retrospective study involving 369 patients in three U.S. cardiac centers. Using existing medical records, TTM findings in a total of 413 reports were judged for equivalence to the findings of subsequent physical examinations in pacemaker clinics. This study found TTM follow-up testing to have a sensitivity of 94.6%, specificity of 98.5%, positive predictive value of 93.3%, and negative predictive value of 98.8%. The study also documents the clinical utility of TTM in identifying various modes of pacemaker malfunctions and instances of significant arrhythmia.

Arrhythmias, Cardiac↗
PubMed1994

Sinus node modification using radiofrequency current in a patient with persistent inappropriate sinus tachycardia.

Radiofrequency catheter modification of the sinus node for persistent inappropriate sinus tachycardia has not been previously reported. This article describes a patient in whom radiofrequency current was used to ablate an incessant automatic tachycardia focus mapped to the region of the sinus node, where a discrete multicomponent electrogram demonstrating earliest atrial activation was recorded. A transient junctional rhythm developed immediately after ablation, with rapid subsequent emergence of a stable rhythm having normal sinus nodal characteristics.

Adult↗
PubMed1990

The cardiac beta-myosin heavy chain isogene is induced selectively in alpha 1-adrenergic receptor-stimulated hypertrophy of cultured rat heart myocytes.

Cardiac hypertrophy produced in vivo by pressure overload is characterized by selective up-regulation of the fetal/neonatal beta-cardiac myosin heavy chain (MHC) isogene. However, a molecular signal for beta-MHC isogene induction has not been identified. We examined cardiac MHC isogene expression in a cell culture model for hypertrophy. alpha-MHC and beta-MHC iso-protein and iso-mRNA levels in cultured cardiac myocytes were quantified during hypertrophy stimulated by the alpha 1-adrenergic agonist, norepinephrine (NE). beta-MHC iso-protein content was increased 3.2-fold vs. control (P less than 0.001), whereas alpha-MHC isoprotein content was not changed significantly (1.4-fold vs. control, P = NS). MHC iso-mRNA levels were quantified by nuclease S1 analysis, using a single oligonucleotide probe. NE increased beta-MHC iso-mRNA content by 3.9-fold vs. control (P less than 0.001), but there was no change in alpha-MHC iso-mRNA (1.1-fold vs. control, P = NS). The NE-stimulated increase in beta-MHC iso-mRNA preceded in time the increase in beta-MHC isoprotein accumulation. The EC50 for NE induction of beta-MHC was 40 nM, and pharmacologic experiments indicated alpha 1-adrenergic receptor specificity. alpha-MHC isogene expression was predominant in control myocytes (68% alpha-isoprotein and 60% alpha-iso-mRNA). In contrast, beta-MHC expression was equal to alpha-MHC or predominant after treatment with NE (51% beta-isoprotein and 69% beta-iso-mRNA). Thus, alpha 1-adrenergic receptor stimulation increases the cellular contents of beta-MHC iso-mRNA and beta-MHC isoprotein during hypertrophy of cultured neonatal rat cardiac myocytes, but does not change the levels of alpha-MHC iso-mRNA or isoprotein. The effect on beta-MHC is mediated primarily at the level of mRNA steady-state level (pretranslational). Activation of the alpha 1-adrenergic receptor is the first identified molecular signal for increased beta-MHC isogene expression in a model of cardiac hypertrophy.

Animals↗
PubMed1989

Transcription of early developmental isogenes in cardiac myocyte hypertrophy.

We have developed a cell culture system to study molecular mechanisms important in myocardial hypertrophy. alpha 1-Adrenergic receptor stimulation produces hypertrophy of neonatal rat cardiac myocytes. Myocyte hyperplasia is not induced by alpha 1 stimulation, although alpha 1-adrenergic receptor-mediated DNA synthesis and cell division have been observed in other types of cells. The myocyte hypertrophic response does not require contractile activity. Activation of the alpha 1 receptor also produces highly specific alterations in gene expression, as measured at the mRNA and protein levels. In particular, there is selective up-regulation of two contractile protein isogenes that are expressed in vivo during early development and in pressure-load hypertrophy, skeletal alpha-actin and beta-myosin heavy chain. Studies with an in vitro transcription assay indicate that stimulation of the alpha 1-adrenergic receptor leads to a distinctive temporal sequence of transcriptional activation. Transcription of the skeletal alpha-actin isogene is induced preferentially to that of cardiac alpha-actin. Thus, early developmental isogene induction in alpha 1-stimulated hypertrophy reflects a fundamental change in the transcriptional program of the cardiac myocyte nucleus. The goal now is to define an intracellular pathway connecting the alpha 1-adrenergic receptor in the plasma membrane to activation of RNA polymerase II on the skeletal alpha-actin gene in the cardiac myocyte nucleus. There is evidence that protein kinase C may be one component of this pathway. A model for alpha 1-mediated transcription is presented.

Animals↗
PubMed1987

The prognostic value of the changes in the mode of ventricular tachycardia induction noted during therapy with a marked reduction of ventricular ectopic activity.

The prognostic significance of changes in the mode of induction of ventricular tachycardia (VT) noted during therapy was studied in 49 patients with sustained VT or ventricular fibrillation. Before treatment, all patients had inducible sustained VT by programmed stimulation (one to three extrastimuli) and frequent (greater than or equal to 30/hr) ventricular premature complexes (VPCs). On the discharge regimen, VT was no longer inducible by programmed stimulation in 22 patients (group 1). Twenty-seven patients (group 2) with persistent induction of VT despite extensive serial drug testings were discharged on a regimen that resulted in a marked reduction of VPCs on Holter monitoring (greater than or equal to 50% reduction of VPCs, greater than or equal to 90% reduction of couplets, and abolition of nonsustained VT). The modes of induction at baseline and on the discharge regimen were compared in each patient in group 2. Induction of VT was more difficult, requiring more aggressive stimulation protocol in 5 of 27 patients, unchanged in 14 patients, and easier in 8 patients. The duration of follow-up was 20 +/- 13 months (mean +/- SD). Arrhythmia-free survival rates at 6, 12, 18, and 24 months were 95%, 89%, 82%, and 73% in group 1, 92%, 84%, 75%, and 75% in group 2, 93%, 83%, 77%, and 69% in 27 patients with noninducibility or harder induction, and 95%, 90%, 79%, and 79% in 22 patients with the same or easier induction, respectively. The differences were not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Value of Holter monitoring in predicting long-term efficacy and inefficacy of amiodarone used alone and in combination with class 1A antiarrhythmic agents in patients with ventricular tachycardia.

The value of two reported and two new ambulatory electrocardiographic (Holter) criteria was studied in 80 patients taking amiodarone for refractory recurrent sustained ventricular tachycardia. In the 80 patients, the four Holter criteria were as follows: I-85% or greater reduction of ventricular premature complexes and abolition of couplets and nonsustained ventricular tachycardia in 74 patients who had 10 or more ventricular premature complexes/h, or any couplets or nonsustained ventricular tachycardia/24 hours at baseline; II-abolition of nonsustained ventricular tachycardia in 51 patients who had nonsustained ventricular tachycardia at baseline; III-85% or greater reduction of ventricular premature complexes and abolition of nonsustained ventricular tachycardia in 64 patients who had 30 or more ventricular premature complexes/h at baseline; and IV-85% or greater reduction of ventricular premature complexes and abolition of nonsustained ventricular tachycardia in 73 patients who had 10 or more ventricular premature complexes/h at baseline. Amiodarone was judged effective in, respectively, 51 of 74, 44 of 51, 51 of 64 and 61 of 73 patients by criterion I, II, III or IV. During the follow-up period (19 +/- 20 months), there were 19 instances of recurrence of ventricular arrhythmia or sudden death. Actuarial arrhythmia-free survival rate at 24 months was 84, 74, 86 and 85%, respectively, in patients with efficacy by criterion I, II, III or IV and 61, 43, 48 and 39%, respectively, in patients with inefficacy (p less than 0.015 for all). Many patients with efficacy by Holter criteria, however, had a recurrence of arrhythmia, suggesting insensitivity of these Holter criteria.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1987

Disopyramide-pyridostigmine interaction: selective reversal of anticholinergic symptoms with preservation of antiarrhythmic effect.

This double-blind, randomized, placebo crossover study was used to evaluate the effects of a cholinesterase inhibitor--slow-release pyridostigmine (180 mg orally every 12 hours)--on the anticholinergic and antiarrhythmic properties of disopyramide. Quantitative side effects questionnaire scores were used to guide disopyramide administration in 20 men with ventricular tachycardia. Disopyramide was given to each patient both with placebo and with active pyridostigmine. The maximal administered dose for each regimen was used in conjunction with corresponding questionnaire scores to calculate an index or estimate of the maximal tolerable dose of disopyramide. Additional evaluations performed at baseline and at each maximal administered dose regimen included tear and saliva quantitation, 24 hour electrocardiogram (ECG), exercise testing and programmed ventricular stimulation. Results showed that the maximal administered dose of disopyramide was greater with active pyridostigmine than with placebo: 295 +/- 75 versus 245 +/- 100 mg every 6 hours (p less than 0.05). The calculated maximal tolerable dose was substantially greater in the presence of pyridostigmine: 355 +/- 90 versus 260 +/- 115 mg every 6 hours (p less than 0.001). Maximal side effects questionnaire scores also reflected decreased anticholinergic activity in the presence of pyridostigmine compared with placebo: 101.9 +/- 2.2 versus 104.6 +/- 2.8, respectively (p less than 0.005). Baseline tear and saliva production was significantly reduced during disopyramide therapy, but was restored toward normal by the addition of pyridostigmine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Comparison of programmed stimulation and Holter monitoring for predicting long-term efficacy and inefficacy of amiodarone used alone or in combination with a class 1A antiarrhythmic agent in patients with ventricular tachyarrhythmia.

The values of two Holter ambulatory electrocardiographic monitoring criteria and one programmed stimulation efficacy criterion reported to be predictive of the efficacy of amiodarone were compared in 70 patients taking amiodarone for sustained ventricular tachyarrhythmias. At baseline, all patients had ventricular tachycardia inducible by programmed stimulation. After amiodarone loading (935 +/- 271 mg for 16 +/- 7 days), efficacy was determined by a programmed stimulation criterion (ventricular tachycardia no longer inducible or less than or equal to 15 beats) and two Holter monitoring criteria (Holter I = greater than or equal to 85% reduction of ventricular premature complexes and abolition of couplets and triplets in 64 patients who had greater than or equal to 10 ventricular premature complexes/h or couplets or triplets or both before therapy; Holter II = abolition of triplets in 41 patients who had triplets before therapy). Amiodarone was effective in 12 of 70 patients by the programmed stimulation criterion, in 49 of 64 patients by Holter criterion I and in 37 of 41 patients by Holter criterion II. In assessing efficacy of amiodarone, programmed stimulation and Holter criteria were discordant in 69% of patients or more (p less than 0.001). There were 16 recurrences or sudden deaths during the entire follow-up period (19 +/- 19 months). Arrhythmia-free survival rates at 24 months of patients with efficacy and inefficacy by each criterion, respectively, were 90 and 78% by programmed stimulation, 84 and 62% by Holter criterion I (p less than 0.05) and 73 and 50% by Holter criterion II (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Automatic implantable cardioverter-defibrillator: patient survival, battery longevity and shock delivery analysis.

The automatic implantable cardioverter-defibrillator (AICD) has been shown to reduce the mortality rate of patients with malignant ventricular tachyarrhythmias. This report describes experience with implantation of 36 automatic implantable cardioverter-defibrillators (AID-B and AID-BR models) in 22 persons over a 44 month patient follow-up period (mean 19.6 months). There were five deaths: two patients died suddenly 22 and 29 months, respectively, after their second implant, one died of congestive heart failure, one died of respiratory failure and one died of catheter sepsis. Although 11 (50%) of the 22 patients never received a countershock for a ventricular tachyarrhythmia and are still alive, the other 11 received one or more spontaneous countershocks. Nine patients (41%) experienced spurious shocks during the follow-up period. Assuming that the first shock for presumed ventricular tachyarrhythmia prevented death, the hypothetical cumulative survival of patients at 42 months would have been 34 +/- 14.1% in the absence of an automatic implantable cardioverter defibrillator rather than the actual survival rate of 59 +/- 16.8%. The cumulative device survival of the 36 AID-B units was 92 +/- 5.62% at 15 months but diminished to 37 +/- 14.4% by 20 months. No unit lasted longer than 22 months. There were 12 battery depletions. The number of shocks emitted did not influence unit longevity. The manufacturer's elective replacement indicator is of uncertain validity. Six units remained active 7 to 17 months after surpassing their replacement indicator. The automatic implantable cardioverter-defibrillator prolongs the life of many patients with otherwise intractable arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Automatic implantable cardioverter/defibrillator: inadvertent discharges during permanent pacemaker magnet tests.

A patient with an automatic implantable cardioverter defibrillator (AICD) received two inadvertent shocks when a magnet was placed over the pacer during a routine permanent pacer check. Analysis of the rhythm strip suggested that both patients' QRS complexes (133 beats/minute) and asynchronous pacer artifacts (70 beats/minute) were counted by the AICD sensing system and exceeded the rate criteria of 153 beats/minute. This resulted in shocks from the AICD during sinus rhythm at 133 beats/minute. To avoid possible inadvertent shocks, an AICD should be deactivated while a magnet is placed over the pacemaker during a permanent pacer check.

Electric Countershock↗
PubMed1987

Antiarrhythmic effects of VVI pacing at physiologic rates: a crossover controlled evaluation.

Ventricular pacing can prevent bradycardia-dependent ventricular ectopic activity (VEA) and is helpful in some cases of drug-refractory ventricular tachycardia (VT). This study is a prospective evaluation of VVI pacing for the control of VEA not related to underlying bradycardia, drug side-effects, or prolonged QT interval syndromes. Twenty-nine patients undergoing serial electrophysiologic-pharmacologic testing for VT control were studied. Eighteen of these patients (12 men; mean age = 60.1) both completed the protocol and had sufficient VEA for analysis. Coronary disease was present in 13 patients, cardiomyopathy in two patients, and one patient each had myocarditis, mitral valve prolapse, and no structural heart disease. Ambulatory (Holter) monitor recordings during VVI pacing were compared with control recordings made in the absence of pacing. VVI pacing rates were 10-15 bpm above the mean daily heart rate (mean = 92 bpm; range = 63-110). Hours from paced recordings were paired with hours from control (prior to analysis) according to time of day to reduce the effects of spontaneous variability in VEA frequency. Overall, VVI pacing reduced ventricular premature complexes (VPCs) 26% from 331 to 245/hour (p less than 0.001). During pacing, couplets (pairs, successive VPCs) were reduced from 6.95 to 1.03/hour (p less than 0.000001) and VT (greater than or equal to 3 successive VPCs) from 0.89 to 0.045 episodes/hour (p less than 0.003). Of 13 patients with couplets, 11 had greater than or equal to 50% reduction and five had greater than or equal to 90% reduction. Baseline VT was eliminated in four out of nine patients during pacing. Pacing did not increase VEA significantly in any patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Electrophysiologic effects and clinical efficacy of mexiletine used alone or in combination with class IA agents for refractory recurrent ventricular tachycardias or ventricular fibrillation.

The electrophysiologic effects and clinical efficacy of mexiletine used alone or in combination with class IA agents were studied in 35 patients with recurrent sustained ventricular tachycardia (VT) or ventricular fibrillation refractory to nonexperimental antiarrhythmic agents. At baseline before therapy, all patients had inducible VT by programmed stimulation (1 to 3 extrastimuli) and frequent (at least 30/hour) ventricular premature complexes (VPCs) during Holter monitoring. Mexiletine therapy was effective by programmed stimulation (VT no longer inducible or 15 or less beats) in 8 and ineffective in 27 patients. Twenty patients were discharged with mexiletine (14 of whom took an additional class IA agent). The discharge regimen was effective by programmed stimulation in 6 of these 20 patients. In 14 patients the discharge regimen was ineffective by programmed stimulation, but all patients had a marked reduction of ventricular ectopic activity (at least 83% reduction of VPCs and abolition of non sustained VT). During the follow-up period of 18 +/- 13 months (mean +/- standard deviation), 4 patients had recurrences (3 with an ineffective regimen by programmed stimulation and 1 with an effective regimen by programmed stimulation). Arrhythmia-free survival rates at 12 and 24 months were 86% and 77%, as determined by the Kaplan-Meier method, in patients with an ineffective regimen by programmed stimulation, and 80% and 80% in patients with an effective regimen by programmed stimulation (p = 0.979 by log rank test).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Is programmed stimulation of value in predicting the long-term success of antiarrhythmic therapy for ventricular tachycardias?

We studied the value of programmed stimulation in assessing the efficacy of antiarrhythmic agents in 52 patients with sustained ventricular tachycardia. All patients in this nonrandomized study had ventricular tachycardia inducible by programmed stimulation and also had frequent ventricular premature complexes (greater than or equal to 30 per hour) on Holter-monitor recordings before therapy. The efficacy of antiarrhythmic agents was assessed by both programmed stimulation and Holter recordings during serial drug testing. A regimen was deemed effective according to the programmed-stimulation criteria in 25 patients (Group 1). Twenty-seven patients in whom tachycardia could still be induced during programmed stimulation despite extensive drug trials were discharged on a regimen that caused a marked reduction of ventricular premature complexes according to Holter monitoring (Group 2). In 23 patients no effective drug regimen was identified by either set of efficacy criteria, and these patients were excluded from the present analysis. Follow-up lasted 18.6 +/- 13.9 months. Rates of arrhythmia-free survival at 12 and 24 months were 88 percent and 72 percent, respectively, in Group 1 and 84 percent and 75 percent in Group 2 (P = 0.637). We conclude that demonstration of antiarrhythmic efficacy by programmed stimulation predicts a good clinical outcome, that inefficacy as shown by the programmed-stimulation protocol used in this study may not preclude a good outcome if there is a marked reduction of spontaneous ventricular premature complexes on Holter monitoring, and that randomized trials should be conducted to validate the results of this observational study.

Anti-Arrhythmia Agents↗
PubMed1986

Susceptibility to atrial fibrillation and ventricular tachyarrhythmia in the Wolff-Parkinson-White syndrome: role of the accessory pathway.

Clinical and electrophysiologic characteristics associated with spontaneous and inducible atrial fibrillation and ventricular tachyarrhythmia were assessed in 20 consecutive patients with Wolff-Parkinson-White (WPW) syndrome undergoing surgical division (n = 12) or transcatheter electrical ablation (n = 8) of accessory pathways. Patients with spontaneous atrial fibrillation were characterized by the trend (not significant) of a shorter antegrade accessory pathway effective refractory period (256 +/- 26 vs 303 +/- 109 msec). However, patients with and without spontaneous atrial fibrillation did not differ with respect to prevalence of structural heart disease (3 of 11 vs 2 of 9), intra-atrial conduction time (34 +/- 10 vs 32 +/- 10 msec), or interatrial conduction time (86 +/- 21 vs 88 +/- 17 msec). Thus, atrial and accessory pathway electrophysiologic properties (per se) were not clear determinants of susceptibility to atrial fibrillation. Among the 20 patients, 10 to 35 beats of nonsustained ventricular tachycardia (seven patients) or ventricular fibrillation (three patients) were induced at electrophysiologic study with one to three programmed extrastimuli. Clinically, a ventricular arrhythmia (ventricular fibrillation during atrial fibrillation) had occurred in only one of these patients. The discordance of these observations was significant (p less than 0.01). Patients with and without inducible ventricular arrhythmias were not distinguished by clinical factors or by electrophysiologic properties of the accessory pathway or ventricles. Accessory pathway conduction was completely or partially eliminated by ablation procedures in 14 of 20 patients. During a mean follow-up of 27 months, atrial fibrillation recurred in two patients with failed ablation procedures and in one patient with left atrial enlargement (despite accessory pathway division) (p = 0.019 vs pre-ablation). Ventricular arrhythmias remained inducible in two patients in whom accessory pathway ablation failed (p = 0.01 vs initial study). However, spontaneous ventricular tachyarrhythmias did not occur during follow-up. We conclude that susceptibility to spontaneous or inducible atrial fibrillation and ventricular tachyarrhythmia in patients with WPW syndrome and no organic heart disease depends primarily on the existence of a functional accessory pathway. These susceptibilities are eliminated by interruption of accessory pathway conduction. Ventricular tachyarrhythmias remain infrequent spontaneous events in the WPW syndrome. Their more frequent induction at electrophysiologic study is not predictive of clinical occurrence.

Atrial Fibrillation↗
PubMed1986

Discordance between ambulatory monitoring and programmed stimulation in assessing efficacy of mexiletine in patients with ventricular tachycardia.

UNLABELLED: Programmed electrical stimulation (PES) and 24-hour Holter monitoring were compared in 30 patients with ventricular tachycardia (VT) or ventricular fibrillation (VF) before and during treatment with mexiletine. Before treatment, all patients had greater than or equal to 30 ventricular premature complexes (VPCs)/hr and 22 patients had nonsustained VT on Holter. All had inducible sustained VT by PES (one to three extrastimuli). Mexiletine was effective in only 23% by PES criteria (VT no longer inducible or less than or equal to 15 beats in duration and effective in 57%, 57%, and 73% by Holter criteria I, II, and III, respectively (Holter I greater than or equal to 50% reduction of VPCs, greater than or equal to 90% reduction of couplets and abolition of nonsustained VT; Holter II greater than or equal to 83% reduction of VPCs and abolition of VT; Holter III abolition of VT in patients who had VT during baseline Holter). Results of PES and Holter were discordant in 67%, 60%, and 55% (PES vs Holter I, II, and III, respectively). The majority (greater than or equal to 75%) of the discordance occurred due to mexiletine appearing effective by Holter criteria but ineffective by PES criteria (suggesting insensitivity of efficacy by Holter criteria and/or nonspecificity of induced VT during treatment with mexiletine). CONCLUSIONS: PES and Holter are discordant in assessing efficacy of mexiletine (p less than 0.05). Efficacy of mexiletine by Holter criteria is easier to achieve than efficacy by PES. The discordance between the two methods, both with very good reported predictive values, calls for randomized clinical follow-up studies to determine sensitivity and specificity of each method in assessing efficacy of mexiletine.

Drug Evaluation↗