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Biomedical subjects

A J Solomon

Publications and source records attributed to A J Solomon.

28 records · Page 2Linked to original sources
PubMed1995

Relation between repolarization and refractoriness during programmed electrical stimulation in the human right ventricle. Implications for ventricular tachycardia induction.

BACKGROUND: Although programmed electrical stimulation is widely used for provoking sustained ventricular tachycardia (VT), the mechanism by which repetitive extrastimulation evokes VT is still little understood. Specifically, it is not clear why several closely coupled extrastimuli are frequently required to induce VT. Although regularly paced human ventricular myocardium exhibits a near constant relation between myocardial repolarization and refractoriness, the effect of repetitive extrastimulation on the relation between repolarization and excitability in the human heart and its relevance for arrhythmia induction by programmed stimulation are unknown. We hypothesized that the induction of VT by repetitive extrastimulation is facilitated by an altered relation between repolarization and refractoriness, and this leads to disturbances in ventricular impulse propagation, which trigger the onset of VT. METHODS AND RESULTS: Twenty-one patients undergoing routine electrophysiological study were paced from the right ventricular apex and outflow tract endocardium with monophasic action potential-pacing catheters placed at both sites simultaneously Monophasic action potential durations (APDs) and effective refractory periods (ERPs) were measured simultaneously at each site, during regular stimulation (S1-S1) at 400-ms cycle length and during three consecutive extrastimuli (S2 through S4) at the closest coupling intervals at which all three extrastimuli still resulted in capture. Measurements further included the repolarization level at which the earliest capture occurred, the ratio between ERP and APD, and the propagation time between the pacing and distant recording site. APD and ERP both shortened progressively with each extrastimulus. APD at 90% repolarization decreased from a baseline (S1) of 238.1 +/- 19.7 ms by 14.9% at S2, 18.9% at S3, and 22.9% at S4 (P < .0001, S1 versus S4). ERP decreased from 233.1 +/- 19.7 ms (S1) to 180.0 +/- 41.9 ms (S3) (P < .0001, S1 versus S3). While ERP shortening occurred mainly on the basis of APD shortening, there was an additional factor that contributed to ERP shortening independent of APD shortening. Each consecutive extrastimulus was able to elicit a propagated response at earlier repolarization levels than the previous one: the earliest capture for S2 occurred at 85.5 +/- 10.2% of complete repolarization, for S3 at 83.9 +/- 10.5%, and for S4 at 78.4 +/- 11.2% (P < .05 for S2 versus S3; P < .05 for S3 versus S4; P < .01 for S2 versus S4). This progressive "encroachment" of the earliest capture stimulus onto the preceding repolarization phase (at progressively less repolarized levels) correlated with a progressive delay of impulse propagation between the pacing site and the second recording site: propagation time increased from baseline (S1) by 10.5 +/- 1.3% with S2 to 19.0 +/- 1.6% with S3 and to 22.5 +/- 2.8% with S4 (P < .05, S4 versus S1). VT was induced in 11 of 21 patients. Nine of these had VT induced only when significant encroachment of extrastimuli on the preceding repolarization phase (< 81.3 +/- 7.0%) and associated conduction slowing (> 16.6 +/- 1.8%) were present. CONCLUSIONS: Repetitive extrastimulation not only shortens APD and subsequently ERP but also alters the ERP/APD relation by allowing capture to occur at progressively less complete repolarization levels. This progressive encroachment onto the preceding repolarization phase is associated with impaired impulse propagation and a high incidence of VT induction. This may help explain how repetitive, closely coupled extrastimulation induces ventricular tachycardia in the human heart.

Aged↗
PubMed1995

Prolongation of conduction time during premature stimulation in the human atrium is primarily caused by local stimulus response latency.

BACKGROUND: Conventional clinical electrophysiological techniques cannot accurately differentiate between local stimulus response latency and propagation time of the atrial response. The purpose of this study was to identify and distinguish local stimulus response latency from impulse propagation time in the human right atrium during programmed electrical stimulation. METHODS: Pacing was performed from two atrial sites (high and low right atrium) in 19 patients, using monophasic action potential recording/pacing combination catheters (interelectrode distance < 2 mm). Local stimulus response latency (interval between stimulus artifact and upstroke of the local monophasic action potential), and propagation time (interval between local and remote monophasic action potential upstroke) were evaluated at a basic cycle length (S1-S1) of 600 ms and as a function of the extrastimulus proximity (interval between extrastimulus and effective refractory period). Data are presented as means +/- SEM. RESULTS: During basic stimulation, local latency was very small (3.8 +/- 1.7 ms). During premature extrastimulation (proximity < 70 ms), local latency increased progressively with decreasing coupling intervals. Prolongation of local latency was most pronounced during stimulation close to the effective refractory period with local stimulus response latency increasing to 18.3 +/- 1.4 ms (380 +/- 7.9%) at 10 ms proximity (P < 0.002) and to 27.9 +/- 3.7 ms (630 +/- 13.2%) at 5 ms proximity, respectively (P < 0.0001). The impulse propagation time between the stimulation site and the remote recording site was on average 54.5 +/- 14.3 ms during basic stimulation, and increased up to 62.1 +/- 13.5 ms (14.0 +/- 8.4%), which was not significant. CONCLUSIONS: The intra-atrial impulse propagation remained essentially unchanged during the entire range of premature stimulation. Local stimulus response latency was negligible and constant during late coupling intervals but increased dramatically when extrastimulation approached the preceding repolarization phase. This has the following clinical impact: first, local stimulus response latency during premature extrastimulation curbs the targeted atrial response interval second, local stimulus response latency, not propagation time, seems responsible for the greater functional than effective refractory period during electrical stimulation; third, local stimulus response latency should be considered in pace mapping for accurate comparison of conduction time before pacing with that during pacing.

Aged↗
PubMed1995

Thermistor guided radiofrequency ablation of atrial insertion sites in patients with accessory pathways.

Radiofrequency ablation has gained acceptance in the treatment of patients with symptomatic Wolff-Parkinson-White syndrome. The purpose of this study was to characterize the relation between temperature and other electroconductive parameters in patients undergoing atrial insertion accessory pathway ablation utilizing a thermistor equipped catheter. The mean temperature and power at sites of atrial insertion ablation are lower than has been previously associated with creation of radiofrequency lesions in the ventricle. While high cavitary blood flow in the atrium may result in cooling, the thinner atrial tissue may require less energy to achieve adequate heating than ventricular myocardium.

Adolescent↗
PubMed1995

5-HT3 receptor-independent inhibition of the depolarization-induced 86Rb efflux from human neuroblastoma cells, TE671, by ondansetron.

The 5-HT3-receptor antagonist, ondansetron, has been shown to have positive effects in selected in-vivo models of memory impairment and anxiety. The exact mechanisms underlying such bioactivities are unknown. In the present work, an 86Rb efflux bioassay was used to show that ondansetron has a unique ability to block voltage-gated potassium channels in TE671 human neuroblastoma cells. This intrinsic potassium-channel-blocking (KCB) property is relatively weak (IC50 20 microM), but is not shared by other 5-HT3-receptor ligands including zatosetron, MDL 72222, LY 278, 584, zacopride, 1-phenylbiguanide, and ICS 205-930 (tropisetron). Pre-incubation of the target neuroblastoma cells with several 5-HT-receptor ligands including 5-hydroxytryptamine, 8-OH-DPAT, ketanserin, 2-methyl-5-HT, as well as a number of potent 5-HT3 agonists and antagonists and two selective neurotoxins, failed to abolish the KCB action of ondansetron. A preliminary structure-activity relationship analysis indicates that the KCB activity of ondansetron is almost entirely attributable to its structural nucleus, 2,3-dihyro-9-methyl-4(1H)-carbazolone. It is hypothesized that the KCB action of ondansetron is mediated through receptors other than 5-HT3 receptors. The KCB activity of ondansetron may be a significant factor in the in-vivo cognition-enhancing activities of this compound, conceivably due to depolarization of the hippocampal synaptic membranes and a consequent augmentation of neurotransmission.

Anti-Anxiety Agents↗
PubMed1993

Radiofrequency catheter ablation of ectopic atrial tachycardia using paced activation sequence mapping.

OBJECTIVES: Although ectopic atrial tachycardia is infrequent, it can be an important clinical challenge. We sought to define an alternative therapeutic approach to this refractory problem. BACKGROUND: Radiofrequency energy catheter ablation has been used to treat a variety of ventricular and supraventricular arrhythmias but has not been proved efficacious in the management of ectopic atrial tachycardia. METHODS: Ten patients (14 to 47 years of age) referred with refractory ectopic atrial tachycardia were studied. Mapping techniques included identification of earliest atrial activation, confirmation of concordance of P wave configuration during spontaneous tachycardia and pacing from the ablation catheter, and paced activation sequence mapping. The paced activation sequence mapping compared the activation sequence at multiple atrial sites during spontaneous tachycardia with that recorded during pacing from the ablation catheter. The catheter was steered to a point where pacing reproduced the spontaneous activation sequence. RESULTS: Foci were right atrial in eight patients and left atrial in two. In 8 of 10 patients, 514 +/- 97 (SE) J and 5.7 +/- 2.3 (SD) J radiofrequency energy applications ablated the ectopic focus. Seven of these eight patients presented with one focus and one had two discrete and stable foci. Ablation was unsuccessful in two patients with multiple foci. No complications occurred. An arrhythmia focus recurred in two patients and one patient underwent successful repeat ablation. The other patient was managed medically. All seven patients with successful ablation are symptom free after 6.5 +/- 3.8 months. CONCLUSIONS: Our preliminary experience suggests that with the use of both paced activation sequence mapping and standard techniques, radiofrequency ablation of ectopic atrial tachycardia may be a safe and effective form of therapy.

Adolescent↗
PubMed1993

Effect on coronary artery anatomy of radiofrequency catheter ablation of atrial insertion sites of accessory pathways.

OBJECTIVES: The purpose of this study was to analyze the effects of radiofrequency catheter ablation of the atrial insertion site of accessory pathways on the angiographic appearance of coronary arteries. BACKGROUND: Radiofrequency catheter ablation of accessory pathways requires the application of energy to the endocardial surface of the atrioventricular groove adjacent to the major epicardial coronary arteries. A systematic analysis of the effect of radiofrequency ablation on coronary arteries has not previously been demonstrated. METHODS: Seventy consecutive patients with 76 accessory pathways (7 right free wall, 44 left free wall, 12 posteroseptal, 8 anteroseptal and 5 midseptal) were studied. Quantitative coronary angiography was performed before, immediately after and a mean of 69 +/- 42 days after radiofrequency catheter ablation. RESULTS: Coronary artery diameter adjacent to the ablating electrode was 2.6 +/- 0.9 mm before ablation, 2.7 +/- 0.9 mm immediately after ablation and 2.7 +/- 1.0 mm at the time of follow-up study. Angiographic findings were unchanged from baseline in 69 of 70 patients immediately after ablation and in all 70 patients at the time of follow-up study. CONCLUSIONS: Radiofrequency catheter ablation of the atrial insertion site of accessory pathways does not result in short-term angiographic changes in coronary artery anatomy.

Adolescent↗
PubMed1992

A simple in vivo model to evaluate the effects of antiarrhythmic agents.

Antiarrhythmic agents alter cardiac conduction, refractoriness, and action potential duration in a rate dependent fashion. A simple in vivo model was developed to measure these variables over a wide range of cycle lengths. Complete heart block was produced in dogs using an 8 French hexapolar ablation catheter, anterior skin electrode, and radiofrequency current (30 W, 13.6 +/- 2.6 seconds). Ventricular pacing and monophasic action potential recordings were performed using a single combination catheter. QRS and action potential durations were measured at multiple cycle lengths and after an abrupt change in paced cycle length. Ventricular effective refractory periods were also measured at multiple cycle lengths. Data obtained during flecainide and d-Sotalol infusions are presented. This simple model allows detailed in vivo evaluation of the electrophysiological effects of antiarrhythmic agents and combinations.

Animals↗
PubMed1991

The signal-averaged electrocardiogram in predicting coronary artery disease.

The ability to noninvasively detect coronary artery disease (CAD) in patients undergoing diagnostic cardiac catheterization was studied using a signal-averaged electrocardiogram. An initial study of 13 patients revealed that a QRS duration greater than or equal to 100 msec, a root mean square voltage in the terminal 40 msec of the QRS less than 50 microV, and a low amplitude signal (LAS) duration greater than 28 msec were suggestive of CAD. These parameters were then used prospectively to examine 40 consecutive patients with chest pain of undetermined etiology referred for cardiac catheterization. Patients with CAD had significantly longer filtered QRS and LAS durations and lower root mean square voltages compared with patients without CAD. The sensitivity, specificity, and positive predictive value of a single parameter ranged from 62% to 76%, 74% to 89%, and 75% to 87%, respectively. Thus the signal-averaged electrocardiogram may be a useful tool in evaluating patients for the presence of CAD.

Adult↗
PubMedDate not supplied

Effect of recent randomized trials on current pacing practice.

The most common indication for a permanent pacemaker is symptomatic bradycardia. An atrial-based pacemaker (dual-chamber or atrial) usually is preferred, except in patients with chronic atrial fibrillation. Several prospective, randomized trials recently have been completed to evaluate new indications for permanent pacemakers. A dual-chamber pacemaker with an optimal atrioventricular interval can reduce the left ventricular outflow tract gradient by >50% in patients with hypertrophic cardiomyopathy. This has been associated with symptomatic improvement in the majority of patients, but an important placebo effect appears likely. Pacing also has been evaluated in patients with medically refractory dilated cardiomyopathy. Despite encouraging initial studies, routine implantation of a permanent pacemaker in dilated cardiomyopathy is not indicated. In patients with cardioinhibitory or mixed vasovagal syncope and carotid sinus hypersensitivity, implantation of a pacemaker markedly decreases syncopal episodes. Pacemaker therapy is clearly indicated in patients with atrial fibrillation associated with symptomatic bradycardia, and exciting new data on the use of pacing to prevent atrial fibrillation appear promising. The best pacing modality for this indication may be dual-site atrial pacing. Finally, permanent pacemakers play an important role in the treatment of symptomatic long QT syndrome, usually in combination with beta-blockers.

Atrial Fibrillation↗