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Biomedical subjects

B B Lerman

Publications and source records attributed to B B Lerman.

At least 55 records · Page 3Linked to original sources
PubMed1995

Metabolic determinants of defibrillation. Role of adenosine.

BACKGROUND: The single most important determinant of cardiac arrest outcome is the duration of ventricular fibrillation (VF) preceding delivery of a high-energy shock, because of the adverse effect of VF duration on defibrillation threshold (DFT). Although a metabolic mechanism has been proposed, hypoxia, metabolic acidosis, or alkalosis do not adversely affect DFT. However, since (1) catecholamines and adenosine levels are markedly increased during hypoxia, (2) exogenous catecholamines decrease DFT, and (3) adenosine is a potent antagonist of the electrophysiological effects of catecholamines on ventricular myocardium, we hypothesized that release of adenosine during prolonged VF adversely affects DFT and that this effect occurs through an antiadrenergic mechanism. METHODS AND RESULTS: DFT was determined in dogs during infusion of adenosine (300 micrograms.kg-1.min-1) and dipyridamole (0.25 mg/kg), an adenosine uptake blocker, a regimen that resulted in adenosine levels in the myocardial effluent equivalent to those achieved after 5 minutes of VF. Adenosine increased transthoracic DFT in each dog by 49 +/- 14% (n = 21) (mean +/- SEM) and transmyocardial DFT in a separate group of 10 dogs by 103 +/- 16%, P = .0003. Pretreatment with the specific A1 adenosine receptor antagonist 8-cyclopentyltheophylline (CPT) 5 mg/kg completely abolished the effects of adenosine on DFT. The effects of adenosine on DFT were also examined in the denervated state (propranolol 0.2 mg/kg plus bilateral vagotomy). In contrast to its effect in the innervated condition, adenosine had no effect on DFT in the same dogs when denervated, 49 +/- 11 versus 53 +/- 10 J (P = NS). CONCLUSIONS: Adenosine significantly increases transthoracic and transmyocardial DFT, effects that are mediated by the A1 adenosine myocardial receptor through an antiadrenergic mechanism. These results suggest that enhanced release of adenosine during VF may have a deleterious effect on defibrillation and that intramyocardial delivery of a specific A1 adenosine antagonist during VF may facilitate defibrillation and significantly reduce defibrillation threshold.

Adenosine↗
PubMed1995

Performance of the signal-averaged electrocardiogram: relation to baseline QRS duration.

Analysis of the duration and terminal components of the filtered QRS complex on the signal-averaged electrocardiogram (ECG) has been widely used for the detection of late potentials. Although filtered QRS duration is strongly related to 12-lead QRS duration, the relation of performance of the signal-averaged ECG to baseline QRS duration has not been critically examined. To examine the relation of test performance of the signal-averaged ECG to 12-lead QRS duration and to test the hypothesis that the difference between filtered and baseline 12-lead QRS duration would reflect more accurately the presence of late potentials than would analysis of the filtered QRS alone, we evaluated signal-averaged and 12-lead ECGs in 144 normal subjects and in 132 patients who were examined by electrophysiologic study and of whom 45 had inducible sustained monomorphic ventricular tachycardia. The signal-averaged ECG was considered positive by standard late potential criteria when the filtered vector QRS duration was > 114 msec and either the root-mean-square voltage of the terminal 40 msec of the filtered QRS was < 20 microV or the low-amplitude signal of the terminal filtered QRS was > 38 msec. A new signal-averaged ECG criterion for the presence of late potentials was developed in the 144 normal subjects on the basis of the difference between the longest filtered QRS duration in any of the orthogonal leads and QRS duration on the baseline 12-lead ECG ("the QRS difference"), which was adjusted by regression analysis for the decreasing QRS difference found with increasing baseline QRS duration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Three-dimensional uniform grid modeling of electrical defibrillation on a data parallel computer.

Finite element modeling has played an increasingly important role in the study of defibrillation. In order to model well the complex anatomical details, a large number of elements are required in the finite element grid, leading to a large set of equations that often cannot be solved effectively with the computational power of conventional computers. In this paper, we describe the use of a data parallel computer to provide the memory and reduction in solution time for solving these large finite element problems. Using a uniform grid and a nodal assembly technique, the discretized problem domain can be mapped efficiently to the parallel computer, allowing the solution of problems with over two million unknowns. The finite element algorithm for a three-dimensional inhomogeneous anisotropic body is described together with its parallel implementation. Test results for a canine torso model constructed from CT images are also presented.

Algorithms↗
PubMed1995

Increased defibrillation threshold due to ventricular fibrillation duration. Potential mechanisms.

The duration of ventricular fibrillation (VF) that precedes a high energy shock has been recognized as a critical determinant of defibrillation outcome. Factors such as metabolic acidosis or alkalosis do not affect outcome. The authors hypothesized that release of myocardial adenosine during VF could potentially mediate the time-dependent effects of VF duration on defibrillation. Defibrillation threshold (DFT) was therefore determined in dogs during concurrent infusion of adenosine and dipyridamole (a nucleoside transport blocker). Transthoracic DFT increased by approximately 50%, whereas transmyocardial DFT increased by approximately 100% in a separate group of dogs. These effects of adenosine on DFT were abolished when the dogs were autonomically denervated, suggesting that the deleterious effects of adenosine on DFT are due to its antiadrenergic mechanism of action. These data indicate that adenosine release during VF can markedly increase DFT. Since adenosine myocardial release during VF is time dependent, it is likely that adenosine plays a significant role in mediating the increase in threshold that is dependent on the duration of VF.

Adenosine↗
PubMed1995

Nonlinear forecasting and the dynamics of cardiac rhythm.

Since the initial development of the electrocardiogram, cardiologists have made dramatic advances in the description and understanding of cardiac arrhythmias. Despite these successes, the analysis of cardiac rhythm has remained largely descriptive. Recently, the principles of nonlinear dynamics, or chaos theory, have been applied to the quantitative analysis of cardiac rhythm in a variety of diverse situations. In chaos theory, three types of signals can be defined: periodic signals, which repeat themselves over some finite time interval, chaotic signals, which, while deterministic, demonstrate complex behavior and do not repeat themselves, and random signals, which are unpredictable and nondeterministic. The technique of nonlinear forecasting defines trajectories in a suitably defined phase space and uses the future evolution of trajectories that are close to each other over short distances to make predictions for times further into the future. The ability to reliably predict the future evolution of the trajectories derived from any signal is an important characteristic of the underlying dynamics of the signal and can therefore used to determine those dynamics. The foundation of nonlinear forecasting is reviewed, and an algorithm is described that can be used to determine the underlying dynamics of a signal and has been applied to the analysis of R-R interval data.

Algorithms↗
PubMed1995

Control of high common mode voltage during transthoracic defibrillation.

A high common mode voltage (Vcm) relative to earth ground is produced on the myocardium during the delivery of a defibrillator pulse and can generate a differential error signal when potential gradients are recorded with bipolar electrodes and isolation amplifiers. The error signal is proportional to Vcm, and therefore, a reduction in Vcm improves the accuracy of the potential gradient data. Experiments were conducted on 5 dogs to determine whether Vcm can be controlled using a bridge circuit. The bridge circuit consisted of a 5 k omega power rheostat in parallel with the transthoracic resistance of the dog. The variable contact of the rheostat was connected to earth ground, and by adjusting the rheostat, Vcm on the myocardium could be varied. In each dog, 20 A shocks were delivered through stainless steel transthoracic electrodes. Point contact electrodes sutured to the epicardium were used to measure Vcm. It was determined that Vcm could be reduced to approximately zero at a given electrode on the heart. In addition, for the 5 dogs studied, the maximum measured Vcm on the heart was only 10% of the transthoracic voltage when the bridge circuit was balanced for an interior point in the heart.

Animals↗
PubMed1995

AV nodal-His-Purkinje reentry: a novel form of tachycardia.

INTRODUCTION: Bundle branch reentry (BBR) typically occurs in patients with dilated cardiomyopathy and infra-Hisian conduction system disease. The macroreentrant circuit of BBR is confined to the His-Purkinje system (HPS) and ventricular myocardium. As such, the atrioventricular (AV) node plays no role in the tachycardia circuit. METHODS AND RESULTS: In the present study, we identified a novel form of wide complex tachycardia in a patient with coronary disease and severe aortic regurgitation. The tachycardia morphology was right bundle branch block with a left superior axis. Ventriculoatrial block was present during tachycardia. An unusual feature of this rhythm was two sequential His-bundle deflections (H and H') for each ventricular beat of tachycardia. The H'V interval was identical to the HV interval during supraventricular rhythm. Changes in the ventricular cycle length (VV) preceded changes in the HH interval, consistent with retrograde activation of the first His-bundle deflection. Changes in the H'H' interval preceded changes in the VV interval, consistent with anterograde activation of the second His-bundle deflection. Tachycardia could be terminated with ventricular extrastimuli that did not capture the proximal HPS as well as with ventricular extrastimuli that advanced the His deflection, consistent with block in the HPS and in the AV node, respectively. Reproducible termination of the tachycardia following the first His deflection was demonstrated with adenosine, consistent with an upper pivot in the AV node. CONCLUSIONS: We have identified a new form of reentrant tachycardia in which the AV node, HPS, and ventricular myocardium each obligatorily participates in the tachycardia circuit, with the left posterior fascicle and right bundle functioning as the anterograde and retrograde limbs, respectively. Unlike BBR, however, the His bundle is activated twice as the wavefront pivots in the AV node. This model requires longitudinal dissociation at the levels of the AV node and His bundle.

Aged↗
PubMed1994

Limitations of adenosine in assessing the efficacy of radiofrequency catheter ablation of accessory pathways.

Adenosine has been shown to reliably confirm the success of accessory pathway catheter ablation by producing transient atrioventricular (AV) block during atrial and ventricular pacing. This is due to the insensitivity of accessory pathway conduction to adenosine (with the rare exception of accessory pathways with decremental conduction properties). However, 4 of 204 consecutive patients who underwent successful accessory pathway ablation (as shown by adenosine-induced transient AV block) had recurrent AV reciprocating tachycardia involving a second, previously nonmanifest accessory pathway. In each case, the second accessory pathway was localized to a site disparate from the original pathway. No pathway showed decremental anterograde or retrograde conduction properties. In 2 patients, adenosine initially did not show the presence of the second concealed accessory pathway, because the refractory period of the accessory pathway was longer than the pacing cycle length used to assess ventriculoatrial conduction. Only when the refractory period of this second accessory pathway was shortened by infusion of isoproterenol did adenosine reveal the presence of the pathway during follow-up electrophysiologic study. In another patient, a non-decremental accessory pathway was shown to be sensitive to adenosine. In the remaining patient, the second accessory pathway may have been transiently injured during the initial study, thereby simulating adenosine sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1994

Physiologic role of atrio-Hisian and nodo-Hisian bypass tracts in supraventricular tachycardia.

Atrio-Hisian bypass tracts are considered to be rare electrophysiologic curiosities. The prevalence and functional significance of these tracts are unknown. We examined the incidence of atrio-Hisian and nodo-Hisian bypass tracts, their electrophysiologic manifestations, and their physiologic role in supraventricular tachycardia in 200 consecutive patients referred for evaluation of supraventricular tachycardia. In one patient it was demonstrated for the first time that a concealed (retrograde only) nodo-Hisian bypass tract functioned as the retrograde limb of orthodromic reciprocating tachycardia. The VA interval was negative during tachycardia, similar to that sometimes observed in atrioventricular nodal reentry. In a second patient an anterograde and retrograde conducting pathway resulted in a pseudo Wolff-Parkinson-White electrocardiographic pattern and served as an "innocent bystander," permitting a rapid ventricular response during atrial flutter. In conclusion, although atrio-Hisian and nodo-Hisian bypass tracts are rare, they are sufficiently prevalent to make them observable in a larger referral series. Most importantly, they may participate as bystanders during supraventricular tachycardia or as either the anterograde or retrograde limbs of reciprocating tachycardia. They may possess features that mimic Wolff-Parkinson-White syndrome and/or AV nodal reentry.

Adult↗
PubMed1994

Differential therapeutic responses of patients with isoproterenol-dependent and isoproterenol-independent vasodepressor syncope.

Orthostatic stress during tilt table testing (TTT) is used to examine patients who may have vasodepressor syncope. This response is thought to be mediated by activation of left ventricular mechanoreceptors. Isoproterenol, by increasing the rate of discharge of these mechanoreceptors, has been proposed to increase the sensitivity of TTT without decreasing its specificity. This mechanism is not, however, totally consistent with recent observations of vasodepressor responses after cardiac transplantation in patients with denervated hearts. These reports and data showing that not all sympathomimetic agents increase the sensitivity of TTT suggest that more than one mechanism may be responsible for a positive TTT result. Therefore we hypothesized that patients with positive TTT results tests not requiring isoproterenol (iso-independent) would have a different clinical and therapeutic response than patients who required isoproterenol (iso-dependent). One hundred sixty-one consecutive patients who underwent TTT for the evaluation of unexplained syncope were included in the study. TTT was performed without and during isoproterenol infusion. A positive TTT result was defined as syncope or presyncope with a sudden decrease in systolic blood pressure and reproduction of the patient's clinical symptoms. Patients with a positive TTT result underwent a second test after 1 to 2 weeks of therapy with an oral beta-blocking agent; if the result remained positive, TTT was performed again with other agents until a satisfactory therapeutic response was obtained. Sixty-six (41%) of 161 patients had a positive result; 18 (27%) were iso-independent, and 48 (73%) were iso-dependent. There were no significant differences in age, gender, or presence of underlying heart disease between these two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1994

Linearity of transthoracic conductance with respect to electrode force and area during high-voltage defibrillation shocks.

Canine transthoracic conductance (GT) was measured during high-voltage defibrillation shocks to test the hypothesis that (GT) is a linear function of electrode force (F) and electrode area (A). Symmetric protocols were used to compensate for changes in (GT) with respect to shock number (n). Stainless steel electrodes were employed with a force-control system for precise selection and control of both F and A at each shock. For a constant A = 60 cm2, GT was linear (r = 0.996, 0.995, 0.971, 0.992, 0.995) over five dogs for 30 N < or = F < or = 70 N. For a constant F = 50 N, GT was linear (r = 0.992, 0.998, 0.994, 0.992) over four dogs for 20 cm2 < or = A < or = 60 cm2, and in one dog (r = 0.996) for 40 cm2 < or = A < or = 90 cm2. The quantitative relationship demonstrated for GT and F and A can be used in the design of experiments and interpretation of results used for validation of numerical defibrillation models.

Animals↗
PubMed1994

Comparison of methods for removal of ectopy in measurement of heart rate variability.

Heart rate variability (HRV) analysis uses variations in heart rate to assess activity of the autonomic nervous system. Ectopic beats can affect HRV by introducing mathematical artifact into the computations of time- and frequency-domain measures. Exclusion of ectopy-containing segments of data from analysis has been used to correct for ectopy, but this technique eliminates data and may bias HRV measurements if ectopic beats are causally associated with changes in autonomic tone. We have assessed algorithms for correcting for ectopy: deletion, in which ectopic beats are removed from the R-R sequence; linear and cubic spline interpolation; and nonlinear predictive interpolation, in which ectopy-free R-R sequences are used as templates for replacing ectopic beats. The null method (no ectopy correction) was evaluated to determine the importance of ectopy correction. These methods were applied to computer-generated sequences created by adding simulated ventricular premature depolarizations to 5-min ectopy-free R-R sequences. The null method resulted in significant alterations in HRV. Deletion and nonlinear predictive interpolation performed superiorly to linear or cubic spline interpolation, which overestimated low-frequency power and underestimated high-frequency power. Thus ectopy correction is necessary for HRV analysis; deletion of ectopic beats performs as well as or better than more complicated methods for these relatively short data samples.

Animals↗
PubMed1994

Evidence for functionally distinct dual atrial inputs to the human AV node.

Although conventional models of the human atrioventricular (AV) node assume a single upper common pathway, animal studies demonstrate dual atrial inputs: an anterior input from the interatrial septum and a posterior input from the crista terminalis (running near the os of the coronary sinus in the posteroseptal region). We hypothesized that functionally distinct dual atrial inputs to the AV node also exist in humans and that the anterior input has a lower safety factor for impulse propagation. To evaluate this hypothesis, we examined 20 patients undergoing radiofrequency ablation of the slow AV nodal pathway for AV nodal reentrant tachycardia who underwent subsequent follow-up testing. After ablation near the os of the coronary sinus (and posterior to the compact AV node), 11 patients had no residual slow pathway conduction [SP(-)], whereas 9 did [SP(+)]. The effective refractory period of the fast AV nodal pathway (FP-ERP) and anterograde AV nodal Wenckebach (AVN-W) cycle length were significantly increased at follow-up in the SP(-) patients (FP-ERP = 336 +/- 71 vs. 387 +/- 103 ms, P = 0.02; AVN-W cycle length = 356 +/- 74 vs. 442 +/- 118 ms, P = 0.03) but not in SP(+) patients. Similarly among 10 patients undergoing radiofrequency ablation of a right posteroseptal accessory pathway (near the os of the coronary sinus), 5 developed impaired AV conduction: abnormal anterograde pacing-induced AVN-W cycle length in 4 patients and 2:1 AV nodal block in 1 patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Mechanism-specific effects of adenosine on atrial tachycardia.

BACKGROUND: Recent reports suggest that adenosine, in addition to terminating supraventricular tachycardia involving the atrioventricular (AV) node, may have antiarrhythmic effects on atrial tachycardia. The electrophysiological effects of adenosine on supraventricular tissue include shortening of action potential duration in atrial myocytes mediated by the potassium current, IKACh,Ado; shortening of action potential duration and hyperpolarization in sinus node cells; and anti-adrenergic electrophysiological effects resulting from inhibition of adenylyl cyclase. We therefore hypothesized that the response of atrial tachycardia to adenosine would be mechanism specific, with termination of atrial tachycardia due to sinus node reentry or cAMP-mediated triggered activity, transient suppression of automatic atrial tachycardia, and an absence of antiarrhythmic effect on tachycardia due to intraatrial reentry. METHODS AND RESULTS: Adenosine (mean +/- SD, 143 +/- 54 micrograms/kg IV) was administered to 27 patients (55 +/- 19 years) in atrial tachycardia whose mechanism was confirmed by electrophysiological study. Adenosine terminated sinus node reentrant tachycardia in 6 of 6 patients and terminated atrial tachycardia due to triggered activity in the 1 patient in whom it was identified. Adenosine transiently suppressed automatic atrial tachycardia in 7 of 7 patients and had no effect in 13 patients with intra-atrial reentrant tachycardia, including 8 patients with atrial flutter. CONCLUSIONS: These findings demonstrate that adenosine's effects on atrial tachycardia are mechanism specific and can be used to differentiate between reentrant tachycardia confined to the region of the sinus node or atria and between nonreentrant atrial tachycardia due to either triggered activity or automaticity.

Adenosine↗
PubMed1994

Role of arterial chemoreceptors in mediating the effects of endogenous adenosine on sympathetic nerve activity.

BACKGROUND: Exogenous adenosine has been shown to increase muscle sympathetic nerve activity (MSNA), blood pressure, heart rate, and ventilation in conscious humans, effects attributed to peripheral chemoreceptor activation. METHODS AND RESULTS: To determine whether endogenous adenosine has similar effects and whether they are mediated through chemoreceptor activation, we examined the effects of dipyridamole, an inhibitor of adenosine reuptake, on sympathetic nerve activity and ventilation. Twenty studies were conducted on separate days in 15 healthy volunteers. We examined responses to dipyridamole 0.56 mg/kg during room air breathing (n = 7), during hyperoxia (100% O2, n = 6), and during room air breathing after pretreatment with aminophylline (n = 7). During room air breathing, dipyridamole increased MSNA from 231 +/- 42 to 504 +/- 136 U/min, heart rate from 65 +/- 3.8 to 96 +/- 4.7 beats per minute, and systolic blood pressure from 129 +/- 3.5 to 140 +/- 4.8 mm Hg; central venous pressure decreased from 5.5 +/- 0.4 to 4.5 +/- 0.3 mm Hg (P < .01), and minute ventilation increased from 7.8 +/- 0.6 to 9.1 +/- 0.5 L/min (P < .01). During peripheral chemoreceptor suppression (with hyperoxia), there was a dissociation of the effects of dipyridamole on ventilation and sympathoexcitation. Effects on ventilation were attenuated, but sympathoexcitatory effects were not. Pretreatment with aminophylline, an adenosine receptor antagonist, either abolished (blood pressure, minute ventilation, and end-tidal CO2) or markedly attenuated (MSNA and heart rate) the effects of dipyridamole during room air breathing. CONCLUSIONS: Augmentation of endogenous adenosine with dipyridamole increases sympathetic nerve activity and ventilation in conscious humans. The ventilatory effects of endogenous adenosine are mediated predominantly by chemoreceptor activation, but the sympathetic and hemodynamic responses to endogenous adenosine are probably mediated by an additional afferent mechanism that is independent of peripheral chemoreceptor activation.

Adenosine↗
PubMed1993

Adenosine induced intraatrial block.

Adenosine, an endogenous nucleoside with potent negative chronotropic and dromotropic effects on the sinus and AV nodes, is thought to have little if any antiarrhythmic effect on normal atrial tissue. However, there may be an electrophysiological basis for an adenosine effect on atrial tissue with atypical conduction properties. We examined the electrophysiological effects of adenosine in a patient with decremental atrial conduction properties. During incremental pacing from the high right atrium there was gradual prolongation of the intraatrial interval between the high right atrium and the low septal atrium, from 180 to 280 msec, until 2:1 intraatrial block occurred at a pacing cycle length of 280 msec. Adenosine (6 mg IV) resulted in transient intraatrial block followed by prolonged intraatrial conduction during high right atrial pacing at a cycle length of 400 msec. Thus, similar to its effects on the AV node and decremental AV accessory pathways, adenosine may also slow and abolish conduction in decremental atrial issue, an effect that is likely attributed to adenosine induced hyperpolarizing K+ current in partially depolarized atrial tissue.

Adenosine↗