PubMed Health⌕ Search

Biomedical subjects

B B Lerman

Publications and source records attributed to B B Lerman.

At least 19 recordsLinked to original sources
PubMed1992

Adenosine-induced atrioventricular block: a rapid and reliable method to assess surgical and radiofrequency catheter ablation of accessory atrioventricular pathways.

Adenosine has been shown to inhibit anterograde and retrograde conduction through the atrioventricular (AV) node while having little or no effect on accessory pathway conduction. Its rapid onset of action and short half-life make it particularly suitable for repetitive measurements. In this study, the utility of adenosine was tested in assessing completeness of accessory pathway ablation. Sixteen patients with an accessory pathway were studied (eight surgical ablations, eight catheter ablations with radiofrequency energy). Before ablation, no accessory pathway was sensitive to adenosine. Twelve patients with pre-excitation showed high grade AV node block with maximal pre-excitation on the administration of adenosine during atrial pacing. Four patients with a concealed accessory pathway demonstrated high grade AV block without evidence of latent anterograde accessory pathway conduction. Preablation ventriculoatrial (VA) block was not observed in any of the 16 patients in response to adenosine during ventricular pacing. Immediately after accessory pathway ablation, all patients developed AV and VA block with the administration of adenosine during atrial and ventricular pacing, respectively. These findings were confirmed during follow-up study 1 week later. Atrioventricular block during atrial and ventricular pacing with adenosine affords a reliable and immediate assessment of successful pathway ablation.

Adenosine↗
PubMed1992

Adenosine-sensitive afterdepolarizations and triggered activity in guinea pig ventricular myocytes.

This study examines the cellular basis and specificity of the effects of adenosine on early afterdepolarizations (EADs), delayed afterdepolarizations (DADs), and triggered activity (TA) induced by various drugs with different mechanisms of action. Membrane potential and currents were measured in isolated guinea pig ventricular myocytes. Adenosine (10-100 microM) significantly (p less than 0.05) reduced the amplitude of DADs and suppressed TA induced by isoproterenol (10-50 nM) and forskolin (1 microM) but not those induced by dibutyryl cAMP (1 microM), ouabain (1-5 microM), and 7.2 mM [Ca2+]o. Adenosine also abolished EADs and TA induced by isoproterenol. In contrast, adenosine failed to abolish EADs and TA induced by quinidine (3 microM) or those that occurred spontaneously (i.e., in the absence of drugs). Transient inward current (ITi) was induced on repolarization after 2-second-long single depolarizing voltage steps or after 12-second-long trains of 300-msec depolarizing pulses. Concomitant with the attenuation of DADs, adenosine suppressed ITi caused by isoproterenol and forskolin but not those induced by ouabain, dibutyryl cAMP, and elevated [Ca2+]o. The amplitude of ITi was dependent on the magnitude of the activating voltage step, but the suppression of ITi by adenosine was not. The selective A1-adenosine receptor antagonist N-0861 (9-methyladenine derivative) antagonized the effects of adenosine on afterdepolarizations, ITi, and TA. In myocytes from guinea pigs treated with pertussis toxin, adenosine failed to attenuate DADs and ITi or abolish TA induced by isoproterenol or forskolin. In parallel experiments, isoproterenol (10 nM) raised cellular cAMP from 5.7 +/- 0.2 to 8.1 +/- 0.1 pmol and the selective A1 receptor agonist cyclopentyladenosine (5 microM) reduced it to 6.5 +/- 0.2 pmol (p less than 0.05). Thus, adenosine specifically attenuates afterdepolarizations and abolishes TA by suppressing ITiS that are associated with stimulation of adenylate cyclase via a pertussis toxin-sensitive A1 receptor-mediated action. In conclusion, the response of TA to adenosine may identify a mechanism of afterdepolarization related to stimulation of adenylate cyclase.

Action Potentials↗
PubMed1990

Clinical relevance of exercise-induced ventricular arrhythmias in suspected coronary artery disease.

Because there is controversy regarding the clinical relevance of exercise-induced ventricular arrhythmias, we analyzed their significance in 383 patients who had undergone both exercise thallium-201 stress-testing and cardiac catheterization. Two-hundred twenty-one patients (58%) had no exercise-induced ventricular arrhythmias while 162 (42%) did. There was no difference between patients with and without exercise-induced ventricular arrhythmias in terms of previous myocardial infarction (p = 0.61), incidence of fixed thallium-201 defects (0.06), number of diseased vessels (p = 0.09) and resting left ventricular ejection fraction (p = 0.06). In contrast, evidence of provocable ischemia (redistribution on thallium-201 and ST-segment depression on the electrocardiogram) were more likely (p less than 0.02) to be seen in patients with exercise-induced ventricular arrhythmias. Discriminant function analysis revealed that these 2 variables best separated patients with and without exercise-induced ventricular arrhythmias. In a 4- to 8-year follow-up, 89 patients had adverse cardiac events. Of these 89, there were 41 deaths, 9 nonfatal myocardial infarctions and 39 coronary revascularization procedures performed later than 3 months after catheterization. Patients with exercise-induced ventricular arrhythmias were more likely (p = 0.01) to have these events than those without these arrhythmias. Moreover, these arrhythmias provided independent prognostic information beyond that provided by the thallium-201 stress test and coronary angiography. We conclude that exercise-induced ventricular arrhythmias are associated with exercise-induced ischemia and provide prognostic information which adds marginally to that provided by other noninvasive and invasive parameters in ambulatory patients being evaluated for chest pain.

Arrhythmias, Cardiac↗
PubMed1990

Reversible myocardial depression in survivors of cardiac arrest.

Three patients under 40-years old who survived cardiac arrest due to ventricular fibrillation were originally diagnosed as having idiopathic dilated cardiomyopathy. Shortly after cardiac arrest, assessment of myocardial function revealed a globally dilated left ventricle in each patient with an estimated ejection fraction between 20% and 30%. Serial assessment of myocardial function, however, showed either normal or near-normal function by 2 weeks postevent. These findings suggest that myocardial stunning due to hypoperfusion during ventricular fibrillation or the effects of transthoracic shocks may result in profound, reversible myocardial depression in survivors of cardiac arrest. Serial evaluation of left ventricular function may be of value in selected survivors of cardiac arrest in order to evaluate time-dependent resolution of myocardial dysfunction and may prevent misdiagnosis of idiopathic dilated cardiomyopathy.

Adult↗
PubMed1990

Nature of defibrillation: determinism versus probabilism.

The gradual transitions that are found between unsuccessful and successful shock strengths in percent success or dose-response curves suggest that defibrillation is a probabilistic phenomenon. This concept appears to be reinforced by the fact that a frequency distribution is observed in defibrillation threshold data and that a dose-response relationship is also obtained by integration of the frequency distribution. The purpose of this study was to investigate whether a deterministic threshold model (based on experimental results) could produce 1) gradual transitions in dose-response curves, and 2) a threshold frequency distribution for individual subjects. In the experimental phase of the study, a linear deterministic relationship was found between transthoracic threshold current and defibrillation episode number (other variables held constant) in pentobarbital-anesthetized dogs. The correlation coefficient for each dog was between 0.77 and 0.98 (P less than 0.01), and both positive and negative slopes were found. Based on these results, threshold current was modeled for computer simulation as a linear function of episode number. The model was thus purely deterministic with no random variability. For each simulated experiment, several parameters were varied: order of shocks (increment, decrement, random order), slope of threshold function, and percent error of the initial threshold. Several hundred computer simulations were performed to determine the effect of varying these parameters. In all cases, threshold-frequency distributions and sigmoidal dose-response curves with gradual transitions were produced. The results of this investigation demonstrate that the apparent probabilistic behavior of defibrillation can be produced by a deterministic relationship.

Animals↗
PubMed1990

Electrophysiological effects of adenosine in the transplanted human heart. Evidence of supersensitivity.

After cardiac transplantation, the denervated donor atria and ventricles demonstrate increased sensitivity to infusions of sympathomimetic amines. Recently, supersensitivity of the canine sinus and atrioventricular (AV) nodes to acetylcholine has also been demonstrated after parasympathetic denervation. Acetylcholine and the endogenous nucleoside adenosine exert similar electrophysiological effects in both the sinus and AV nodes, and share a common transduction process. We, therefore, hypothesized that after orthotopic cardiac transplantation, the donor (denervated) sinus node would demonstrate greater sensitivity to exogenous adenosine than the recipient (innervated) sinus node. The effects of incremental doses of intravenous adenosine (37-112 micrograms/kg) on changes in sinus cycle length (SCL) (delta SCLmax%), changes in PR interval (delta PRmax%), time to peak effect (sec), and duration of electrophysiological effects (sec) were prospectively measured in 28 orthotopic cardiac transplant patients and nine control subjects. The baseline SCL was 795 +/- 71 msec for the control subjects, 891 +/- 43 msec for the recipient atria, and 700 +/- 18 msec for the donor atria (p less than 0.05, donor vs. recipient). The delta SCLmax% for each dose of adenosine was similar in the innervated control and recipient atria. In contrast, the donor sinus node demonstrated a threefold to fourfold increased response to adenosine as compared with the recipient sinus node and a threefold to sixfold increased response as compared with control subjects. Similarly, the donor AV node demonstrated a threefold to fivefold increase in PR interval as compared with control subjects. The duration of sinus node slowing in the denervated atria was threefold to fivefold longer than in the recipient and control atria (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1990

Effect of epicardial patch electrodes on transthoracic defibrillation.

To improve survival rates in patients undergoing surgical ablative procedures for malignant ventricular tachycardia (VT), a frequent practice is to implant epicardial patch electrodes at the time of map-guided surgery. After operation, patients with inducible VT often receive an automatic internal cardioverter/defibrillator (AICD) implant, whereas patients with noninducible VT usually do not. In the event that spontaneous, hypotensive VT or ventricular fibrillation should subsequently occur in the patient with noninducible VT, however, transthoracic defibrillation and resuscitation may prove difficult, because the patch electrodes are insulated with silicone rubber that can reduce the amount of current traversing the myocardium and thus can increase transthoracic defibrillation threshold (DFT). In this study, DFT was determined in mongrel dogs to test the hypothesis that epicardial patch electrodes elevate threshold. This study was also designed to assess the effect of patch electrode orientation and size on DFT. In the first protocol (perpendicular orientation), small epicardial patch electrodes (surface area, 30 cm2) were sutured to the epicardial surfaces of the anterior right and posterior left ventricles in 15 dogs so that the center axes of the patch electrodes were coincident and perpendicular to the coincident center axes of the transthoracic electrodes. The effect of two large epicardial patch electrodes (surface area, 53 cm2) on transthoracic DFT was also examined in eight of these dogs. In the second protocol (parallel orientation), small patch electrodes were sutured to the lateral surfaces of the right and left ventricles in seven dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Intrathoracic current flow during transthoracic defibrillation in dogs. Transcardiac current fraction.

To achieve transcardiac threshold current during transthoracic defibrillation, a considerably larger current must be delivered to the thorax to compensate for the shunting effect of the lungs, the thoracic cage, and other elements of the torso. This shunting effect is thus an important determinant of transthoracic defibrillation threshold and can be quantified by the transcardiac current fraction (FC, the ratio of transcardiac to transthoracic threshold currents). Previous estimates of FC have ranged from as low as 3% to as high as 45%. The purpose of of this study was to quantify both FC and the major intrathoracic current pathways. Transthoracic and intrathoracic voltages and currents were simultaneously measured during high-voltage transthoracic shocks in 20 dogs. With correction factors determined from another set of 12 dogs, these raw data were corrected to compensate for field distortion caused by the presence of the intrathoracic electrodes, and the adjusted data were fit to a resistive network model. The results showed that 82% of the transthoracic current was shunted by the thoracic cage, while 14% was shunted by the lungs. The remaining 4% (FC) is the portion that passed through the heart. There was good agreement between the two independent methods used to calculate FC. Analysis based on the model indicated that FC was 3.7%, whereas FC determined by direct measurement with calibrated electrodes was 4.2%. Therefore, the results of this study, in contrast to earlier estimates of FC, show that defibrillation in dogs is achieved by only 4% of the total transthoracic current.

Animals↗
PubMed1990

Relation between transcardiac and transthoracic current during defibrillation in humans.

Conceptually, transthoracic defibrillation threshold current can be considered a function of at least two quantities. It is directly proportional to the transcardiac threshold current and inversely proportional to the transcardiac current fraction (FC) or the ratio of transcardiac and transthoracic current. Although experimental and theoretical estimates of FC have been as high as 45%, previous measurements in humans have not been made. This study was designed to quantify FC in humans. During intraoperative testing of the automatic implantable cardioverter defibrillator, transthoracic rescue shocks of 200-400 J were delivered when the device failed to defibrillate. Simultaneous transthoracic voltage (VT) and transcardiac voltage (VC) between two implanted epicardial patch electrodes were measured. The ratio, VC/VT, was 0.04 +/- 0.03 (mean +/- SD) in 10 patients. In 16 dogs, a comparison was made between direct measurement of FC and VC/VT. FC was determined with a specially designed electrode system, which was calibrated to account for field distortion introduced by the electrodes. There was no significant difference between FC and VC/VT, which were both approximately 0.05, suggesting that VC/VT was statistically equivalent to FC. The results of this study, therefore, indicate that during transthoracic defibrillation in humans, approximately 4% of transthoracic current traverses the heart. This relatively small percentage of current results from the existence of parallel pathways, such as the thoracic cage and lungs, which shunt current around the heart.

Adolescent↗
PubMed1989

Nonventricular arrhythmias as precursors of ventricular fibrillation in patients with out-of-hospital cardiac arrest.

Ventricular tachycardia (VT) and ventricular fibrillation (VF) are the most common arrhythmias documented at the time of resuscitation in survivors of out-of-hospital cardiac arrest unassociated with an acute myocardial infarction. However, 20% and 40% of these patients will not manifest inducible ventricular arrhythmias during subsequent electrophysiologic studies. The optimal management of these patients has been controversial. In a consecutive series of 100 survivors of out-of-hospital cardiac arrest with documented VF, six were identified by either clinical or electrophysiologic data as having a nonventricular arrhythmia as the immediate precursor of VF. Two of these patients had rapid, hypotensive supraventricular arrhythmias induced with programmed cardiac stimulation. In four patients, bradyarrhythmias (sinus arrest two; atrioventricular block two) preceded and caused the episode of VF. Therapy directed at these nonventricular arrhythmias prevented recurrence of cardiac arrest in all patients. In survivors of out-of-hospital cardiac arrest, nonventricular arrhythmias represent a treatable potential etiology that may be overlooked during the patient's evaluation.

Adolescent↗
PubMed1989

Coronary artery bypass grafting in patients with ventricular fibrillation.

The role of coronary artery revascularization in the management of survivors of cardiac arrest remains controversial. Patients with sustained monomorphic ventricular tachycardia rarely respond to revascularization, but the response of patients with ventricular fibrillation as their basic arrhythmia has not been characterized. Coronary artery bypass grafting was performed in 8 patients with a history of cardiac arrest known to be caused by ventricular fibrillation without preceding sustained monomorphic ventricular tachycardia. All patients had critical double-vessel or triple-vessel coronary artery disease, and 7 of 8 had wall motion abnormalities from a prior myocardial infarction. After successful operation, 5 patients had no spontaneous arrhythmias and no inducible arrhythmias at a postoperative electrophysiological study. Three patients, however, had spontaneous, recurrent episodes of ventricular fibrillation unassociated with recurrent ischemia. Clinical factors were not useful predictors of response. The effect of coronary artery revascularization in patients with ventricular fibrillation is unpredictable, and full postoperative electrophysiological evaluation is necessary to judge the success of the procedure.

Cardiac Pacing, Artificial↗
PubMed1989

Stability of electrophysiological parameters after acute amiodarone loading: implications for patient management.

The appropriate timing of electrophysiological study in patients treated with amiodarone is uncertain. Twenty patients with coronary artery disease in whom sustained ventricular tachycardia was still inducible after 9 +/- 1 days of amiodarone loading (1,200-1,400 mg/day) underwent repeat electrophysiological testing after an additional month of maintenance therapy (400 mg/day). Compared with baseline, both short- and long-term amiodarone therapy caused significant changes in QTc, right ventricular effective refractory period, and ventricular tachycardia cycle length. However, there was no significant change in electrophysiological parameters between the end of the acute amiodarone loading period and 1 month of additional therapy. Sustained ventricular tachycardia remained inducible in 19 of 20 patients after 1 month of maintenance therapy. Amiodarone and desethylamiodarone plasma concentrations remained stable after amiodarone loading, but did not correlate with the magnitude of electrophysiological changes from baseline. These data suggest that electrophysiological testing after 9 days of high dose amiodarone therapy may accurately reflect long-term electrophysiological effects.

Aged↗
PubMed1989

Electrophysiologic effects of dipyridamole on atrioventricular nodal conduction and supraventricular tachycardia. Role of endogenous adenosine.

Exogenous adenosine has been shown to have potent electrophysiologic effects and antiarrhythmic properties within the atrioventricular (AV) node. Endogenous adenosine, a nucleoside with an increased release signaled by ischemia and hypoxia, is not believed to exert significant effects during homeostatic conditions. Recent experimental evidence suggests, however, that under normoxic conditions, the amount of adenosine released may be sufficient to mediate some of its physiologic effects. This study was designed to test the hypothesis that in humans the electrophysiologic effects of endogenously released adenosine on AV nodal conduction can be demonstrated under normoxic conditions by inhibiting uptake and degradation of the nucleoside. In the first protocol, the effects of intravenous dipyridamole (0.56 mg/kg bolus i.v., 5 micrograms/kg/minute infusion), a nucleoside-transport blocker that elevates endogenous plasma levels of adenosine, on AV nodal conduction were evaluated in seven patients. At a constant atrial paced cycle length, dipyridamole increased the AH interval from 110 +/- 19 to 164 +/- 26 msec, p = 0.002 (+/- SEM). Aminophylline (5.6 mg/kg i.v.), a competitive antagonist of adenosine, completely reversed the effects of dipyridamole on AV nodal conduction. Similarly, dipyridamole increased the cycle length at which pacing-induced AV nodal Wenckebach occurred, from 348 +/- 31 (control) to 388 +/- 33 msec (dipyridamole) (p = 0.002). In a second protocol, the effects of intravenous dipyridamole were evaluated in another group of six patients who had supraventricular tachycardia (SVT) in which the AV node was part of the reentrant circuit.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1988

Usefulness of adenosine for arrhythmias in infants and children.

Adenosine was administered to 25 infants and children (11 patients after presenting with a sustained arrhythmia, and 14 during a diagnostic electrophysiologic study) to determine its electrophysiologic effects. Adenosine was given as an intravenous bolus (starting dose 37.5 micrograms/kg, and increased by 37.5 micrograms/kg increments until an effect was seen). Adenosine caused tachycardia termination or transient increased atrioventricular (AV) block in all 25 patients. Seven patients had tachycardia requiring only the atria for perpetuation and developed increased AV nodal block (minimum effective adenosine dose range 37.5 to 350 micrograms/kg, mean 131). Thirteen had AV reciprocating tachycardia or AV node reentry tachycardia (minimum effective adenosine dose range 37.5 to 225 micrograms/kg, mean 114). Four other patients received adenosine to rule out preexcitation (minimum effective adenosine dose range 37.5 to 375 micrograms/kg, mean 165). One of the 25 patients had junctional ectopic tachycardia and adenosine administration caused retrograde AV block. Six of the 25 (24%) had noticeable but minor side effects. One patient had sustained bradycardia (2 to 3 minutes requiring temporary pacing). Adenosine is a safe and effective agent in the evaluation and treatment of infants and children with arrhythmias.

Adenosine↗