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Biomedical subjects

B B Lerman

Publications and source records attributed to B B Lerman.

At least 109 records · Page 6Linked to original sources
PubMed1986

Adenosine-sensitive ventricular tachycardia: evidence suggesting cyclic AMP-mediated triggered activity.

Catecholamine-induced triggered activity is thought to be caused by intracellular calcium overload mediated by elevation of intracellular cyclic AMP (cAMP). Although shown to occur in isolated preparations, evidence supporting its clinical existence has been lacking. Electrophysiologic studies were performed in four patients with structurally normal hearts who had exertionally related sustained ventricular tachycardia (VT). Programmed stimulation reproducibly initiated and terminated VT in all patients. Induction of tachycardia was also facilitated by infusion of isoproterenol. Adenosine, an endogenous nucleoside, whose only known electrophysiologic effect on ventricular myocardium and Purkinje fibers is antagonism of catecholamine-induced stimulation of intracellular cAMP production, reproducibly terminated all episodes of VT. The tachycardia was also terminated by intravenous verapamil and by the Valsalva maneuver and/or carotid sinus massage. Beta-Adrenergic receptor blockade with propranolol either terminated or prevented induction of VT during programmed stimulation or catecholamine challenge. Adenosine was also administered during VT to 14 patients whose arrhythmias fulfilled standard criteria for reentry, two of whom also had exercise-induced VT. Adenosine, at a dose (112.5 to 225 micrograms/kg iv) sufficient to cause either sinus slowing/arrest or ventriculoatrial block during ventricular pacing, failed to slow or terminate any episode of VT in these patients. Verapamil and autonomic modulation were also ineffective in this group of patients. Adenosine, verapamil, vagal maneuvers (acetylcholine), and beta-adrenergic receptor blockade are all known to decrease the slow-inward calcium current either directly by modulating calcium channels or indirectly by inhibiting production of cellular cAMP. Therefore the observation in this study that interventions that lower intracellular cAMP either terminate or prevent induction of VT in patients with structurally normal hearts and exercise-induced VT suggests that the mechanism of tachycardia may be cAMP-mediated triggered activity.

Adenosine↗
PubMed1985

Diagnostic and therapeutic use of adenosine in patients with supraventricular tachyarrhythmias.

Adenosine has been shown to affect both sinus node automaticity and atrioventricular (AV) nodal conduction. The effects of increasing doses of intravenous adenosine were assessed in 46 patients with supraventricular tachyarrhythmias. Adenosine reliably terminated episodes of supraventricular tachycardia in all 16 patients with AV reciprocating tachycardia, in 13 of 13 patients with AV nodal reentrant tachycardia and in 1 of 2 patients with junctional tachycardia with long RP intervals. Adenosine produced transient high grade AV block without any effect on atrial activity in six patients with intraatrial reentrant tachycardia, four patients with atrial flutter, three patients with atrial fibrillation and in single patients with either sinus node reentry or an automatic atrial tachycardia. The dose of adenosine required to terminate episodes of supraventricular tachycardia was variable (range 2 to 23 mg). Side effects were minor and of short duration. These results demonstrate that adenosine is useful for the acute therapy of supraventricular tachycardia whenever reentry through the AV node is involved. When arrhythmia termination is not affected, atrial activity may be more readily analyzed during adenosine-induced transient AV block.

Adenosine↗
PubMed1985

Automaticity of the Kent bundle: confirmation by phase 3 and phase 4 block.

Automaticity in the Kent anomalous atrioventricular bundle has been postulated to occur on the basis of electrocardiographic recordings. This hypothesis was confirmed using intracardiac recordings and programmed stimulation in a patient with pre-excitation. It was supported, in part, by demonstrating the presence of phase 3 and phase 4 block in the Kent bundle during decremental atrial pacing. The existence of automaticity in the Kent bundle may explain the manifestation of intermittent pre-excitation in certain patients. Furthermore, the presence of phase 3 and phase 4 block makes the likelihood of rapid antidromic conduction over the Kent bundle pathway unlikely within this subgroup.

Atrial Fibrillation↗
PubMed1985

Sustained ventricular tachyarrhythmias within 2 months of acute myocardial infarction: results of medical and surgical therapy in patients resuscitated from the initial episode.

Sustained ventricular tachycardia or fibrillation that develops during the early recovery period after acute myocardial infarction is a common clinical problem whose management remains controversial. Fifty-three patients who survived an initial episode of sustained ventricular tachycardia or fibrillation occurring between 3 and 60 days (mean +/- SD 21 +/- 16) after myocardial infarction were evaluated. Most of these patients had had a large (peak creatine kinase = 1,729 +/- 882 IU) complicated infarction. Forty-two (79%) of the 53 patients had had repetitive sustained ventricular arrhythmias and the condition of 19 of these could not be stabilized with drug therapy. Twenty-eight patients received medical therapy only. Twenty-four survived and were discharged from the hospital. Twenty-five patients underwent infarctectomy or aneurysmectomy either on an emergency basis (16 patients) or electively because of coexistent heart failure or angina (9 patients). Intraoperative mapping was attempted in these patients but was completely successful in only 13 (52%). Operative mortality was 16% with all deaths occurring in patients who were in shock before surgery. Five of 21 surgically treated survivors required long-term antiarrhythmic therapy. Twenty-one of 24 patients medically treated remain alive and well after 15 +/- 10 months of follow-up. Nineteen of 21 surgically treated patients remain alive and well after 17.9 +/- 11 months. One of these patients required reoperation for severe mitral regurgitation. These results confirm the poor medical prognosis of sustained ventricular tachyarrhythmias that present during the first 2 months after myocardial infarction but demonstrate that an acceptable rate of survival can be achieved with a combined medical and surgical approach to therapy.

Adult↗
PubMed1985

Role of invasive electrophysiologic studies in the evaluation and treatment of supraventricular tachycardia.

Electrophysiologic studies have provided new insights into the mechanisms responsible for supraventricular arrhythmias and have enabled investigators to evaluate with precision the acute effects of pharmacologic, physiologic, electrical, and surgical interventions. Not all patients with supraventricular arrhythmias require invasive studies, however, since empiric drug trials will often be adequate for management. At present, the clinical indications for study include the following: (1) for diagnosis of tachycardia mechanism when scalar ECG analysis is uncertain; (2) for assessment of risk of future life-threatening arrhythmia; and (3) as a rapid means of assessing future therapy when sporadic arrhythmias are likely to be poorly tolerated. Innovations that include surgical and catheter ablations of tachycardia pathways and antitachycardia pacing devices hold great promise and in the future, will provide nonpharmacologic options for patients poorly controlled by or intolerant of drug therapy.

Cardiac Catheterization↗
PubMed1985

Mechanoelectrical feedback: independent role of preload and contractility in modulation of canine ventricular excitability.

Mechanoelectrical feedback, defined as changes in mechanical state that precede and alter transmembrane potential, may have potential importance in understanding the role of altered load and contractility in the initiation and modulation of ventricular arrhythmias. To assess the independent effects of preload and contractility on myocardial excitability and action potential duration, we determined the stimulus strength-interval relationship and recorded monophasic action potentials in isolated canine left ventricles contracting isovolumically. The strength-interval relationship was characterized by three parameters: threshold excitability, relative refractory period, and absolute refractory period. The effects of a threefold increase in left ventricular volume or twofold increase in contractility on these parameters were independently assessed. An increase in preload did not change threshold excitability in 11 ventricles but significantly shortened the absolute refractory period from 205 +/- 15 to 191 +/- 14 ms (P less than 0.001) (mean +/- SD). Similarly, the relative refractory period decreased from 220 +/- 18 to 208 +/- 19 ms (P less than 0.002). Comparable results were observed when contractility was increased as a result of dobutamine infusion in 10 ventricles. That is, threshold excitability was unchanged but the absolute refractory period decreased from 206 +/- 14 to 181 +/- 9 ms (P less than 0.003), and the relative refractory period decreased from 225 +/- 17 to 205 +/- 18 ms (P less than 0.003). Similar results were obtained when contractility was increased with CaCl2, indicating that contractility associated changes were independent of beta-adrenergic receptor stimulation. An increase in preload or contractility was associated with shortening of the action potential. A threefold increase in preload and twofold increase in contractility were associated with a decrease in action potential duration of 22 and 24 ms, respectively. There was a significant linear correlation between action potential duration and excitability (absolute refractory period). The similar effects of increased preload and contractility on threshold excitability and refractoriness can be explained by the action these perturbations have on the time course of repolarization. Therefore, excitability of the ventricle is sensitive to and is modulated by alteration of load or inotropic state. The similar effects of either increased preload or contractility on excitability may be mediated by a common cellular mechanism which results in a rise in intracellular free Ca2+ and secondary abbreviation of the action potential.

Action Potentials↗
PubMed1985

Extended subendocardial resection. A surgical approach to ventricular tachyarrhythmias that cannot be mapped intraoperatively.

The optimal surgical management of patients with sustained, uniform-morphology ventricular tachycardia is endocardial activation sequence mapping during ventricular tachycardia and directed resection and/or cryoablation of the involved endocardium. The results of these procedures are superior to those obtained with nondirected aneurysmectomy. The optimal operative procedure when stable uniform ventricular tachycardia cannot be induced intraoperatively is uncertain. Between April, 1982, and April, 1984, intraoperative endocardial mapping was attempted on 33 patients with prior ventricular tachycardia. There were six perioperative deaths. Completely satisfactory intraoperative electrophysiologic maps were obtained in only 17 of the remaining 27 patients (63%). In 10 of these 27 patients, stable ventricular tachycardia could not be induced in the operating room, and satisfactory mapping thus could not be performed. In the first three of these 10 patients, limited subendocardial resection was performed either in regions with fractionated activity during sinus rhythm (two patients) or in regions suggested by preoperative catheter mapping (one patient). Ventricular tachycardia recurred postoperatively in two of these three patients. In the next seven patients, all visible endocardial scar around the border of the aneurysm was resected. Clinical ventricular tachycardia could not be induced at postoperative electrophysiologic study and has not recurred in these seven patients. These results suggest that complete endocardial resection provides an acceptable operative approach when intraoperative electrophysiologic mapping is not satisfactory.

Cardiac Catheterization↗
PubMed1984

Prognosis in patients with intra-Hisian conduction disturbances.

Intra-Hisian delay is usually associated with fascicular conduction abnormalities. We report our experience in 23 patients who had intra-Hisian delay as their only conduction defect. First-degree intra-Hisian delay (His bundle deflection greater than or equal to 30 msec) was present in 17 patients, 5 of whom also had split His potentials. Three of these patients received permanent pacemakers, all of whom had a history of syncope. Higher degrees of intra-Hisian delay were observed either spontaneously or in response to atrial pacing in 6 patients. Five of these patients were treated with permanent pacing, 4 of whom had symptomatic bradyarrhythmias and/or syncope. No patient has had a recurrence of symptoms following pacemaker insertion during the mean 31-month follow-up. No patient with first-degree intra-Hisian delay not receiving a pacemaker developed symptomatic bradyarrhythmias or syncope during a mean follow-up of 21 months.

Adult↗
PubMed1984

Myocardial injury and induction of arrhythmia by direct current shock delivered via endocardial catheters in dogs.

Although electrical ablation of ventricular tachycardia via percutaneous catheters has been recently accomplished in human beings, little is known of its pathologic or arrhythmogenic effects. We studied 21 open-chest anesthetized dogs in which an endocardial electrode catheter was percutaneously introduced into the left ventricle. Direct current (DC) shock was delivered by a standard defibrillator through the distal electrode to a back paddle. Cross-sectional two-dimensional echocardiographic studies were performed in the plane of the catheter (confirmed by epicardial metal beads), and blood flow was determined by the microsphere technique before DC shock and when the animals were killed 2 to 8 days later. Of 11 dogs receiving a total of 100 to 400 J, only three survived 48 hr compared with nine of 10 receiving 50 J and all three control dogs. Holter monitoring demonstrated sustained ventricular tachycardia (VT) (greater than or equal to 30 sec) in all 11 dogs monitored (six received greater than or equal to 100 J), beginning within 5 hr of the DC shock; three control dogs had no VT. Two dogs that died suddenly while being monitored showed ventricular fibrillation. Histologic examination revealed hemorrhagic contraction band necrosis in the shock zone, a type of injury similar to that observed in reperfusion necrosis. Necrosis of the left ventricle was 0.5% to 5%. There was no significant difference in necrosis between dogs receiving 100 J or more and those receiving 50 J (2.5 vs 1.7 g; p greater than .10). Percent systolic thickening determined in eight equally divided regions around the left ventricle showed no difference between the shock zone, perishock zone, or remote normal zone in dogs receiving 50 J.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Disopyramide: evaluation of electrophysiologic effects and clinical efficacy in patients with sustained ventricular tachycardia or ventricular fibrillation.

The efficacy of disopyramide in the management of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) was evaluated in 50 patients by programmed ventricular stimulation: 38 patients had coronary artery disease (16 with left ventricular aneurysm), 8 had other cardiac diseases, and 4 had no apparent heart disease. Disopyramide was administered orally for 72 hours (dosage 400 to 1,600 mg/day), resulting in a plasma level of 3.6 +/- 1.2 micrograms/ml (mean +/- standard deviation [SD]). Disopyramide prevented induction of sustained ventricular tachyarrhythmias in 17 patients (34%) and failed to prevent induction in 33 patients (66%). Plasma levels were not significantly different regardless of response to disopyramide. The VT cycle length in patients responding to disopyramide was shorter than in nonresponding patients (225 +/- 51 ms versus 281 +/- 70 ms, p = 0.005). Disopyramide increased VT cycle length in those patients in whom it was ineffective (failed to prevent induction) from 281 +/- 70 ms to 347 +/- 64 ms (p less than 0.001). Ventricular refractory periods, QRS, and QTc durations significantly increased after disopyramide administration. Of the 17 patients in whom tachyarrhythmias were noninducible on disopyramide, 11 were discharged on disopyramide and followed up for 19 +/- 9 months; 9 of them remained free of VT. Heart failure developed in 2 of these patients. One other patient in whom disopyramide was ineffective had irreversible heart failure and died. It is concluded that disopyramide (1) prevents induction of ventricular tachyarrhythmias in one third of patients studied and remains clinically effective in approximately 80%, (2) is more frequently effective in rapid tachycardias, (3) prolongs the VT cycle length when ineffective, and (4) may produce marked hemodynamic embarrassment in patients with significant left ventricular dysfunction.

Adult↗
PubMed1983

Electrophysiologic evaluation of syncope in patients with bifascicular block.

Thirteen patients with syncope and bifascicular block were evaluated by electrophysiologic study (EPS) including programmed stimulation. The mean age was 62 years. Six patients had coronary artery disease, three had cardiomyopathy, and four showed no evidence of organic heart disease. Holter monitoring and neurologic evaluation were nondiagnostic in all patients prior to EPS. EPS demonstrated inducible ventricular tachycardia (VT) in four patients, an HV interval greater than or equal to 70 msec in four, intra- and infra-His block with atrial pacing in one, and was nondiagnostic in four patients. Four of six patients with an HV interval greater than or equal to 70 msec or pacing-induced infranodal block were treated with permanent pacemakers, four of four patients with VT received antiarrhythmic therapy, and three of four patients with nondiagnostic studies received no therapy (one patient received a permanent pacemaker). During a mean follow-up period of 19 months (range 3 to 60 months) all but three patients have been free of syncope. One patient with VT did not take prescribed antiarrhythmic therapy, another patient with VT died suddenly; the remaining patient had a normal study and basilar migraines were subsequently diagnosed. We conclude that: (1) ventricular tachycardia may be a significant cause of syncope in patients with bifascicular block and was induced by programmed stimulation in approximately one third of patients studied; (2) EPS including programmed stimulation is helpful in delineating both the etiology of syncope and appropriate treatment in patients with bifascicular block. A negative study may also be of prognostic value.

Adolescent↗
PubMed1983

Tachyarrhythmias associated with programmable automatic atrial antitachycardia pacemakers.

A multiprogrammable automatic antitachycardia pacemaker (Cybertach-60), connected to a tined "J" wire electrode, was positioned in the right atrial appendage in three patients with recurrent supraventricular tachycardia (SVT). Mechanisms of SVT included atrioventricular (AV) nodal reentry (two patients) and reciprocating tachycardia using an accessory pathway (one patient). Indications for implantation included frequent symptomatic episodes, multiple drug failures, and reproducible termination of the arrhythmia by the automatic pacemaker during electrophysiologic studies. Following discharge, multiple episodes of pacemaker malfunction were recorded. The three types of malfunction included: undersensing with induction of SVT by a single atrial premature depolarization, oversensing of extraneous electromechanical potentials triggering burst pacing which initiated SVT, and inappropriate burst pacing in response to sinus tachycardia with and without initiation of SVT. Treatment with a beta-blocking agent prevented pacemaker triggering by sinus tachycardia, and replacement of the electrode catheter resolved pacemaker triggering by electromechanical potentials. One patient required removal of the pacemaker because undersensing could not be corrected by repositioning the atrial electrode. This report illustrates three potential complications that may result with either normal or faulty sensing when employing automatic atrial antitachycardia pacemakers for control of SVT. It also stresses the importance of careful electrophysiologic evaluation before implantation and meticulous follow-up after implantation.

Adult↗
PubMed1982

Aortic stenosis associated with systemic lupus erythematosus.

Hemodynamically significant valvular lesions have been rarely reported sequelae of Libman-Sacks endocarditis complicating systemic lupus erythematosus (SLE). Furthermore, embolic phenomena associated with these vegetations have not been clearly documented. We present a report of critical aortic stenosis associated with SLE in a patient who had received corticosteroid treatment for several years. An embolus, histologically identical with the aortic valve vegetation, was found in the left anterior descending artery at necropsy. There was no evidence of rheumatic heart disease, bacterial endocarditis or a bicuspid aortic valve. Recent reports suggest an increased incidence of significant valvular dysfunction in patients with SLE who have received long-term corticosteroid treatment.

Adult↗
PubMed1980

Hemodialysis-exchange transfusion for treatment of thrombotic thrombocytopenic purpura.

Remission in thrombotic thrombocytopenic purpura (TTP) was achieved in two patients after repeated exchange transfusion. Since both patients had renal insufficiency, exchange was performed with hemodialysis. This provided optimal volume control and facilitated the rapid exchange of blood. The infusion of plasma did not maintain the clinical improvement achieved with exchange transfusion. Until a concentrate of the putative factor deficient in TTP becomes available, an exchange procedure remains the most expeditious method for the replacement of any deficient factor. The procedure of hemodialysis can be adapted to perform exchange transfusion safely and efficiently.

Acute Kidney Injury↗