Search PubMed⌕ Search

Biomedical subjects

D G Benditt

Publications and source records attributed to D G Benditt.

At least 109 records · Page 6Linked to original sources
PubMed1987

Calcium uptake by cardiac sarcoplasmic reticulum in human dilated cardiomyopathy.

To determine the biochemical basis of abnormal diastolic properties in human dilated cardiomyopathy calcium uptake by the sarcoplasmic reticulum in ventricular homogenates of biopsy specimens from 21 patients with dilated cardiomyopathy was compared with that in nine normal controls. As a group, patients with cardiomyopathy had considerably lower calcium uptake rates (3.3(0.6) nmol.mg-1.min-1 vs 6.5(0.5) nmol.mg-1.min-1, p less than 0.01). Calcium uptake rates correlated modestly with resting haemodynamic values and significantly with plasma noradrenaline concentrations but not with plasma renin activity. These results show that sarcoplasmic reticulum function is impaired in human dilated cardiomyopathy and that this impairment is related both to the severity of haemodynamic dysfunction and to the extent of sympathetic nervous system activation.

Adolescent↗
PubMed1987

Effects of transplantation on atrioventricular nodal accommodation and hysteresis.

In the present study, atrioventricular nodal accommodation and hysteresis characteristics were evaluated in awake, unsedated dogs, before (n = 10) and after cardiac transplantation (n = 10). Chronically instrumented animals were atrially paced at a cycle length (CL) of 400 ms, followed by an abrupt decrease in pacing CL to 300 ms, followed by an abrupt return in pacing CL to 400 ms (with pacing sustained for 60 s at each CL). Atrioventricular nodal conduction characteristics (assessed by AH intervals) were simultaneously monitored. Under control conditions, AH intervals lengthened rapidly after an abrupt decrease in pacing CL [mean time for AH interval lengthening to stabilize (Tonset) = 2 +/- 1 s], whereas AH intervals lengthened more slowly (P less than 0.05) after transplantation (Tonset = 41 +/- 4 s). Similarly, after an abrupt increase in pacing CL, control AH intervals shortened rapidly [mean time for AH interval to return to base line (Tonset) = 5 +/- 1 s], whereas AH intervals shortened more slowly (P less than 0.05) after transplantation (Tonset = 42 +/- 5 s). Thus accommodation appears to be an intrinsic atrioventricular nodal response (present after cardiac denervation by transplantation) to abrupt, sustained atrial CL changes. Furthermore equivalence (P = NS) in atrioventricular nodal accommodation responses to symmetric CL decreases and increases after transplantation suggests that hysteresis [i.e., nonequivalence (P less than 0.05) in atrioventricular nodal accommodation responses], as seen under control conditions, results primarily from extrinsic (neural) modification of intrinsic atrioventricular nodal responses to symmetric CL changes.

Adaptation, Physiological↗
PubMed1987

Single-chamber cardiac pacing with activity-initiated chronotropic response: evaluation by cardiopulmonary exercise testing.

In this study, sequential cardiopulmonary exercise testing was used to assess the physiologic benefits of a single-chamber ventricular pacing system that utilizes a piezoceramic sensor to adjust heart rate by detecting "physical activity." An initial exercise test was conducted with the pacemaker programmed (based on a randomization table) to either the fixed rate (VVI, 70 beats/min) or rate-variable (VVI-Act) mode, and the results were compared with those obtained during a second exercise test in which the pacemaker was programmed to the alternate pacing mode. A 1.5 to 2 hr rest period was permitted between exercise tests, each of which consisted of a symptom-limited constant speed (3.0 mph) Balke protocol with 2 min stages commencing at 0.0% grade with increments of 2.5% at end of each stage. Compared with findings during fixed-rate VVI pacing, VVI-Act pacing was associated with greater exercise-induced positive chronotropic response (mean maximum heart rate VVI-Act 128 +/- 15.3 beats/min vs VVI 90 +/- 28.4 beats/min; p less than .01), prolongation of exercise duration (VVI-Act 10.2 +/- 3.8 min vs VVI 7.7 +/- 2.5 min; p less than .01), increased peak oxygen consumption (VVI-Act 1617 +/- 656 ml O2/min vs VVI 1325 +/- 451 ml O2/min; p less than .01), and onset of anaerobic threshold at a higher oxygen consumption (VVI-Act 1208 +/- 343 ml O2/min vs VVI 1064 +/- 377 ml O2/min: p less than .01). Additionally, of 44 comparable exercise stages tested in the two pacing modes, perceived exertion (assessed by a numerical grading system) was lower in 38 of 44 instances during VVI-Act compared with VVI pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Follow-up evaluation of infant paroxysmal atrial tachycardia: transesophageal study.

We report results of follow-up transesophageal electrophysiologic studies in 35 infants seven to 27 months old (mean, 12 months) in whom paroxysmal atrial tachycardia (PAT) using an accessory atrioventricular (AV) connection had been previously evaluated by transesophageal study in the first 2 months (mean, 14 days) of life. No infants were receiving antiarrhythmic drug therapy at the time of follow-up study. To evaluate AV conduction and initiate PAT, a standard transesophageal pacing protocol was used: single extrastimuli in sinus rhythm, incremental pacing to second-degree AV block, and burst pacing at cycle lengths near those resulting in second-degree AV block. If PAT was not initiated during the baseline period, the protocol was repeated during the infusion of isoproterenol and after administration of atropine. At follow-up study, PAT was reinitiated in 24 of 35 (68%) infants, six of whom had exhibited recent spontaneous recurrence of PAT. AV nodal function did not differ in those with and those without inducible PAT. However, when initial and follow-up studies were compared, changes in antegrade conduction of the accessory AV connection were observed, since only five of 10 infants with preexcitation at initial study continued to exhibit preexcitation at follow-up study (1/5 infants only after isoproterenol). Additionally, changes in retrograde conduction of the accessory AV connection were observed; the ventriculoatrial interval in PAT induced at follow-up study increased by 20 to 40 msec in eight of 24 infants and by 50 to 80 msec in five of 24 infants compared with the interval at initial study.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrioventricular Node↗
PubMed1987

Potentiation of cardiac electrophysiologic effects of verapamil after autonomic blockade or cardiac transplantation.

Cardiac electrophysiologic effects of verapamil in vivo are the result of both direct and indirect actions on the heart (the latter due to augmentation of sympathetic neural tone, diminution of parasympathetic neural tone, and increased circulating catecholamines). In this study we assessed the interaction of verapamil's direct and indirect actions on electrophysiologic properties of the heart in awake, previously instrumented, unsedated dogs. After administration of intravenous verapamil (0.2 mg/kg), electrophysiologic effects were assessed serially over a 1 hr period in 10 awake dogs before (group 1 studies) and during pharmacologic autonomic blockade (group 2 studies), and in a subset of these dogs (n = 5) after orthotopic cardiac transplantation (group 3 studies). In group 1 dogs, sinus cycle length (SCL) initially shortened after verapamil (postverapamil 379 +/- 50 msec vs baseline of 494 +/- 72 msec, p less than .001) and subsequently gradually prolonged. In groups 2 and 3, transient SCL shortening was absent. SCL prolonged promptly after verapamil, and sinus arrest developed in two of 10 group 2 and two of five group 3 animals. Verapamil exerted a negative dromotropic effect on atrioventricular node conduction in all three experimental groups, as assessed by drug-induced changes in minimum cycle length with sustained 1:1 atrioventricular conduction and measurements of atrioventricular node effective and functional refractory period. However, compared with findings in group 1, this negative dromotropic effect occurred more rapidly and was markedly potentiated in groups 2 and 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Sensor-triggered, rate-variable cardiac pacing. Current technologies and clinical implications.

Conventional implantable dual-chamber cardiac pacemakers adjust heart rate and maintain normal atrial and ventricular contraction by tracking "native" atrial electrical activity and pacing the ventricles after a predetermined programmable atrioventricular delay. However, in patients with symptomatic bradyarrhythmias, optimal function of "atrial-tracking" devices may be limited by concomitant sinoatrial disease. Provision of chronotropic response during physical exertion or emotional stress may be achieved by using physiologic sensors to alter pacing rate independently of atrial activity. Additional systems using sensor technologies are being developed. Future pacing systems will have dual-chamber pacing capability and may use several sensors coupled synergistically in order to take advantage of particular strengths of each. Physiologic sensor technology may be of diagnostic value in both antitachycardia devices and implantable cardioverter and defibrillator systems.

Bradycardia↗
PubMed1987

Morphine suppression of digitalis-induced ventricular arrhythmias.

The purpose of the study was to investigate the effect of morphine on digitalis-induced arrhythmias. Seventeen normokalemic dogs [serum potassium 3.9 +/- 0.3 mEg/L (+/- 1 S.D.)] and 19 hypokalemic dogs (serum potassium 2.2 +/- 0.3 mEg/L) were allocated to a morphine pretreatment group (morphine sulfate 3 mg/kg) or to a control group without morphine. Ouabain was administered by a constant infusion of 150 micrograms/kg/hr following an initial bolus of 20 micrograms/kg until animals developed ventricular tachycardia. In hypokalemic dogs, morphine pretreatment significantly (p less than 0.05) increased the digitalis dose required to initiate ventricular tachyarrhythmias (66 +/- 14 vs 37 +/- 11 micrograms ouabain/kg). In normokalemic dogs morphine did not affect the relationship between digitalis dose and arrhythmias. Thus, morphine pretreatment reduces the tendency for hypokalemia to potentiate digitalis-induced ventricular arrhythmias.

Animals↗
PubMed1986

Modes of onset ("initiating events") for paroxysmal atrial tachycardia in infants and children.

Observations of spontaneous onset of paroxysmal atrial tachycardia (PAT) in infants and children have been infrequently reported. This study reports on modes of spontaneous onset of PAT in 22 infants and 8 children in whom onset of PAT was recorded during continuous electrocardiographic recording. During PAT, all 30 patients used the normal specialized atrioventricular conduction system for ventricular activation, with atrial activation occurring through an accessory atrioventricular connection (orthodromic reciprocating tachycardia). Wolff-Parkinson-White syndrome was present in 7 patients. Analysis of the mode of onset of PAT revealed that infants initiated PAT with atrial extrasystoles or sinus acceleration (a gradual shortening of the P-P interval). In 10 infants more than 10 PAT onsets were recorded, and in these infants the mode of onset was sinus acceleration. In 7 infants, both atrial extrasystole and sinus acceleration were observed to initiate PAT. In the older children, onset of PAT followed atrial extrasystole (3 patients), ventricular extrasystole (2 patients), and sinus pause with junctional escape (3 patients). It has been previously recognized that the natural history of these "initiating events" varies with patient age. Variations in frequency of spontaneous episodes of PAT may relate to chronologic variations in frequency and type of initiating events.

Adolescent↗
PubMed1986

Transesophageal study of recurrent atrial tachycardia after atrial baffle procedures for complete transposition of the great arteries.

Transesophageal study was used for diagnosis and treatment of 51 episodes of tachycardia in 13 patients with complete transposition of the great arteries who had undergone atrial baffle procedure. At the time of atrial baffle procedure, patients were 6 to 36 months old (mean 23). Tachycardia (1 to 17 episodes per patient) first occurred 1 to 23 days (4 patients) or 1.8 to 12 years (9 patients) after atrial baffle. Transesophageal study was performed using a bipolar silicone rubber-coated catheter. Tachycardia conversion was accomplished with stimulation bursts using 4 to 10 stimuli 9.9 ms in duration at 20 to 28 mA and an interstimulus interval of 50 to 100 ms less than the atrial cycle length. All tachycardia episodes had regular atrial cycle lengths ranging from 200 to 350 ms. In 12 patients, second-degree atrioventricular (AV) block was observed during tachycardia, suggesting primary atrial tachycardia. However, in 1 patient, occurrence of AV block always resulted in tachycardia termination, suggesting the presence of AV reentrant tachycardia. Transesophageal stimulation converted 48 of 51 tachycardia episodes to sinus/junctional rhythm. Ten tachycardia episodes in 6 patients were transiently converted to atrial fibrillation lasting 3 seconds to 28 minutes before spontaneous conversion to sinus junctional rhythm. Conversion attempts were unsuccessful on 3 occasions. Acceleration of ventricular rate after stimulation necessitated DC cardioversion on 1 occasion. Conversion was not achieved in 2 tachycardia episodes using stimuli less than 10 mA. Transesophageal study is a safe and effective minimally invasive technique for diagnosis and treatment of tachycardia in infants and children who have had atrial baffle for transposition of the great arteries.

Child, Preschool↗
PubMed1986

Intracavitary electrode catheter cardioversion of atrial tachyarrhythmias in the dog.

This study examined factors determining efficacy of intracavitary cardioversion of atrial tachyarrhythmias in closed chest, anesthetized dogs with talc pericarditis. Electrode catheters were positioned transvenously with the cathode in the right atrial appendage. In Group 1 dogs (n = 6), three anode sites (superior and inferior venae cavae ostia and mid-right atrium) were tested with graded energy shocks to determine the lowest effective cardioversion energy at each anode position. In Group 2 dogs (n = 9), multiple cardioversion attempts with energy levels of 0.01 to 5.0 J were used to evaluate reproducibility of energy thresholds. In Group 3 dogs (n = 6) without talc-induced pericarditis, atrial pathologic study was done after five intracavitary shocks (0.5 or 5.0 J). In Group 1, cardioversion was achieved with 0.75 J or less with no significant difference in minimal effective cardioversion energies among the three anode positions tested. In Group 2, 98 (26%) of 372 cardioversion attempts were successful. Intra-animal minimal effective cardioversion energies varied widely, and timing of shocks relative to atrial electrograms did not influence efficacy. Complications were infrequent and included delayed sinus rhythm recovery, transient atrioventricular block and ventricular fibrillation. Ventricular fibrillation occurred in 9 (2.4%) of 372 shocks, and was associated with higher delivered energies (6 of 9 with greater than or equal to 1.0 J) and with shocks delivered 116 to 180 ms after onset of the QRS complex. In Group 3, two dogs had no histologic damage, three dogs had multiple small foci of subendocardial necrosis and in one dog these foci coalesced to involve half the atrial wall thickness. Thus, low energy cardioversion of atrial tachyarrhythmias is feasible using intracavitary electrodes. Synchronization of energy delivery to the QRS complex is important to minimize risk of ventricular fibrillation.

Animals↗
PubMed1986

Electrophysiologic effects of papillary muscle traction in the intact heart.

In this study we used transmural multipolar electrodes, sonomicrometers implanted within the left ventricular wall, and cardiac electrical stimulation techniques to examine the effect of transient mechanical posterior papillary muscle traction on local myocardial electrophysiologic characteristics. Nine open-chest dogs were atrially paced (cycle length 400 msec) followed by insertion of timed premature extrastimuli at left ventricular epicardial pacing sites either in the vicinity of (traction zone) or remote from (nontraction zone) the site of papillary muscle traction. Electrophysiologic recordings were made before and during periods of intermittent papillary muscle traction of predetermined timing, application rate (25 cm/sec), and duration (170 msec). Papillary muscle traction was applied in late diastole just before the last beat of each atrial drive train. In seven of nine dogs application of transient papillary muscle traction resulted in significantly earlier local ventricular activation (mean activation advancement 30 +/- 13 msec), altered QRS morphology of the last conducted atrial drive-train beat, and relative prolongation of ventricular functional refractory period in the traction zone. Conversely, in nontraction zones in these seven dogs, early activation did not occur and refractoriness remained unchanged as tested by a locally placed extrastimulus. In two of nine dogs traction failed to induce early activation and changes in refractoriness did not occur. Alterations in regional myocardial blood flow (assessed by radioactive microsphere technique) did not appear responsible for the observed changes, since there was no demonstrable traction-induced difference in regional blood flow between the traction and nontraction zones.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Electrophysiologic properties of the myocardial infarction border zone: effects of transient aortic occlusion.

This study used transmural multipolar electrodes, ventricular pressure monitoring, and cardiac electrical stimulation techniques to examine the effects of transient aortic occlusion on ventricular refractoriness in a canine model of recent myocardial infarction. Six previously instrumented resting awake dogs were atrially paced, followed by timed premature extrastimuli inserted at epicardial pacing sites adjacent to an apical left ventricular (LV) myocardial infarction or in an LV control zone remote from the myocardial infarction. Electrophysiologic and pressure recordings were obtained before and during periods of transient aortic occlusion. Aortic occlusion was applied before the last beat of an eight-beat atrial pacing sequence and resulted in increased peak LV pressure (92.8 +/- 27.7 mm Hg, p = 0.003). Aortic occlusion shortened LV effective refractory period (ERP) recorded from the myocardial infarction border zone in both the subepicardial (-17.0 +/- 11.8 msec, p = 0.019) and subendocardial (-17.7 +/- 10.9 msec, p = 0.011) regions, whereas LVERP of the control zone was unchanged. Conduction latency of premature beats at equivalent coupling intervals and maximum latency observed were unchanged by aortic occlusion. atrioventricular conduction interval shortened in association with aortic occlusion. Thus transient aortic occlusion reduced ventricular refractoriness in the border zone adjacent to the myocardial infarction while control zone refractoriness was minimally or not changed. Heterogeneity of ventricular myocardial refractoriness may result from mechanical dysfunction, potentially increasing susceptibility to arrhythmias.

Animals↗
PubMed1985

Electrophysiologic effects of flecainide acetate and its major metabolites in the canine heart.

Flecainide acetate, an investigational class 1 antiarrhythmic agent, undergoes biotransformation in man with production of 2 major metabolites: meta-O-dealkylated flecainide (S-24623) and the meta-O-dealkylated lactam of flecainide (S-26191). This study compared the effects of flecainide, S-24623 and S-26191 on cardiac electrophysiologic characteristics in the anesthetized dog. Each dog received 2 dose levels of 1 of the 3 test compounds after control measurements. Flecainide (2 and 4 mg/kg in 8 dogs), S-24623 (4 and 8 mg/kg in 8 dogs) and S-26191 (4 and 10 mg/kg in 7 dogs) were administered intravenously in dilute solution. Of the 3 compounds, only flecainide significantly prolonged sinus cycle length (p less than 0.01). However, both flecainide and S-24623 significantly prolonged minimum atrial paced cycle length with 1:1 atrioventricular conduction, atrioventricular nodal effective and functional refractory periods, and right ventricular effective refractory period. Metabolite S-26191 exhibited qualitatively similar but much weaker electrophysiologic actions. The maximal electrophysiologic effects of flecainide and S-24623 were approximately equivalent, but the metabolite was about one-half as potent on a milligram-permilligram basis, and lacked marked effects on infranodal (HV interval) conduction. S-26191 was less than one-tenth as potent as flecainide. Therefore, since both flecainide metabolites occur primarily in the conjugated form in plasma (i.e., free metabolite concentrations are low), it is unlikely that these compounds either potentiate flecainide's antiarrhythmic action or increase susceptibility to drug toxicity in the clinical setting.

Animals↗
PubMed1985

Electrophysiological effects of transient aortic occlusion in intact canine heart.

This study utilized sonomicrometers transmural multipolar electrodes and cardiac electrical stimulation techniques to examine the effect on myocardial electrophysiological characteristics of altering ventricular systolic mechanical properties by transient aortic occlusion. Nine anesthetized open-chest dogs were atrially paced, and timed extrastimuli were inserted during alternate drive-train sequences at right or left ventricular (RV, LV) epicardial sites to measure ventricular effective refractory period (ERP). Sonomicrometer measurements of LV systolic mechanical parameters and both RV and LV electrophysiological findings were determined prior to and during periods of transient aortic occlusion. Aortic occlusion was applied just prior to the last beat of each eight-beat atrial drive train and released immediately following the programmed ventricular extrastimulus. Aortic occlusion increased LV systolic pressure (+42 +/- 26.6 mmHg, P less than 0.01) and diminished segmental stroke shortening (0.100 +/- 0.059 mm, P less than 0.02), shortening fraction (0.086 +/- 0.048, P less than 0.001), mean velocity of stroke shortening (0.444 +/- 0.186 mm/s, P less than 0.001), and stroke work (P less than 0.001). LV epicardial and endocardial ERP were prolonged as a result of aortic occlusion (5 +/- 7.2 and 6 +/- 6.5 ms, respectively, P less than 0.05), whereas RV ERP was unchanged. Latency of premature beats at equivalent coupling intervals was unaltered. ERP prolongation correlated most strongly with reductions of segmental stroke shortening (r = 0.928, P less than 0.001), shortening fraction (r = 0.901, P less than 0.001), and mean shortening velocity (r = 0.819, P less than 0.01). Thus transient aortic occlusion prolonged LV refractoriness, and electrophysiological changes closely paralleled the severity of systolic mechanical disturbance.

Animals↗
PubMed1985

Carotid sinus hypersensitivity: evaluation of the vasodepressor component.

The basis of the vasodepressor response in patients with carotid sinus hypersensitivity (CSH) is unknown, and prevention of recurrent vasodepressor-induced hypotension in these patients has not been possible. In this study we assessed the effectiveness of atrioventricular sequential pacing and pharmacologic interventions in the prevention of carotid sinus massage (CSM)-induced vasodepressor responses in eight patients with CSH. Maintenance of constant heart rate (80 beats/min) and atrioventricular synchrony (atrioventricular interval 150 msec) with sequential pacing did not significantly alter mean CSM-induced fall in systolic pressure (CSM control, -60 +/- 12 mm Hg vs CSM with atrioventricular sequential pacing, -48 +/- 19 mm Hg). Similarly, neither pharmacologic muscarinic blockade nor combined muscarinic and beta-adrenergic blockade significantly attenuated CSM-induced fall in systolic pressure (CSM with atropine, -43 +/- 16 mm Hg; CSM with atropine plus propranolol, -47 +/- 18 mm Hg; both p = NS vs atrioventricular sequential pacing alone). On the other hand, intravenous norepinephrine and oral ephedrine blunted the CSM-induced drop in systolic pressure (CSM with norepinephrine, -19 +/- 12 mm Hg; CSM with ephedrine, -21 +/- 11 mm Hg; both p less than .01 vs atrioventricular sequential pacing alone). Thus, vasodepressor responses were not prevented by control of heart rate, maintenance of atrioventricular synchrony, pharmacologic muscarinic blockade, or combined muscarinic and beta-adrenergic blockade, but were attenuated by drugs believed to be predominantly alpha-adrenergic agonists. Consequently, atrioventricular sequential pacing alone may be inadequate to prevent hypotension in patients with pronounced vasodepressor responses, whereas administration of vasoconstrictors such as ephedrine may diminish symptoms.

Aged↗
PubMed1985

Periodic procainamide for paroxysmal tachycardia.

We evaluated the efficacy of a single oral dose of procainamide to terminate paroxysmal tachycardia, when procainamide was taken shortly after onset of tachycardia, a regimen we have termed "periodic procainamide." In 12 patients (mean age 15 years) with non-life-threatening tachycardia (orthodromic reciprocating tachycardia, 8/12; ventricular tachycardia, 3/12; atrial flutter, 1/12) in whom intravenously administered procainamide (15 mg/kg at 1 mg/kg/min) terminated tachycardia, efficacy of a single oral dose of procainamide (25 mg/kg) to terminate tachycardia was tested during electrophysiologic study. After oral administration of procainamide, tachycardia was terminated and could not be reinitiated in 11 of 12 patients (9/12 less than 75 min, 2/12 greater than 120 min after administration). Time of tachycardia termination approximately coincided with the time of peak serum concentration of procainamide after the single oral dose. Delayed response or failure of procainamide to terminate tachycardia was associated with delayed and diminished peak serum procainamide concentration. After evaluation, 10 responders were instructed to take a single dose of procainamide when tachycardia occurred. During a mean follow-up of 9 months (range 2 to 17) seven of 10 patients had an opportunity to use periodic procainamide on one to more than 100 occasions; four of 10 patients have not had recurrence of tachycardia. Tachycardia was successfully terminated in six of seven patients using the periodic regimen and could not be terminated on the first out-of-hospital use in one of seven patients. Success of periodic procainamide was predicted during evaluation by rapid termination of tachycardia after oral administration.

Administration, Oral↗