Biomedical subjects

D E Mann

Publications and source records attributed to D E Mann.

At least 55 records · Page 3Linked to original sources

PubMed1988

Electrophysiological effects of acute ventricular dilatation in the isolated rabbit heart.

We examined the effects of left ventricular dilatation on epicardial pacing threshold, conduction velocity, and effective refractory period (ERP) in the isolated, retrograde perfused rabbit heart. Left ventricular size was modified by acutely changing the volume of a fluid-filled balloon anchored within the vented left ventricle. Increases in left ventricular volume, associated with increases in left ventricular end-diastolic pressure from 0 +/- 1 to 35 +/- 2 mm Hg, were not associated with significant changes in pacing threshold or conduction velocity. The left ventricular ERP decreased significantly with an added volume of 1.5 ml (91.4 +/- 5.5 msec) compared with starting volume (117.7 +/- 3.8 msec, p less than 0.01). Right ventricular ERP did not change significantly with increases in left ventricular volume. The left and right ventricular ERPs were comparable at starting volume (117.7 +/- 3.8 and 117.6 +/- 3.5 msec, respectively; p = NS) but were significantly different with an added volume of 1.5 ml (91.4 +/- 5.5 and 112 +/- 5.6 msec, p less than 0.05). These changes were independent of coronary perfusion pressure and paced cycle length, suggesting that ischemia is an unlikely explanation for the observed effects. Changes in left ventricular volume decreased left ventricular ERP in a regionally heterogeneous manner, increasing the temporal dispersion of recovery over the left ventricle nearly twofold. Induced ventricular arrhythmias (ventricular tachycardia or fibrillation) were significantly more frequent at high (35%) than at low (3%) volumes during left ventricular pacing. We conclude that ventricular dilatation is associated with increased dispersion of refractoriness in this model, a finding that correlates with propensity for reentrant arrhythmias.

Animals↗

PubMed1988

Detection of histamine in human placental perfusate and the effect of histamine releasers.

Studies on full-term human placentas were conducted to determine whether the vasogenic actions of certain agents on perfused placental vasculature are due to histamine release. Compound 48/80 and morphine were selected because they liberate the autacoid via different mechanisms. Initially, a control effluent was collected prior to each drug challenge and again collected throughout the rise and fall in perfusion pressure. The drugs were given alone and in the presence of a 50 mcg dose of histamine free base (HFB) to assess the release of stored histamine and also to serve as a control. Following extraction in n-butanol and recovery in 0.1 N HCl, all effluents were fluoresced with o-phthalaldehyde and assayed for histamine content via spectrophotofluorometry. A baseline histamine level was discovered in the majority of placental effluents collected prior to the administration of any agent. No significant increases above this initial level occurred following treatment with compound 48/80 alone. However, small but significantly elevated amounts of histamine appeared in the placental effluent when compound 48/80 was given 10 minutes after the initial 50 mcg dose of HFB. This agent also caused a slight increase in placental perfusion pressure after each administration. Results obtained with morphine do not appear to support the hypothesis that significant amounts of histamine are released by this agent in the perfused human placenta.

Female↗

PubMed1988

Chronic supraventricular tachycardia can cause severe ventricular dysfunction, which can be surgically repaired.

A 19-year-old woman with a history of chronic supraventricular tachycardia was admitted with acute left ventricular dysfunction (ejection fraction = 0.26). Surgical division of the accessory conduction ventriculoatrial pathway resulted in complete recovery and improved ejection fraction (0.55 one year after operation). The purpose of this report is to indicate that (1) chronic supraventricular tachycardia can cause ventricular dysfunction, (2) surgical repair of the tachycardia reverses ventricular dysfunction, and (3) progressive left ventricular dysfunction is an indication for surgical intervention in the management of chronic supraventricular tachycardia.

Adult↗

PubMed1987

Electrophysiology of Ethmozine (moricizine HCl) for ventricular tachycardia.

Moricizine HCl, an antiarrhythmic phenothiazine drug, was investigated for its efficacy against ventricular tachycardia (VT) in a group of 60 patients from 8 institutions using electrophysiologic testing before and after oral administration. Moricizine HCl significantly prolonged PR, QRS, AH and HV intervals and cycle length for atrioventricular nodal block, but had minimal or no effect on repolarization or cardiac refractory periods. Induction of sustained VT (in 33 patients) and nonsustained VT (in 14 patients) occurred at baseline. During moricizine HCl therapy, sustained VT was induced in 31 patients and nonsustained VT in 7 patients. In individual patients, suppression of VT induction was obtained in 18% of patients with sustained VT and in 27% of patients with nonsustained VT. Cycle length of induced VT was significantly prolonged by moricizine HCl therapy. During prospective follow-up of 37 patients, electrophysiologic study predicted recurrence of nonrecurrence of VT with a sensitivity value of 82% and specificity of 65%.

Adult↗

PubMed1987

Effects of upright posture on anterograde and retrograde atrioventricular conduction in patients with coronary artery disease, mitral valve prolapse or no structural heart disease.

To assess the effects of posture on anterograde and retrograde atrioventricular conduction, electrophysiologic testing was performed in 25 patients in both the supine and 45 degrees upright positions on a tilt table. Retrograde conduction was present during ventricular pacing in 17 patients in the supine position; all 17 continued to manifest retrograde conduction in the upright position. In all patients with absent retrograde conduction while supine, retrograde conduction could not be demonstrated while upright. Upright posture significantly (p less than 0.05) shortened the sinus cycle length (from 808 +/- 34 to 678 +/- 26 ms, mean +/- standard error of the mean), AH interval during sinus rhythm (78 +/- 6 to 69 +/- 6 ms), and AH interval during atrial pacing at cycle length 500 ms (123 +/- 13 to 91 +/- 9 ms). Total atrioventricular conduction time during atrial pacing shortened significantly (from 169 +/- 13 to 136 +/- 10 ms), as did ventriculoatrial conduction time during ventricular pacing (from 192 +/- 9 to 178 +/- 7 ms). Upright posture also significantly shortened both anterograde block cycle length (390 +/- 20 to 328 +/- 17 ms) and retrograde block cycle length (466 +/- 27 to 354 +/- 18 ms). However, the effect of upright posture on retrograde block cycle length was significantly greater than on anterograde block cycle length: a 21% decrease retrograde vs a 14% decrease anterograde (p less than 0.05). These effects may produce clinically important changes in characteristics of arrhythmias that depend on the properties of anterograde and retrograde conduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrioventricular Node↗

PubMed1987

Efficacy of class Ib (lidocaine-like) antiarrhythmic agents for prevention of sustained ventricular tachycardia secondary to coronary artery disease.

The effects of lidocaine, tocainide and mexiletine were examined in 17 patients with coronary artery disease and chronic, recurrent, sustained ventricular tachycardia (VT) or ventricular fibrillation and inducible VT. Eleven patients presented with sustained VT; 6 patients had had an episode of sudden death from which they had been resuscitated. All patients were refractory to conventional antiarrhythmic agents. Lidocaine prevented induction of VT in only 3 patients (18%). Tocainide prevented induction of VT in only 1 lidocaine-responsive patient. Mexiletine prevented VT induction in 1 patient who had responded to lidocaine but not tocainide. Neither tocainide nor mexiletine was effective in preventing induction of VT in any patient who did not respond to lidocaine. Lidocaine terminated VT in 3 patients, but this did not predict noninducibility with lidocaine, tocainide or mexiletine. Cycle length of VT was prolonged slightly by lidocaine (control 311 +/- 14 ms, lidocaine 361 +/- 26 ms, p less than 0.05), tocainide (344 +/- 16 ms, p less than 0.05) and mexiletine (371 +/- 27 ms, mean +/- standard error of the mean, p less than 0.05). Thus, class lb agents are infrequently effective in preventing induction of VT in this group of patients, electrophysiologic inefficacy of lidocaine is highly predictive of continued inducibility with tocainide and mexiletine, and termination of VT with lidocaine does not correlate with its ability to prevent VT induction.

Adult↗

PubMed1987

Prospective comparison of right and left ventricular stimulation for induction of sustained ventricular tachycardia.

Thirty-eight patients who had sustained monomorphic ventricular tachycardia (VT) or sudden cardiac death underwent programmed ventricular stimulation. To assess the relative efficacy of right and left ventricular (RV and LV) stimulation, a tandem protocol with 1 to 4 extrastimuli and burst pacing was used. Each step of the protocol was performed in a rotating sequence at the RV apex, basal RV septum and LV apex. Sustained VT was induced from the RV apex in 26 patients, right ventricle (either site) in 27, and LV apex in 24, and spontaneous VT was reproduced from those sites in 11, 14 and 12 patients, respectively. In the 23 patients who had sustained VT induced from both ventricles, RV stimulation always required fewer or the same number of extrastimuli for induction. At every stage of the protocol, the cumulative yield of sustained VT was consistently greater from the right ventricle than from the left ventricle. After delivering 4 extrastimuli and burst pacing, LV stimulation only increased the yield of sustained VT by 1 patient, and spontaneous VT by 3 patients. Inducibility or noninducibility in the right ventricle generally predicted the same outcome in the left ventricle. Previously undocumented VT or ventricular fibrillation was induced from the right ventricle in 19 patients and from the left ventricle in 13. Thus, LV stimulation was less efficacious than RV stimulation. LV stimulation increased the yield over RV stimulation only minimally and did not reduce the number of extrastimuli required to induce sustained VT.

Cardiac Catheterization↗

PubMed1987

Two different patterns of entrainment of ventricular tachycardia.

In a patient with two morphologic forms of ventricular tachycardia, rapid pacing from different ventricular sites produced two distinctively different patterns of entrainment. Pacing from sites contralateral to the site of emergence of ventricular tachycardia caused progressive fusion. Following pacing, the interval (return interval) between the first tachycardia beat (return beat) and the preceding beat was equal to the pacing cycle length. Near the site of emergence, the local electrogram of the return beat was morphologically identical to that of the preceding paced beats. In contrast, pacing from sites ipsilateral to the site of emergence did not cause fusion. The return intervals increased with decreasing pacing cycle lengths. The local electrogram of the return beat was morphologically different from that of the preceding paced beats. Using a model of ventricular reentrance, both patterns of responses can be explained. Pacing impulses arising from sites contralateral to the site of emergence activate the latter orthodromically. Fusion occurs between the emerging tachycardia wavefront and the next pacing wavefront. In contrast, pacing impulses arising from sites ipsilateral to the site of emergence activate the latter antidromically. Fusion is not observed because collision within the area of slow conduction prevents the emergence of the tachycardia during pacing.

Adult↗

PubMed1986

Effects of quinidine versus procainamide on the QT interval.

Eighteen patients were given quinidine and procainamide separately to evaluate whether prolongation of the QT interval by type Ia antiarrhythmic agents is a drug-specific phenomenon. Doses were titrated to achieve standard trough therapeutic levels of quinidine (2 to 5 micrograms/ml) and procainamide (4 to 12 micrograms/ml). In 16 of the 18 patients, the increase in corrected QT interval (QTc) was greater with quinidine than with procainamide, averaging 78 +/- 10 ms (+/- standard error of the mean) with quinidine and 39 +/- 7 ms with procainamide (p less than 0.001). The greater degree of QTc prolongation with quinidine than with procainamide was not due to differences in sinus cycle length, QRS duration, serum potassium level or concomitant drug therapy. Differences in relative drug level did not appear to account for the greater effect of quinidine. Thus, at frequently used plasma levels, quinidine prolongs QTc to a greater degree than does procainamide. This effect does not appear to be due to the comparison of "nonequivalent" drug levels.

Adult↗

PubMed1986

Electrophysiologic evaluation of pirmenol for sustained ventricular tachycardia secondary to coronary artery disease.

The efficacy and electrophysiologic effects of pirmenol were evaluated in 21 patients with a history of sustained ventricular tachycardia (VT) and coronary artery disease. Intravenous pirmenol (0.7- to 1.1-mg/kg bolus, followed by a 35- to 40-micrograms/kg/min infusion) significantly prolonged the PR, QRS, QT and corrected QT intervals, HV interval and right ventricular effective refractory period, and shortened the sinus cycle length and atrioventricular nodal block cycle length. All 21 patients had inducible VT (20 sustained, 1 nonsustained) during programmed stimulation in the control state. After intravenous pirmenol, 5 patients (24%) no longer had inducible VT. In those in whom VT was still inducible, the VT cycle length was prolonged significantly. The 5 patients who responded to intravenous pirmenol were given oral pirmenol (200 to 250 mg every 8 hours) for 1 to 3 days and retested with programmed stimulation. In 4 of these 5, VT could not be induced with oral pirmenol administration; in 1 patient sustained VT was induced and pirmenol therapy was discontinued. Oral pirmenol suppressed recurrent VT during a follow-up of 315 +/- 133 days in 4 patients. However, pirmenol therapy was discontinued in 2 patients because of possible deleterious effects (worsened heart failure in 1 patient and elevated liver function test results in 1). Thus, pirmenol, a type IA antiarrhythmic drug, had an overall efficacy of approximately 19% in patients with sustained VT secondary to coronary artery disease.

Adult↗

PubMed1986

Effect of increased current, multiple pacing sites and number of extrastimuli on induction of ventricular tachycardia.

Reproduction of spontaneously occurring ventricular tachycardia (VT) and induction of previously undocumented VT were studied prospectively in 98 patients: 48 with documented sustained VT or ventricular fibrillation, 25 with nonsustained or exercise-induced VT, and 25 with no documented VT. Patients received 1 to 4 ventricular extrastimuli and ventricular burst pacing at 2 right ventricular (RV) sites, first at twice late diastolic threshold, and then at 10 mA using a prospective, tandem study design. Spontaneously occurring VT was reproduced in 37 of 48 patients (77%) at twice late diastolic threshold and in 1 other patient (2%) at 10 mA. VT was reproduced at both RV sites in 17 of 48 patients (35%) and at 1 site in 20 of 48 patients (42%) at twice late diastolic threshold. A previously undocumented VT was induced in 7 of 25 patients (28%) with no documented VT at twice diastolic threshold and 14 of 25 patients (56%) at 10 mA. A previously undocumented VT was induced in 33 of 73 patients (45%) with a history of sustained or nonsustained VT at twice late diastolic threshold and in 47 of 73 patients (64%) at 10 mA. In patients with documented sustained VT, the use of up to 4 ventricular extrastimuli at multiple RV sites increases the sensitivity of the test. In patients without documented VT, the induction of previously undocumented VT with more than 3 ventricular extrastimuli limits the specificity of the test. Increased current provides only a slight advantage over 4 ventricular extrastimuli at twice late diastolic threshold in terms of reproduction of spontaneously occurring VT, but leads to a marked increase in induction of previously undocumented VT.

Aged↗

PubMed1985

Effect of bradycardia on dispersion of ventricular refractoriness.

The effect of bradycardia on dispersion of ventricular refractoriness was evaluated. Refractory periods were measured at 3 right ventricular sites in 16 patients with severe bradycardia (average heart rate 39 +/- 5 beats/min) and were compared with those measured in 11 control subjects, (average heart rate 72 +/- 12 beats/min). Patients with bradycardia had significantly longer effective (377 +/- 36 ms) and functional (421 +/- 39 ms) refractory periods (ERP and FRP) than control subjects (ERP 296 +/- 25 ms, FRP 346 +/- 18 ms) (p less than 0.001). However, dispersion of refractoriness was similar in the 2 groups. Dispersion of ERP was 43 +/- 38 ms and FRP was 48 +/- 35 ms in patients with bradycardia. In control subjects dispersion of ERP was 37 +/- 12 ms, and FRP was 36 +/- 20 ms. Pacing of 120 beats/min significantly decreased ERP and FRP in both groups. Pacing shortened dispersion significantly in control subjects. In patients with bradycardia, pacing failed to significantly decrease dispersion. Compared with control subjects with normal heart rates, patients with bradycardia have longer absolute refractory periods but do not have significantly increased dispersion of refractoriness. Single and double, twice threshold ventricular extrastimuli (S2 and S3) failed to induce ventricular tachycardia in any patient during bradycardia. Bradycardia alone does not appear to be a factor in the induction of ventricular tachyarrhythmias.

Adult↗

PubMed1985

Permanent triggered antitachycardia pacemakers in the management of recurrent sustained ventricular tachycardia.

Permanent pacemakers capable of triggered ventricular stimulation were implanted in 28 patients with a history of sustained ventricular tachycardia or fibrillation. Noninvasive programmed ventricular stimulation was performed on 125 occasions during follow-up periods ranging from 1 to 25 months and was used to assess the efficacy of antiarrhythmic drug therapy, drug or dosage changes and left ventricular endocardial resection. Drug or dosage changes based on noninvasive programmed ventricular stimulation were made in 19 of the 28 patients. In addition, 126 episodes of spontaneous sustained ventricular tachycardia were terminated noninvasively in nine patients. It is concluded that a permanent pacemaker capable of triggered ventricular stimulation is useful in patients with ventricular tachycardia or fibrillation that is difficult to control.

Adult↗

PubMed1985

Importance of pacing site in entrainment of ventricular tachycardia.

Transient entrainment by pacing has been demonstrated during various tachyarrhythmias, including ventricular tachycardia. A patient is described who had two morphologically distinct forms of sustained ventricular tachycardia induced by programmed stimulation. Entrainment of both configurations of ventricular tachycardia was demonstrated. Evidence for entrainment included the presence of different degrees of fusion between paced and ventricular tachycardia complexes at different pacing cycle lengths, and the observation that the last entrained beat was always unfused and identical in configuration to the ventricular tachycardia complexes. Termination of ventricular tachycardia only occurred at pacing cycle lengths at which there was loss of fusion. Catheter endocardial mapping suggested a septal origin of both configurations of ventricular tachycardia. Demonstration of entrainment was dependent on pacing site, being seen only during pacing in the ventricle opposite from that showing earliest activation during ventricular tachycardia. Thus, when attempting to entrain ventricular tachycardia, multiple pacing sites in both ventricles should be used.

Bundle-Branch Block↗

PubMed1985

Emergency defibrillation using a temporary pacing electrode catheter.

Direct application of electrical current to the heart utilizing special equipment such as implantable defibrillators or specially designed catheters has been useful in patients with recurrent ventricular tachyarrhythmias. We describe a patient who developed intractable ventricular fibrillation (VF) during the course of electrophysiologic testing. VF continued for 50 minutes, during which time multiple transthoracic shocks of 360 joules failed to convert the arrhythmia. Intracardiac shocks were then delivered via a transvenous 6 French standard quadripolar pacing catheter positioned in the right ventricular apex by direct application of the defibrillator paddle to the catheter, with the patient lying on the posterior paddle. Energy of up to 300 joules failed to defibrillate the patient, but use of 360 joules delivered in this fashion defibrillated the patient twice. Despite the protracted time of cardiac arrest, the patient recovered without sequelae. We report this case to demonstrate that VF refractory to transthoracic defibrillation may be converted by intracardiac shocks using a temporary pacing catheter without special equipment.

Cardiac Catheterization↗

PubMed1984

Conduction system abnormalities in symptomatic mitral valve prolapse: an electrophysiologic analysis of 60 patients.

This study examined the site of atrioventricular (AV) block in mitral valve prolapse (MVP). Sixty symptomatic patients with MVP underwent electrophysiologic study; 49 had documented arrhythmias and 28 had syncope. Eight patients had spontaneous second- or third-degree AV block and 10 had chronic bundle branch block. Electrophysiologic study revealed abnormal sinus node function in 8 patients, prolonged HV interval in 10, intra-Hisian delay in 9, and functional bundle branch block in 15. Dual AV nodal pathways were demonstrated in 24 patients. Comparison with 101 similarly symptomatic patients without MVP revealed a greater prevalence of dual AV nodal pathways in the MVP patients. Infranodal conduction abnormalities and dual AV nodal pathways are frequently revealed by electrophysiologic testing in symptomatic patients with MVP.

Adolescent↗

PubMed1984

Influence of alpha- and beta-adrenergic antagonists on dopamine-induced responses in the isolated heart of Mercenaria mercenaria.

Agents with predominantly adrenergic antagonistic properties (the alpha-blockers, phentolamine and tolazoline, and the beta-blocker propranolol), and those with suspected alpha-blocking capabilities [hydralazine and 3,3'-(4,4'-biphenylene)bis(2,5-diphenyl-2H-tetrazolium chloride) (neotetrazolium chloride); I] were added individually to a bath containing an isolated Mercenaria mercenaria heart. Two and one-half minutes later, dopamine was added to the bath as the second drug and cardiac responses were noted. Pretreatment with saline controls, followed by dopamine 2.5 min later, produced results that were identical with those which occurred after the administration of dopamine alone, i.e., marked stimulation and cardiac arrest. Pretreatment with phentolamine and I were the only procedures that prevented dopamine-induced cardiac arrest. Phentolamine, tolazoline, and hydralazine generally produced positive inotropic responses when initially added to the bath, whereas propranolol mimicked the effects caused by the addition of dopamine alone or after saline pretreatment. The M. mercenaria heart appears to possess an adrenergic receptor of an alpha-configuration.

Adrenergic alpha-Antagonists↗

PubMed1984

Electrophysiologic effects of ethmozin in patients with ventricular tachycardia.

Ten patients with recurrent episodes of ventricular tachycardia (VT) had electrophysiologic studies in the basal state and on chronic oral ethmozin (12.1 +/- 0.6 SE mg/kg/day). Ethmozin significantly prolonged the AH interval (basal: 75 +/- 8 SE msec; ethmozin: 91 +/- 10 msec, p less than 0.05), the HV interval (51 +/- 3; 66 +/- 5 msec, p less than 0.01), and the QRS duration (101 +/- 4; 118 +/- 4 msec, p less than 0.001). Atrial and ventricular refractory periods and the corrected QT interval were not significantly affected by ethmozin. VT was induced in 7 of 10 patients in the basal state by means of programmed right ventricular extrastimulation or rapid burst ventricular pacing. On oral ethmozin nine patients had inducible VT. VT cycle length was consistently prolonged on ethmozin (250 +/- 13; 326 +/- 14 msec, p less than 0.001). Four of the seven patients with VT on basal ambulatory monitoring had total abolition of spontaneous VT on ethmozin. Ethmozin failed to prevent induction of VT in most patients despite significant reductions in ventricular arrhythmia on ambulatory monitoring. Further studies comparing VT induction with ambulatory monitoring in patients on ethmozin are needed to confirm these findings and to define the clinical significance of this dissociation.

Adult↗