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Biomedical subjects

A E Epstein

Publications and source records attributed to A E Epstein.

At least 91 records · Page 5Linked to original sources
PubMed1991

Inability of the signal-averaged electrocardiogram to determine risk of arrhythmia recurrence in patients with implantable cardioverter defibrillators.

Signal-averaged electrocardiography has been used to identify patients at risk for arrhythmic death after myocardial infarction. Since patients with implantable cardioverter defibrillators (ICDs) are at high risk for arrhythmic events, they should also be expected to have a high incidence of abnormal signal-averaged electrocardiograms (SAECGs). However, whether the SAECG can discriminate patients who will have arrhythmia recurrence and receive appropriate ICD shocks from those who will have no recurrence and no shocks is unknown. This study examines the usefulness of the SAECG to separate appropriate users from non-users of the ICD. Fifty patients with ICDs participated in this study. Those who received a shock preceded by symptoms, a shock without preceding symptoms but with electrocardiographic documentation of ventricular fibrillation or ventricular tachycardia, or a shock while asleep were classified as ICD users. All other patients were classified as nonusers. The SAECG was classified as normal if the QRS duration on the standard electrocardiogram was less than or equal to 110 msec and if the total filtered QRS duration was less than 120 msec, the root-mean square voltage of the terminal 40 msec was greater than 25 muV, and the terminal low amplitude signal duration measured less than 38 msec. The SAECG was classified as abnormal if the QRS duration on the standard electrocardiogram was less than or equal to 110 msec and any one of these three criteria were outside the "normal range." The SAECG was classified as indeterminate if the QRS duration on the standard 12-lead electrocardiogram was greater than 110 msec. For the entire group of 50 patients, 8 (16%), 12 (24%), and 30 (60%) had normal, abnormal, and indeterminate SAECGs, respectively. Of the 22 ICD users, 1 (5%), 5 (23%), and 16 (73%) patients had normal, abnormal, and indeterminate SAECGs, respectively. Of the 28 ICD nonusers, 7 (25%), 7 (25%), and 14 (50%) patients had normal, abnormal, and indeterminate SAECGs, respectively. ICD users had lower left ventricular ejection fractions (P = 0.0002), a higher incidence of ventricular tachycardia (P = 0.04), prior exposure to a greater number of antiarrhythmic drugs (P = 0.04), and a lower likelihood for survival (P = 0.02) compared to the ICD nonusers. There was no statistically significant difference between the ICD users and nonusers as stratified by SAECG classification regardless of whether or not the interminate studies were included or excluded from the analysis.(ABSTRACT TRUNCATED AT 400 WORDS)

Arrhythmias, Cardiac↗
PubMed1991

Analysis and predictors of pulmonary vascular resistance after cardiac transplantation.

Elevated pulmonary vascular resistance is a known risk factor for early death from acute right ventricular failure after orthotopic cardiac transplantation. Patients in whom the elevated pulmonary vascular resistance is due primarily to increased left atrial pressure ("reactive") frequently have normalization of resistance after transplantation, but few studies have detailed the time course and magnitude of these changes. To analyze the response of pulmonary vascular resistance to cardiac transplantation, we analyzed data from 4353 right heart catheterizations on all 182 patients undergoing cardiac transplantation between 1981 and Jan. 1, 1990. Before transplantation 18% of patients had a pulmonary vascular resistance greater than 4 WU, 16% had a pulmonary artery systolic pressure greater than 60 mm Hg, and 16% had a transpulmonary gradient greater than 14 mm Hg. In the overall group of patients, pulmonary vascular resistance (mean value 2.63 WU), transpulmonary gradient (mean value 9.9 mm Hg), and pulmonary artery systolic pressure (mean value 48.0 mm Hg) were normalized within 1 week of cardiac transplantation. In patients with a high preoperative pulmonary vascular resistance (greater than or equal to 4 WU), the resistance fell promptly within 1 week of transplantation but continued to be slightly elevated throughout the period of follow-up. By multiple regression analysis, pulmonary vascular resistance at 1 week and 1 year after transplantation was significantly correlated with the pretransplantation resistance. Pulmonary vascular resistance anytime after transplantation was related to preoperative resistance, body surface area, and pulmonary artery diastolic pressure. Inferences: (1) As a group, cardiac transplant recipients have a normal pulmonary vascular resistance, transpulmonary gradient, and pulmonary artery systolic pressure within 1 week after transplantation with little change thereafter for at least several years. (2) Patients with reversible elevation of pulmonary vascular resistance before cardiac transplantation typically have a reactive and a fixed component. Cardiac transplantation relieves the reactive but not the fixed component. As a result, pulmonary vascular resistance early (within 1 week) and late after transplantation will have fallen but not completely normalized.

Cardiac Catheterization↗
PubMed1990

Evidence for a central site of action to explain the negative chronotropic effect of atropine: studies on the human transplanted heart.

The chronotropic response to atropine is biphasic; low doses cause slowing of the sinus rate and high doses cause acceleration. Although it is accepted that atropine functions as a competitive antagonist at high doses, the mechanism of the negative chronotropic response at low doses is controversial. Specifically, it is unclear whether the effect is mediated centrally or peripherally. Since at the time of cardiac replacement all central nervous system connections to the heart are severed, the transplanted heart is a unique model for separating these effects. Graded doses of atropine sulfate (0.5, 1.0, 2.0, 4.0, 8.0 and 40.0 micrograms/kg body weight) were administered to 12 human heart transplant recipients to test the hypothesis that the bradycardiac effect of low dose atropine is centrally mediated. The baseline sinus cycle lengths of the decentralized donor and innervated native sinus nodes were 694 +/- 20 and 733 +/- 27 ms, respectively. At the 0.5 and 1.0 microgram/kg doses, the cycle lengths of the native sinus node increased by 29.1 +/- 13.5 and 23.1 +/- 14.2 ms, respectively. At the 2.0 micrograms/kg dose the sinus cycle length again shortened to control. At the maximal dose of atropine the sinus cycle length shortened by 138.3 +/- 29.7 ms compared with control. In contrast, the decentralized donor sinus node exhibited a flat dose response to atropine. High dose atropine (40 micrograms/kg) caused no change in the donor heart's atrial effective refractory period, corrected sinus node recovery time, or sinoatrial conduction time measured by either the Strauss or the Narula method.(ABSTRACT TRUNCATED AT 250 WORDS)

Atropine↗
PubMed1990

Effect of pacing rate on the human atrial strength-duration curve.

The effect of rapid pacing on the atrial constant voltage stimulation threshold in humans has not been defined at rates applicable to those of antitachycardia pacing. The effect of pacing rate on the atrial strength-duration relation was determined in 10 patients at pacing rates between 125 and 300 beats/min to explore excitability over the range of rates used for permanent antitachycardia pacing systems. Two points that define the strength-duration curve were measured at each pacing rate: rheobase voltage--the lowest stimulus voltage that results in capture at a pulse duration of 2 ms; and chronaxie pulse duration--the threshold pulse duration at twice rheobase voltage. A permanent, tined, J-shaped pacing lead with a high current density and low polarization electrode was positioned in the right atrial appendage for cathodal stimulation. A constant voltage output, incorporating a fast recharge pulse designed to minimize electrode polarization, was used for stimulation. There was a significant increase in rheobase voltage (p = 0.009), chronaxie pulse duration (p = 0.001) and minimal threshold stimulus energy (p = 0.05) at pacing rates greater than 225 beats/min. A rheobase voltage greater than 5 V occurred in three patients at pacing rates greater than or equal to 275 beats/min. At a pacing rate of 300 beats/min, rheobase voltage had increased in 8 of 10 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1990

Significance of ventricular tachyarrhythmias complicating cardiac catheterization: a CASS Registry Study.

Ventricular tachycardia and ventricular fibrillation are recognized complications of cardiac catheterization. Despite numerous reports documenting the frequency of these occurrences, their significance has not been systematically examined. Accordingly, the outcome of 108 patients who experienced either ventricular tachycardia or ventricular fibrillation during coronary angiography between 1975 and 1979 in the Coronary Artery Surgery Study (CASS) Registry were examined. There were 20,142 patients analyzed. Patients with ventricular tachyarrhythmias had more objective evidence of left ventricular impairment, clinical heart failure, and ventricular arrhythmia recorded as a clinical symptom. The overall 5-year survival rates were 83% and 88% for patients with and without ventricular tachyarrhythmias, respectively (p = 0.07). When ventricular function, age, gender, angina, and previous myocardial infarction were added in a stepwise Cox survival analysis, the presence of arrhythmias was not significant (p = 0.66). At 5 years, 80% of the medically treated patients and 82% of the surgically treated patients remained alive (p = 0.95). The only statistically significant differences in the patients with ventricular arrhythmias who were treated medically or surgically were age (medically treated patients 52 +/- 10 years, surgical patients 57 +/- 9 years, p = 0.01) and number of diseased vessels (p less than 0.001). In a stepwise Cox survival analysis, functional impairment secondary to congestive heart failure was the only significant covariate to affect survival in the medical and surgical groups (p = 0.0001). Surgical therapy itself was not significant (p = 1.00). The incidence of sudden death during 5 years for patients with and without ventricular tachyarrhythmias during catheterization was 5% and 4%, respectively (p = 0.28).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗
PubMed1990

Torsade de pointes and T-U wave alternans associated with arsenic poisoning.

Arsenic intoxication is a common form of heavy metal poisoning. Although arsenic-induced circulatory collapse, seizures, and syncope are well known, the potential for serious ventricular arrhythmias is less well recognized. Reported in this study are two cases of arsenic poisoning causing torsade de pointes. Furthermore, marked prolongation of the QT-U interval and the rarely observed phenomenon of T-U wave alternans are demonstrated. Thus, arsenic intoxication may be complicated by prolongation of the QT-U interval and torsade de pointes. T-U wave alternans occurs in the presence of a long QT-U interval and may be an electrocardiographic warning sign of torsade de pointes.

Adult↗
PubMed1990

Paradoxical effects of exercise on the QT interval in patients with polymorphic ventricular tachycardia receiving type Ia antiarrhythmic agents.

We analyzed the results of exercise testing performed in the absence of all antiarrhythmic drugs in 11 case patients with newly documented polymorphic ventricular tachycardia in response to type Ia antiarrhythmic agents. These results were compared with those found in 11 control patients matched for age, sex, and heart disease to determine whether the response of the QT interval to exercise testing was abnormal in patients who developed worsening of arrhythmia while taking antiarrhythmic drugs. QT, RR, and QTc intervals (by Bazett's method) were evaluated at rest and at 3 minutes of exercise in both groups. At rest, there was no significant difference in the QT interval (410 +/- 13 vs. 386 +/- 11 msec), RR interval (890 +/- 56 vs. 781 +/- 43 msec), or corrected QT interval (438 +/- 10 vs. 438 +/- 4 msec) in the case patients and the control patients. Both groups demonstrated a similar chronotropic response to exercise. The QT interval shortened in both groups with exercise (p less than 0.001), but the degree of shortening tended to be greater in the control patients (to 310 +/- 9 msec) than in the case patients (to 357 +/- 11 msec) (p = 0.06). Thus, there was a paradoxical increase in the QTc interval in the patients who experienced a proarrhythmic effect of type Ia drugs but not in the control patients (to 482 +/- 8 vs. 431 +/- 5 msec; p less than 0.001). Ten of 11 case patients but only one of 11 control patients had an increase in QTc interval of more than 10 msec with exercise (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1990

Resetting of ventricular tachycardia by single extrastimuli. Relation to slow conduction within the reentrant circuit.

Although both transient entrainment and resetting with single extrastimuli have been demonstrated during sustained ventricular tachycardia related to previous myocardial infarction, the relation between these phenomena has not been defined. Because transient entrainment is only demonstrated when the mechanism of a tachycardia is reentry with an excitable gap, the resetting response to timed premature extrastimuli was studied in patients with ventricular tachycardia and correlated with the ability to demonstrate transient entrainment. The importance of the location of pacing and recording electrodes relative to regions of slow conduction within the reentry circuit for demonstrating specific characteristics of the resetting response after single extrastimuli was examined in 16 patients with 21 distinct morphologies of ventricular tachycardia related to coronary artery disease. At electrophysiological study, intracardiac electrograms were recorded simultaneously from four sites in the right ventricle and four sites in the left ventricle during ventricular tachycardia. Both resetting and transient entrainment could be demonstrated for 18 of the 21 (86%) ventricular tachycardias. The resetting response at each intracardiac recording site was defined as orthodromic or antidromic, based on the conduction time from the pacing stimulus to the recording site and the morphology of the captured (advanced) electrogram. An orthodromic resetting response was associated with demonstration of transient entrainment at 76 of 82 (93%) recording sites, implying that the pacing site was proximal and the recording site was distal to a region of slow conduction. In contrast, an antidromic resetting response was associated with transient entrainment at only six of 154 (4%) recording sites, suggesting that the pacing site was not separated from the recording site by a region of slow conduction (p = 0.001). The return cycle at the site of pacing exceeded the tachycardia cycle length in all episodes of ventricular tachycardia. At orthodromically activated recording sites, however, resetting was associated with a return cycle less than the tachycardia cycle length. Thus, orthodromic resetting demonstrates that a pause is not an integral part of the resetting response but that premature extrastimuli preexcite the reentrant circuit by entering the excitable gap, conducting through a region of slow conduction, and emerging distally without a change in activation sequence. In all episodes of ventricular tachycardia, the slope of the return cycle at the pacing site was determined by the conduction properties to the orthodromically activated sites, with increasing patterns (n = 6) produced by progressive conduction delay in the reentrant circuit at shorter coupling intervals and flat patterns (n = 3) produced by a constant orthodromic conduction interval.(ABSTRACT TRUNCATED AT 400 WORDS)

Cardiac Pacing, Artificial↗
PubMed1990

Current role of the automatic implantable cardioverter-defibrillator in the treatment of life-threatening ventricular arrhythmias.

The automatic implantable cardioverter-defibrillator (AICD) has become widely accepted as an effective treatment for patients with ventricular fibrillation or hemodynamically unstable ventricular tachycardia. The use of an antitachycardia pacemaker in combination with the AICD has also provided an effective therapy for patients with hemodynamically stable ventricular tachycardia that is refractory to antiarrhythmic drugs. The risk of sudden cardiac death following implantation of an AICD in patients with malignant ventricular tachyarrhythmias is lower than has been observed during treatment with amiodarone, direct operations for ventricular tachycardia, or conventional antiarrhythmic drug therapy guided by either noninvasive or invasive electrophysiologic testing. Although the impact of this device on the subsequent risk of sudden death is widely recognized, the effect on overall mortality is more controversial. Careful preoperative evaluation, electrophysiologic testing, and patient selection are critical for the successful use of antitachycardia devices. Clinical trials of AICDs with the capability for antitachycardia and bradycardia pacing, programmable pulse energy and waveform, and extensive memory will soon begin in the United States. Despite considerable limitations in the currently available technology, future developments in implantable antitachycardia devices offer the greatest promise for improving the outcome of patients at risk for sudden cardiac death from ventricular arrhythmias.

Anti-Arrhythmia Agents↗
PubMed1989

Rate-modulated cardiac pacing based on transthoracic impedance measurements of minute ventilation: correlation with exercise gas exchange.

The relation of pacing rate to physiologic variables of metabolic demand was examined in 10 consecutive patients with a minute ventilation-sensing, rate-modulating ventricular pacemaker implanted for complete heart block. All patients had paroxysmal (seven patients) or chronic (three patients) atrial fibrillation and were referred for catheter ablation of the atrioventricular junction. Treadmill exercise testing with measurement of expired gas exchange and respiratory flow was performed before ablation and 4 weeks after pacemaker implantation, with the pacemaker programmed to both the fixed-rate VVI and rate-modulating minute ventilation VVIR pacing modes in random sequence. The relation of pacing rate to oxygen consumption (VO2), expired carbon dioxide concentration (VCO2), respiratory quotient, tidal volume, respiratory rate and minute ventilation was determined during exercise in the rate-modulating minute ventilation pacing mode. Pacing rate was highly correlated with minute ventilation (r = 0.89), respiratory quotient (r = 0.89), VCO2 (r = 0.87), tidal volume (r = 0.87), VO2 (r = 0.84) and respiratory rate (r = 0.84). The mean exercise duration increased from 8.3 +/- 2.8 min in the fixed rate pacing mode to 10.2 +/- 3.4 min in the rate-modulating, minute ventilation mode (p = 0.0001). The maximal VO2 increased from 13.4 +/- 3.4 to 16.3 +/- 4.1 cc/kg per min (p = 0.0004). The maximal heart rate achieved in the minute ventilation pacing mode was 136 +/- 9.7 beats/min, similar to that observed in the patient's intrinsic cardiac rhythm before ablation (134.9 +/- 30.1 beats/min, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Prospective evaluation of transesophageal pacing for the interruption of atrial flutter.

PURPOSE: Although transesophageal pacing has been used successfully for the interruption of cardiac arrhythmias, the efficacy of this technique for the interruption of spontaneous atrial flutter remains poorly defined. The utility of transesophageal pacing to interrupt atrial flutter that was persistent despite standard antiarrhythmic drug therapy (mean duration: 70.3 days; range: one day to more than 365 days) was studied prospectively in 39 consecutive patients. PATIENTS AND METHODS: After written informed consent was obtained from each patient, transesophageal pacing was performed with a programmable stimulator, using the distal electrode as the cathode and the proximal electrode as the anode. All patients continued to receive a type 1 antiarrhythmic drug or amiodarone throughout the period of transesophageal pacing. The response to transesophageal pacing was classified as follows: (1) direct conversion; (2) indirect conversion; or (3) failure to interrupt atrial flutter. RESULTS: The mean stimulus amplitude and pulse duration required for atrial capture were 19.8 +/- 7.5 mA and 18.4 +/- 7.9 msec. Atrial flutter was successfully converted to sinus rhythm by transesophageal pacing in 82% of patients. In 38% of patients, atrial flutter was converted directly to sinus rhythm without another intervening arrhythmia (direct conversion). The mean pacing rate required for direct conversion was 341 +/- 27 beats/minute. In 44% of patients, the cycle length of atrial flutter was accelerated to less than 180 msec or was converted to atrial fibrillation with spontaneous conversion to sinus rhythm within 24 hours (mean 8.4 +/- 9.3 hours, indirect conversion). The mean pacing rate inducing accelerated atrial flutter or transient atrial fibrillation was 372 +/- 61 beats/minute (p = NS compared to direct conversion). Atrial flutter was not interrupted or atrial fibrillation was induced that did not spontaneously convert to sinus rhythm within 24 hours in an additional seven patients (18%). The underlying cardiac disease, age, previous drug therapy, atrial size, atrial flutter cycle length, history of prior atrial fibrillation, left ventricular function, and concomitant medical illnesses did not predict the efficacy of transesophageal pacing. CONCLUSION: The present study suggests that transesophageal pacing is highly effective for interrupting spontaneous atrial flutter that does not terminate with standard antiarrhythmic drug therapy.

Adult↗
PubMed1989

Preferential effect of procainamide on the reentrant circuit of ventricular tachycardia.

Transient entrainment was used to test the hypotheses that 1) procainamide prolongs the cycle length of ventricular tachycardia in patients with coronary artery disease because it has a preferential effect on the reentrant tachycardia circuit, and 2) regions of slow conduction in the reentrant circuit are more susceptible to the effect of procainamide than are other areas of the ventricles. In five patients with prior myocardial infarction, sustained ventricular tachycardia with identical QRS configuration was inducible before and after intravenous infusion of procainamide. Transient entrainment of ventricular tachycardia was demonstrated at two or more cycle lengths by rapid pacing in the baseline state and after procainamide. Rapid pacing was performed from the same site during sinus rhythm at the cycle lengths that demonstrated transient entrainment of ventricular tachycardia. The conduction interval to the transiently entrained site during ventricular tachycardia (orthodromic interval) was compared with the conduction interval to the same site during pacing in sinus rhythm (antidromic interval). The mean tachycardia cycle length increased by 27% after procainamide administration (p = 0.002). The antidromic conduction intervals were prolonged by 9% (p = 0.06) compared with a 28% increase in the mean orthodromic conduction interval (p = 0.002). The difference between the orthodromic and antidromic conduction intervals increased by 40% (p = 0.003). Prolongation of the tachycardia cycle length after procainamide administration correlated positively with increases in the orthodromic conduction intervals (r = 0.94, p = 0.02) but not with changes in the antidromic intervals (r = -0.08, p = NS). The effect of procainamide on the difference between correlated strongly with changes in the cycle length of ventricular tachycardia (r = 0.97, p = 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1989

Comparison of endocardial and epicardial programmed stimulation for the induction of ventricular tachycardia.

Twenty-seven patients who had pairs of stainless steel wire electrodes placed on the right and the left ventricle during cardiac surgery underwent both epicardial and endocardial programmed ventricular stimulation to assess the inducibility of ventricular tachycardia. Twenty-six of the patients had coronary artery disease and were studied to evaluate map-guided surgery for treatment of ventricular arrhythmias. Burst ventricular pacing and up to three ventricular extrastimuli coupled to two drive train cycle lengths were delivered from the right and left ventricular epicardial wire electrodes and from endocardial catheter electrodes placed at the apex and outflow tract of the right ventricle. Ventricular tachycardia was reproducibly induced in three patients by both endocardial and epicardial stimulation. In one patient ventricular tachycardia was reproducibly induced by epicardial stimulation, but nonreproducible, nonsustained ventricular tachycardia was induced by endocardial stimulation. Ventricular tachycardia remained inducible by both endocardial and epicardial stimulation in three instances (two patients) during drug therapy. A negative study (less than 10 consecutive ventricular beats induced) was obtained in 23 patients by both endocardial and epicardial stimulation. The patients were followed up for 12 to 43 months (average 31). Sudden death or documented ventricular tachycardia occurred in two of the three patients with a positive study by both endocardial and epicardial stimulation. Nineteen (83%) of the 23 patients with concordantly negative studies remained free of arrhythmias. On the basis of concordant results of endocardial and epicardial stimulation (p = 0.001) these results suggest that epicardial stimulation of the right and the left ventricle is an acceptable method to assess the postoperative inducibility of ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1989

Combined automatic implantable cardioverter-defibrillator and pacemaker systems: implantation techniques and follow-up.

The automatic implantable cardioverter-defibrillator (AICD) effectively prevents death due to ventricular tachycardia or ventricular fibrillation. Some patients who need an AICD also require cardiac pacing to treat symptomatic bradycardia, bradycardia after defibrillation, or to provide a rate floor to reduce the frequency of bradycardia-related ventricular arrhythmias. Some patients also can benefit from antitachycardia pacing. A mapping technique to implant a pacemaker and AICD sensing leads is presented. For patients with a pacemaker who later need an AICD, the left ventricle is mapped with use of the AICD rate-sensing electrodes to identify a site at which the minimal pacemaker stimulus and maximal ventricular electrogram amplitudes are recorded. An external cardioverter-defibrillator that has amplifiers similar to those in the AICD is used to monitor the rate-sensing electrogram. For patients with an implanted AICD, pacemaker implantation is undertaken by mapping the right ventricle with the pacemaker lead while the AICD is in standby mode; the AICD beep monitor is then used to determine a site where pacemaker stimulus detection by the AICD does not occur. Eight patients underwent implantation of a combined AICD-pacemaker system (four ventricular antitachycardia pacemakers, three ventricular demand pacemakers and one atrial demand pacemaker). Neither inhibition of AICD arrhythmia detection nor double counting occurred. Satisfactory AICD-pacemaker function was shown in all patients postoperatively, and no pacemaker malfunction was observed. Thus, with currently available technology, a combined AICD-pacemaker system can be implanted with satisfactory function of both devices and without adverse device-device interactions.

Aged↗
PubMed1989

Active fixation atrial leads: randomized comparison of two lead designs.

Active fixation leads have reduced the incidence of lead dislodgement in patients with permanent pacemakers. However, theoretic concern that the tissue trauma associated with a myocardial screw-helix may increase the chronic pacing threshold of active compared to passive fixation leads has remained. Whether active fixation leads with a stimulating electrode that is independent of the fixation mechanism are associated with a lower chronic pacing threshold than leads utilizing a screw-helix for both fixation and stimulation is unknown. The present prospective, randomized study compared the acute and chronic atrial pacing and sensing characteristics of two unipolar active fixation leads, one utilizing a screw-helix for both fixation and electrical stimulation, the other with an active porous tip electrode and an electrically inactive helix. Patients were randomized to receive either a Medtronic 6957J lead with an electrically active myocardial screw-helix or a Cordis 329-101P lead with an inactive helix and a porous tip electrode. The baseline characteristics of the groups were comparable. At implantation, the 329-101P lead had a lower mean voltage threshold than the 6957J lead (0.61 +/- 0.16 V vs 1.05 +/- 0.34 V, P = 0.0004). There were no significant differences in atrial electrogram amplitude, slew rate, or lead impedance between the groups. At 6 weeks follow-up, there were no differences in the mean threshold voltage (1.85 +/- 0.36 vs 1.93 +/- 0.69 V), impedance (528 +/- 81 vs 530 +/- 118 ohms), or atrial electrogram amplitude (2.63 +/- 0.50 vs 2.42 +/- 0.95 mV) between the two leads. At long-term follow-up (mean 16.2 +/- 2.8 months, range 13.1-20.0 months) there were no significant differences in voltage threshold (1.65 +/- 0.61 vs 1.97 +/- 0.64 V), impedance (565.5 +/- 81.6 vs 617.7 +/- 146.7 ohms), or atrial electrogram amplitude (2.79 +/- 0.75 vs 3.10 +/- 1.53 mV). Thus, these results suggest that active fixation leads in the atrium with an electrode that is independent of the fixation mechanism do not provide chronic stimulation thresholds or electrogram amplitudes that are superior to those obtained with leads utilizing a myocardial screw-helix as both the active electrode and the fixation device.

Adult↗
PubMed1989

Entrainment of ventricular tachycardia by AV nodal reentrant tachycardia.

Endocardial recordings from a patient with both sustained ventricular tachycardia and AV nodal reentrant tachycardia are presented that demonstrate spontaneous transient entrainment of ventricular tachycardia by AV nodal reentrant tachycardia. During electrophysiological catheterization, there were repeated episodes of spontaneous conversion from a wide to a narrow QRS morphology following the induction of ventricular tachycardia. With conversion from the wide to the narrow QRS, the ventricular deflection in the coronary sinus electrograms demonstrated an abrupt change in morphology, indicating a change in activation sequence at this site from the wavefront of depolarization emerging from the ventricular tachycardia circuit to a wavefront conducting over the His-Purkinje system. However, the right ventricular apex electrogram demonstrated a constant morphology with a decrease in cycle length equal to that of the other intracardiac electrograms, indicating a constant direction of activation from the ventricular tachycardia circuit, and that ventricular tachycardia had been transiently entrained by AV nodal reentrant tachycardia. In addition, rapid atrial pacing during ventricular tachycardia narrowed the QRS and demonstrated transient entrainment of the right ventricular apex electrogram. Although transient entrainment of a tachycardia is evidence supporting reentry with an excitable gap as the probable mechanism, its demonstration has required the use of rapid pacing techniques. This case is a spontaneously occurring example of transient entrainment of one tachycardia circuit by another, a phenomenon that has not been previously described.

Aged↗
PubMed1989

Arrhythmias after orthotopic cardiac transplantation. Prevalence and determinants during initial hospitalization and late follow-up.

The prevalence of arrhythmias after orthotopic cardiac transplantation in the era of cyclosporine immunosuppression is unknown. Accordingly, we analyzed telemetry data from the initial hospitalization period for 33 cardiac transplant procedures and from 100 hospital readmissions in 23 long-term survivors. Prevalence of arrhythmias was analyzed in relation to immunosuppressive regimen, occurrence of acute rejection, and other clinical and hemodynamic variables. Atrial and ventricular arrhythmias were recorded in 55% and 79% of patients during initial hospitalization and in 39% and 43% of long-term survivors, respectively. Compared with cyclosporine-treated patients, atrial (24% vs. 88%, p less than 0.001) and ventricular (65% vs. 94%, p = 0.085) arrhythmias during the initial hospitalization were more prevalent in patients receiving azathioprine. There was no difference in the prevalence of arrhythmias during initial hospitalization between patients experiencing acute rejection and those who did not. Potential associations between arrhythmia occurrence and a prolonged donor heart ischemic time (p = 0.022), elevated pulmonary arterial pressure (p = 0.01), and a lower ejection fraction (p = 0.009) were noted. These data suggest that arrhythmias occur in the majority of patients during the initial hospitalization for transplantation, even in those who never experience acute rejection. Ventricular arrhythmias are common in patients treated with either immunosuppressive regimen; however, atrial arrhythmias are less prevalent in patients receiving cyclosporine. Arrhythmias tend to occur in the setting of altered hemodynamics.

Adult↗