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Biomedical subjects

K A Ellenbogen

Publications and source records attributed to K A Ellenbogen.

At least 91 records · Page 5Linked to original sources
PubMed1995

Late occurrence of incessant atrial tachycardia following the maze procedure.

We report a patient with incessant atrial tachycardia and AV nodal reentrant tachycardia tachycardia and AV nodal reentrant tachycardia beginning almost 18 months following a successful maze procedure. Both tachycardias were cured by radiofrequency ablation. We speculate that the right atrial tachycardia may have been related to the maze procedure. Finally, we believe this report should emphasize the importance of careful and long-term follow-up of all patients undergoing the maze procedure. Proper evaluation of the place of this therapy greatly depends on reporting of all short- and long-term complications of this new procedure.

Aged↗
PubMed1995

Baseline arterial pressure affects sympathoexcitatory responses to ventricular premature beats.

The seconds to minutes before sudden cardiac death are characterized by fluctuations of arterial pressure, cardiac rhythm, and probably sympathetic nerve activity. We explored the interrelations among these factors in seven patients undergoing clinical electrophysiological testing. We measured muscle sympathetic nerve activity (SNA) and arterial pressure responses to ventricular premature beats induced throughout the cardiac cycle under three conditions: 1) lowered arterial pressure and elevated SNA produced by intravenous nitroprusside, 2) baseline arterial pressure and SNA during saline infusion, and 3) elevated arterial pressure and decreased SNA activity produced by intravenous phenylephrine. Sympathetic responses to premature beats were inversely related to diastolic pressure. The magnitude of the sympathetic response was directly related to the prevailing arterial pressure and inversely related to baseline SNA. These data demonstrate that sympathoexcitation evoked by ventricular dysrhythmias is determined importantly by the prevailing arterial pressure and possibly by the background R-R interval and level of sympathetic activity. This effect may influence hemodynamic and electrophysiological stability during dysrhythmias.

Adult↗
PubMed1994

Lessons learned from data logging in a multicenter clinical trial using a late-generation implantable cardioverter-defibrillator. The Guardian ATP 4210 Multicenter Investigators Group.

OBJECTIVES: This study examined patterns of implantable cardioverter-defibrillator use as documented by data logging. BACKGROUND: Implantable cardioverter-defibrillators are accepted therapy for malignant ventricular tachyarrhythmias; however, relatively little is known about their patterns of use. Incorporation of data-storage capacities into these devices provides insight into long-term defibrillator function. METHODS: Stored data-logging information was retrieved from 401 implanted cardioverter-defibrillators in 393 patients over an average of 303 days of follow-up. RESULTS: A total of 91,443 detections were recorded in 299 patients. One hundred-six patients (26%) had detections due to supraventricular tachycardias, electrical noise or other causes, resulting in inappropriate therapy delivery to 92 patients (23%). Two hundred eighty-one patients recorded 66,276 episodes of ventricular tachycardia or ventricular fibrillation. Of these, 74.4% episodes terminated spontaneously without any delivered therapy, 22.1% terminated after antitachycardia pacing, and 1.7% terminated after shock therapy. Antitachycardia pacing was activated without formal testing in 47% of all patients receiving this therapy and was successful in 96% of all episodes receiving this therapy. Acceleration of tachycardia to shock therapy occurred in 1.3% of all episodes and in 30.5% of patients receiving antitachycardia pacing. Thirty-four patients (8.7%) died during follow-up. Mortality was associated with patient age, heart failure functional class at implantation and frequency of shocks received during follow-up (all p < or = 0.05). CONCLUSIONS: Most ventricular tachyarrhythmia detections by this noncommitted implantable cardioverter-defibrillator resolve spontaneously, whereas the majority receiving therapy can be treated with antitachycardia pacing. Mortality after implantable cardioverter-defibrillator implantation is associated with age, heart failure class and frequency of shocks received during follow-up. Data-logging capabilities provide valuable insights into the patterns of defibrillator use.

Algorithms↗
PubMed1994

Sensing/pacing lead complications with a newer generation implantable cardioverter-defibrillator: worldwide experience from the Guardian ATP 4210 clinical trial.

OBJECTIVES: This report describes the sensing/pacing lead complications that developed during a worldwide clinical trial of a new implantable cardioverter-defibrillator. BACKGROUND: The reliability of the leads used for sensing and pacing with the implantable cardioverter-defibrillator has not been adequately studied. METHODS: The Guardian ATP 4210 was implanted in 302 patients. The sensing/pacing leads consisted of either two unipolar epicardial electrodes or a bipolar endocardial electrode from a variety of manufacturers. RESULTS: During a mean follow-up period of 380 days, 39 patients (12.9%) required reoperation because their device developed sensing/pacing lead system complications. The most common clinical presentation was device oversensing (multiple tachycardia or noise detections or inappropriate shocks), which was observed in 27 patients, whereas elevated pacing thresholds were seen in 10 patients. Forty-one (11.8%) of 347 implanted lead systems required revision. The mean time to revision was 156 +/- 145 days. Actuarial lead survival rate at 1 and 3 years was 89% and 79%, respectively. Epicardial lead systems required significantly (p < 0.05) more revision than did endocardial systems, but when adapter problems were excluded, the revision rates of epicardial and endocardial leads were similar. Causes of lead system failures included adapter connection problems, lead dislodgement and insulation disruption. Predictors of lead revision were use of an epicardial lead system or an adapter. CONCLUSIONS: A high rate of sensing/pacing lead complications was found with this newer generation implantable cardioverter-defibrillator. The enhanced diagnostic and data storage capabilities of this implantable cardioverter-defibrillator facilitated the recognition and troubleshooting of these complications. These findings emphasize the need for careful surveillance and testing of implantable cardioverter-defibrillator sensing/pacing leads during follow-up.

Aged↗
PubMed1994

Safety of pacemaker implantation in patients with transvenous (nonthoracotomy) implantable cardioverter defibrillators.

While several reports have documented the safety of implantation of transvenous pacemakers in patients with epicardial patch-based implantable cardioverter defibrillators (ICDs), the implantation of transvenous pacemakers in patients with transvenous (nonthoracotomy) ICDs has not been well-described. We present three patients with transvenous ICDs who subsequently underwent implantation of transvenous pacemakers without complication. Technical considerations and a testing, protocol for detection of pacemaker-ICD interactions are discussed.

Aged↗
PubMed1993

Doppler echocardiographic assessment of an impedance-based dual-chamber rate-responsive pacemaker.

Rate-responsive pacing allows patients with chronotropic incompetence to achieve more physiologic heart rate responses to exercise. One sensor currently being investigated uses impedance-derived measurements of changes in right ventricular stroke volume to alter the pacing rate. Correlation of pacemaker-derived measurements of stroke volume with an accepted method of stroke volume measurement has not been performed. The relative changes in impedance-derived stroke volume were compared in 10 patients with an impedance-based dual-chamber rate-responsive pacemaker (Precept DR, Cardiac Pacemakers, Inc.) with simultaneous Doppler echocardiographic measurements of right and left ventricular stroke volume. These comparisons were made during pacing at 2 heart rates (70 and 100 beats/min) and 3 AV intervals (150, 200 and 250 ms) while in a supine resting state, during lower body negative pressure to -30 mm Hg, and while performing 25% maximal handgrip. Pacemaker-derived stroke volume decreased by 7 to 11% and Doppler time-velocity integral measurements decreased by 14 to 19% in response to an increase in pacing rate (p = NS). There was also no significant difference by either technique in the mean stroke volume change when the atrioventricular interval was varied. Both techniques detected a decrease in stroke volume during lower body negative pressure, ranging from -7 to -20% by pacemaker, and -17 to -38% by Doppler. Overall, the pacemaker stroke volume measurements responded in an appropriate direction to each intervention, signaling the pacemaker's ability to detect directional change in stroke volume. The Precept DR may aid in the programming of parameters such as atrioventricular interval and heart rate by allowing for optimization of stroke volume in individual patients.

Adult↗
PubMed1993

Radiofrequency catheter ablation of sinus node reentrant tachycardia.

Sinus node reentrant tachycardia is a relatively uncommon (5%-15%) form of recurrent paroxysmal supraventricular tachycardia (SVT). We describe a case of symptomatic sinus node reentrant tachycardia in a 67-year-old male with ischemic heart disease, congestive heart failure, and depressed ventricular function. Adenosine administered during an electrophysiology study caused prolongation of the tachycardia cycle length due to atrial cycle length prolongation (without atrio-His prolongation) prior to tachycardia termination. Right atrial mapping revealed the earliest site of atrial activation in the high lateral right atrium just below the superior vena cava. Low energy (10 and 20 W) radiofrequency lesions were applied at this site with termination of the tachycardia within 3 seconds of radiofrequency energy delivery. Tachycardia could not be reinduced after delivery of the radiofrequency lesions. The sinus node function immediately and 6 weeks after radiofrequency catheter ablation remained normal and the patient was without clinical recurrence of SVT. Mapping of sinus node reentrant tachycardia and elimination of the reentrant circuit with radiofrequency catheter ablation is possible without causing sinus node dysfunction. Adenosine causes prolongation of the atrial cycle length followed by termination of sinus node reentrant tachycardia.

Adenosine↗
PubMed1993

Can amiodarone pulmonary toxicity be predicted in patients undergoing implantable cardioverter defibrillator implantation?

Implantable cardioverter defibrillator (ICD) implantation is rapidly becoming accepted as primary therapy for malignant ventricular arrhythmias. Many patients undergoing ICD implantation are on concomitant antiarrhythmic drugs to decrease shock frequency, slow tachycardia rate, and suppress supraventricular arrhythmias. Amiodarone is a potent antiarrhythmic agent that is also frequently used in the treatment of patients with refractory ventricular arrhythmias. Ten to forty percent of patients undergoing ICD implantation will also be taking amiodarone. It has been reported to cause pulmonary toxicity in about 5% of patients per year. Acute amiodarone toxicity presenting as adult respiratory distress syndrome has been reported much less frequently. Although perioperative morbidity due to amiodarone has been described, the risk, predictability, and consequences of acute pulmonary toxicity from amiodarone in patients undergoing ICD implantation have not been previously described. We reviewed the records of 99 consecutive patients undergoing ICD implantation at our institution from October 1987 to April 1992. Thirty-nine patients were taking 480 +/- 230 mg of amiodarone (median 400 mg, lower 20th percentile 400 mg, upper 80th percentile 800 mg) for 291 +/- 554 days prior to ICD implantation. Ten patients taking amiodarone developed acute pulmonary toxicity clinically manifesting as diffuse pulmonary infiltrates on chest radiography and adult respiratory distress syndrome with hypoxia (arterial pO2 < 60 mmHg) without evidence of pneumonia or elevated pulmonary capillary wedge pressure (PCW < or = 15 mmHg). Of the 60 patients not taking amiodarone none developed adult respiratory distress syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Measurement of ventricular electrogram amplitude during intraoperative induction of ventricular tachyarrhythmias.

Adequate sensing of ventricular tachycardia (VT) and ventricular fibrillation (VF) is necessary for proper functioning of an implantable cardioverter defibrillator (ICD). Several ICDs currently undergoing investigation have programmable fixed gain sensitivity for tachycardia detection. If intracardiac electrogram amplitude decreases below the programmed sensitivity during VT or VF, detection of a ventricular arrhythmia may be delayed or missed. The mean amplitude of intracardiac electrograms (ICEGM) recorded with bipolar epicardial or transvenous sensing leads was measured in 63 patients during induced VT and VF recorded in the operating room at the time of ICD implantation. The mean amplitude of the ICEGM during 41 episodes of VF in 15 patients decreased from 14.9 +/- 0.9 mV during sinus rhythm to 8.8 +/- 0.7 mV at 1 second, 9.7 +/- 0.7 mV at 5 seconds, and 9.4 +/- 0.7 mV at 10 seconds (p < 0.0001 vs sinus rhythm ICEGM) with endocardial leads. The mean amplitude of the ICEGM recorded during 173 episodes of VF in 43 patients with epicardial leads decreased from 10.4 +/- 0.3 mV in sinus rhythm to 7.8 +/- 0.3 mV at 1 second, 8.3 +/- 0.3 mV at 5 seconds and 8 mV at 10 seconds (p <0.0001 vs sinus rhythm ICEGM). The mean amplitude of epicardial and transvenous ICEGMs recorded during 34 episodes of monomorphic VT decreased from 18.5 +/- 1.8 mV (epicardial) and 14.4 +/- 2.0 mV (transvenous) during sinus rhythm (p = 0.15, epicardial vs transvenous) to 16.0 +/- 1.7 mV (epicardial) and 13.7 +/- 1.9 mV (transvenous) at 10 seconds (< 10% of baseline amplitude).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1992

Role of calcium antagonists for heart rate control in atrial fibrillation.

Atrial fibrillation is one of the most common symptomatic sustained arrhythmias seen in clinical practice. Many patients with atrial fibrillation and a ventricular response greater than 120 beats/min will experience cardiac symptoms. In the past, control of heart rate in these patients consisted of administration of intravenous digoxin, but this often proved to be ineffective or limited by toxicity. Recently, intravenous beta blockers such as esmolol have been used to slow the ventricular rate during atrial arrhythmias, but in some studies their use has been limited by hypotension. Alternatively, a bolus of an intravenous calcium antagonist, e.g., diltiazem or verapamil, may be administered to achieve acute slowing of the ventricular response. An intravenous bolus of diltiazem or verapamil may be effective, but use of either may be limited by its short duration of action and the inability to administer repeated boluses to tightly control or "fine tune" the heart rate. However, a new bolus plus maintenance infusion technique with diltiazem has shown promise in initial studies. It appears that in the future, continuous infusion techniques with intravenous calcium antagonists will be available that provide safe and effective sustained control of the ventricular response during atrial arrhythmias.

Atrial Fibrillation↗
PubMed1992

Sympathoinhibition and hypotension in carotid sinus hypersensitivity.

Carotid sinus reflex hypersensitivity is a known cause of syncope in humans. The condition is characterized by cardioinhibition and vasodepression, each to varying degrees. The extent and importance of sympathoinhibition has not been determined in patients with carotid sinus hypersensitivity. This study reports on the extent of sympathoinhibition measured directly directly during carotid massage with and without atrioventricular sequential pacing, in a patient with symptomatic carotid sinus reflex hypersensitivity. Carotid massage elicited asystole, hypotension and complete inhibition of muscle sympathetic nerve activity. Carotid massage during atrioventricular pacing produced similar sympathoinhibition, but with minimal hypotension. Therefore, sympathoinhibition did not contribute importantly to the hypotension during carotid massage in the supine position in this patient. Further investigations are required to elucidate the relation of sympathoinhibition to hypotension in patients with carotid sinus hypersensitivity in the upright position.

Carotid Sinus↗
PubMed1992

Influence of lidocaine on human muscle sympathetic nerve activity during programmed electrical stimulation and ventricular tachycardia.

Lidocaine directly affects conduction and refractoriness of ventricular myocardium, and may also indirectly affect these electrophysiologic properties by inhibition of cardiac sympathetic nerve traffic. Both effects may play important roles in preventing ventricular arrhythmias in humans. To determine if lidocaine has a direct effect on sympathetic nerve activity, the effects of a 100 mg lidocaine bolus followed by a 2 mg/min infusion of lidocaine on muscle sympathetic nerve activity was assessed in seven patients during programmed ventricular stimulation with single extrastimuli (premature ventricular contractions [PVCs]) in sinus rhythm, and in seven patients during induced hemodynamically stable monomorphic ventricular tachycardia. During single extrastimuli, the mean (+/- SEM) area of PVC-associated bursts of sympathetic nerve activity was unaffected by lidocaine (1101 +/- 16 units pre-lidocaine versus 1075 +/- 19 units following lidocaine; p = 0.30). Likewise, the transient decrease in blood pressure with induced PVCs was similar before and after lidocaine infusion (p = 0.46). In seven patients with induced monomorphic ventricular tachycardia, tachycardia cycle length did not change after the lidocaine bolus (393 +/- 18 versus 399 +/- 17 msec; p = 0.34) but increased during lidocaine maintenance infusion (428 +/- 17 msec; p = 0.01). After induction of ventricular tachycardia, systolic pressure decreased from 150 +/- 6 to 117 +/- 9 mm Hg at 1 minute of tachycardia, to 109 +/- 6 mm Hg during the lidocaine bolus, and rebounded to 126 +/- 8 mm Hg during the lidocaine maintenance infusion (p = 0.04, bolus versus infusion).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗