PubMed Health⌕ Search

Biomedical subjects

K A Ellenbogen

Publications and source records attributed to K A Ellenbogen.

At least 109 records · Page 6Linked to original sources

Implantation of cardioverter defibrillators in the post-sternotomy patient.

In an attempt to minimize the hazards of redo sternotomy or thoracotomy in patients who have undergone previous cardiac procedures, a technique has been developed for cardioverter defibrillator implantation that involves dissection through a left subcostal incision and placement of extrapericardial defibrillation patches. This approach was used in 22 consecutive patients who required an implantable cardioverter defibrillator 4 to 156 months after previous median sternotomy. Defibrillation threshold energy was less than or equal to 20 J in every patient. Ninety-one percent of patients were extubated during the first 24 hours and were transferred out of the intensive care unit by the second postoperative day. One patient died of an acute myocardial infarction 3 days postoperatively (1/22, 4.5%). It was necessary to replace one lead for mechanical failure of an adapter, one patch required repositioning, and 1 patient needed drainage of a persistent pleural effusion (3/22, 13.6%). No further complications occurred during 3 to 27 months of follow-up. Advantages of the subcostal approach included prompt extubation, a single incision, and minimal morbidity. This approach is safe and effective, and is the method of choice for implantation of a cardioverter defibrillator in patients who have undergone prior sternotomy.

Adult↗

Differentiation between monomorphic ventricular tachycardia and sinus tachycardia based on the right ventricular evoked potential.

The differentiation between ventricular tachycardia (VT) and sinus tachycardia (ST) is problematic in some patients with implantable defibrillators and/or antitachycardia pacemakers. The integral of the ventricular endocardial evoked response, or paced depolarization integral (PDI), has been demonstrated to undergo characteristic changes with a variety of stimuli including catecholamines, pacing rate, and exercise. We hypothesized that the PDI recorded from a unipolar transvenous right ventricular endocardial catheter would differentiate VT from ST. The PDI was calculated from a unipolar pacing stimulus, delivered via a cathode in the right ventricular apex, and the reference electrode, a quadripolar catheter positioned in the superior vena cava. PDIs were measured in 22 patients during VT and sinus rhythm. The PDI measured during sinus rhythm was 579 +/- 240 microV-sec and the PDI during VT was 894 +/- 411 microV-sec (P < 0.001). In a subset of seven patients, PDIs were measured during VT, sinus rhythm, and ST induced by catecholamine infusion or exercise. In this subset, the PDI during sinus rhythm was 645 +/- 295 microV-sec, during ST 588 +/- 308 microV-sec (9% decrease from sinus, P = 0.05), and during VT 863 +/- 342 microV-sec (33.9% increase, P = 0.01). These data indicate that the measurement of the PDI is potentially useful in differentiating VT from ST.

Algorithms↗

Short-term reproducibility over time of right ventricular pulse pressure as a potential hemodynamic sensor for ventricular tachyarrhythmias.

The implantable cardioverter defibrillator (ICD) has been shown to effectively terminate episodes of ventricular tachyarrhythmias. Multiple investigators have suggested that the incorporation of hemodynamic sensors may allow ICDs to differentiate between hemodynamically unstable and stable ventricular tachyarrhythmias (VT), as well as differentiate ventricular from supraventricular tachycardias. Right ventricular (RV) pulse pressure has been shown to possess acceptable characteristics as a sensor for incorporation in ICDs. We sought to determine the short-term reproducibility of RV pulse pressure measurements by comparing RV pulse pressure measured during two separate episodes of VT in each of ten study patients. The mean VT cycle length for VT episode 1 was 293 +/- 15 msec, and was 298 +/- 15 msec for VT episode 2 (P = NS). The decrease in mean arterial pressure was 40 +/- 7 mmHg in episode 1 and 37 +/- 7 mmHg in episode 2 (P = NS). The decrease in RV pulse pressure during episode 1 was -13 +/- 2 mmHg, and -12 +/- 2 during episode 2 (P = NS). The decrease in RV pulse pressure during episodes of VT at two different times during a single electrophysiology study is highly reproducible, suggesting that RV pulse pressure may be a reliable sensor over time.

Aged↗

Sudden death in patients with congestive heart failure: future directions.

Sudden, unexpected cardiac death continues to be a major clinical problem in patients with congestive heat failure. This review summarizes the current state of knowledge regarding the identification and management of these patients. The roles of ambulatory ECG monitoring, electrophysiological testing, signal-averaged ECG, and other methods of predicting increased risk of sudden death are discussed. The modes of sudden cardiac death and the potential mechanisms of ventricular arrhythmias in congestive heart failure are reviewed. Current therapeutic options including antiarrhythmic drugs, neurohormonal blockade, and automatic implantable cardioverter defibrillators are discussed. Finally, future directions and ongoing clinical investigations of the management of these complex patients are considered.

Arrhythmias, Cardiac↗

Failure of a second and third generation implantable cardioverter defibrillator to sense ventricular tachycardia: implications for fixed-gain sensing devices.

Failure to sense ventricular tachycardia and/or ventricular fibrillation by implantable cardioverter defibrillators (ICDs) is rare. We report a case in which persistent undersensing of monomorphic and polymorphic ventricular tachycardia occurred with a second and third generation ICD using fixed-gain sensing. This occurred despite adequate R wave sensing during sinus rhythm. The use of an endocardial sensing lead did not correct the problem. Failure to sense ventricular tachycardia in the third generation device with fixed-gain sensing occurred late after implantation and was discovered only at follow-up electrophysiology testing of the ICD. This problem could not be corrected by reprogramming of the device, and was not related to lead dislodgement. Placement of a new device with an automatic-gain sensing algorithm and use of previously implanted epicardial leads with better sensing characteristics provided appropriate sensing of ventricular tachyarrhythmias. The case illustrates the importance of testing the sensing of all ventricular arrhythmias in patients with fixed-gain ICD's. Follow-up electrophysiology testing and evaluation of epicardial and endocardial leads may be necessary in certain cases to ensure adequate sensing of ventricular tachyarrhythmias late after implantation.

Algorithms↗

Clinical characteristics and outcome of patients with high defibrillation thresholds. A multicenter study.

BACKGROUND: Successful defibrillation by an implantable cardioverter-defibrillator (ICD) depends on its ability to deliver shocks that exceed the defibrillation threshold. This study was designed to identify clinical characteristics that may predict the finding of an elevated defibrillation threshold and to describe the outcome of patients with high defibrillation thresholds. METHODS AND RESULTS: The records of 1,946 patients from 12 centers were screened to identify 90 patients (4.6%) with a defibrillation threshold greater than or equal to 25 J. Excluding three patients who received ICDs that delivered greater than 30 J, there were 81 men and six women with a mean age of 59.5 +/- 10.1 years, a mean left ventricular ejection fraction of 0.32 +/- 0.14, and a 76% prevalence of coronary artery disease. Sixty-one patients (70%) were receiving antiarrhythmic drugs, and 45 (52%) were receiving amiodarone. Seventy-one patients (82%) received an ICD. Death occurred in 27 patients--19 of the 71 (27%) with an ICD (eight arrhythmic), and eight of the 16 (50%) without an ICD (four arrhythmic). Actuarial survival for all patients at 5 years was 67%. Actuarial survival rates at 2 years for patients with and without an ICD were 81% and 36%, respectively (p = 0.0024). Actuarial survival at 5 years for the ICD patients was 73%; no patient without an ICD has lived longer than 32 months. Actuarial survival free of arrhythmic death in the ICD patients at 5 years was 84%. Although the only variable to predict survival was ICD implantation (p = 0.003), it is entirely possible that in this retrospective analysis, clinical selection decisions to implant or to not implant an ICD differentiated patients destined to have better or worse outcomes, respectively. CONCLUSIONS: Antiarrhythmic drug use may be causally related to the finding of an elevated defibrillation threshold. When patients with high defibrillation thresholds receive an ICD, arrhythmic death remains an important risk (42% of deaths in these patients were arrhythmia related, with 16% actuarial incidence at 5 years). Vigorous testing to optimize patch location can potentially benefit patients by enhancing the margin of safety for effective defibrillation.

Adult↗

Pharmacokinetics and pharmacodynamics of intravenous diltiazem in patients with atrial fibrillation or atrial flutter.

BACKGROUND: Diltiazem, a calcium channel blocker, has been shown to be safe and effective in the treatment of patients in atrial fibrillation and/or atrial flutter. However, there have been no pharmacokinetic/pharmacodynamic studies of diltiazem in these patients. METHODS AND RESULTS: The pharmacokinetics and pharmacodynamics of intravenous diltiazem were determined in 32 patients with atrial fibrillation or atrial flutter (mean +/- SD age, 66 +/- 7 years; mean baseline heart rate, 131 +/- 10 beats per minute) after 20 mg or 20 mg followed by 25-mg bolus doses and a 10 and 15 mg/hr infusion for 24 hours. After the 10 and 15 mg/hr infusions of diltiazem, mean +/- SD elimination half-life was 6.8 +/- 1.8 and 6.9 +/- 1.5 hours, volume of distribution was 411 +/- 151.8 and 299 +/- 70.8 I, and systemic clearance was 42 +/- 12.4 and 31 +/- 8.3 l/hr, respectively. Percentages of the plasma concentrations of the principal metabolites desacetyldiltiazem and N-desmethyldiltiazem to diltiazem were < 15% and < 10%, respectively. Thirty of 32 patients maintained response throughout the 24-hour infusion of diltiazem. Using a sigmoidal Emax pharmacodynamic model, a strong relation (mean +/- SD r2, 0.78 +/- 0.2) was observed between plasma diltiazem concentration and percent heart rate reduction. Mean +/- SD Emax (maximum percent reduction in heart rate from baseline) and EC50 (plasma diltiazem concentration that achieves half Emax) were 52 +/- 17% and 110 +/- 84 ng/ml, respectively. The model predicts that mean plasma diltiazem concentration of 79, 172, and 294 ng/ml are required to produce a 20%, 30%, and 40% reduction in heart rate, respectively. A relation between plasma diltiazem concentration and percent change in systolic blood pressure (SBP) or diastolic blood pressure (DBP) from baseline was not observed (mean +/- SD r2, SBP/DBP: 0.35 +/- 0.24/0.36 +/- 0.2). There were no untoward side effects observed. CONCLUSIONS: First, the pharmacokinetics of diltiazem in patients with atrial fibrillation or atrial flutter is nonlinear with an apparent dose-dependent decrease in systemic clearance with increasing infusion rate. Second, using a sigmoidal Emax model, there is a strong relation between plasma diltiazem concentration and percent heart rate reduction. Third, the plasma concentrations of the principal metabolites desacetyldiltiazem and N-desmethyldiltiazem are low and are not expected to contribute significantly to the pharmacodynamics of intravenous diltiazem in these patients.

Aged↗

Effects of cardiac denervation on atrioventricular nodal accommodation and hysteresis.

Conduction through the atrioventricular (AV) node is significantly altered by changes in autonomic tone. AV nodal accommodation (time-dependent changes in AV nodal conduction after a sudden change in atrial cycle length) and AV nodal hysteresis (asymmetry of AV nodal accommodation after directionally opposite atrial pacing cycle length changes) have been characterized in humans. Studies in dogs after cardiac transplantation suggest that the rapid phase of AV nodal accommodation is altered following ablation of neural input to the AV node. To determine if cardiac denervation alters AV nodal accommodation and hysteresis in humans, 13 patients after orthotopic cardiac transplantation and 12 control patients with normal AV nodal function were studied. Atrial pacing was performed for 1 minute at different pacing cycle lengths and AH or AV intervals were measured after cycle length changes. The rapid phase of accommodation is defined as the time required for the AV interval to reach 75% of the final AV interval. During abrupt changes from long to short pacing cycle lengths, the rapid phase of accommodation took 3.2 +/- 1.0 and 4.3 +/- 1.0 beats in control subjects and transplant patients, respectively (p = not significant [NS]). When going from short to long pacing cycle lengths, the rapid phase of accommodation took 1.7 +/- 1.2 and 2.1 +/- 1.8 beats in control subjects and transplant patients, respectively (p = NS). Hysteresis of 1.5 +/- 1.3 and 2.1 +/- 1.4 beats was noted in the control and transplant groups, respectively (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

A placebo-controlled trial of continuous intravenous diltiazem infusion for 24-hour heart rate control during atrial fibrillation and atrial flutter: a multicenter study.

The safety and efficacy of a 10- to 15-mg/h continuous infusion of intravenous diltiazem were evaluated in 47 patients with atrial fibrillation or flutter who first responded to 20 mg or 20 mg followed by one or more 25-mg bolus doses of open label intravenous diltiazem. Of the 47 patients, 44 responded to the bolus injection and were randomized under double-blind conditions to receive either a continuous infusion of intravenous diltiazem (10 to 15 mg/h) (23 patients) or placebo (21 patients) for up to 24 h. Seventeen (74%) of the 23 patients receiving diltiazem infusion and none of the 21 with placebo infusion maintained a therapeutic response for 24 h (p less than 0.001). Over 24 h, patients receiving diltiazem infusion lost response significantly more slowly than did those receiving placebo infusion (p less than 0.001). Nonresponders to the double-blind infusion were given an additional bolus injection of open label intravenous diltiazem and administered an open label 24-h intravenous diltiazem infusion. The overall proportion of patients maintaining a response to a 24-h infusion of intravenous diltiazem under double-blind or open label conditions combined was 83% (34 of 41). Efficacy of the 24-h infusion of intravenous diltiazem was similar in elderly versus young patients, those who did versus those who did not receive digoxin and those weighing less than 84 versus greater than or equal to 84 kg. However, intravenous diltiazem appeared to be more effective in atrial fibrillation than in atrial flutter. No significant untoward effects were noted.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Sympathetic neural responses to induced ventricular tachycardia.

Although sympathetic mechanisms play a major role in buffering abrupt arterial pressure reductions, including those that occur during tachyarrhythmias, human sympathetic nervous system responses to ventricular tachycardia have not been measured. Muscle sympathetic nerve activity was recorded directly from the peroneal nerve in 16 patients during diagnostic induction of 19 episodes of sustained monomorphic ventricular tachycardia (average rate 189 beats/min, range 130 to 250). Average systolic and diastolic pressures decreased from 149/78 to 61/49 mm Hg by 10 s and increased toward baseline levels to 88/64 mm Hg by 1 min of ventricular tachycardia. Average sympathetic nerve activity increased by 92% at 10 s in direct proportion to arterial pressure reductions and in inverse proportion to ventricular rate and remained 83% above baseline levels at 1 min. The late recovery of arterial pressure during ventricular tachycardia was related significantly to the magnitude of early sympathetic responses. Sympathetic activity tended to lose its discrete bursting pattern during ventricular tachycardia, and power spectral analysis showed that the large sympathetic peaks at the heart rate frequency present during sinus rhythm are absent during ventricular tachycardia. This study is the first to delineate human sympathetic nervous system responses to ventricular tachycardia. The results suggest that in the patients studied, large early sympathetic surges differed from those that occur during sinus rhythm and contributed to hemodynamic stability during ventricular tachycardia.

Aged↗

A prospective study of changes in right ventricular dP/dt during ventricular tachycardia.

The automatic implantable cardioverter defibrillator (AICD) has significantly decreased mortality in high risk ventricular tachycardia (VT) patients. The AICD provides treatment based on ventricular rate, sometimes leading to high energy shocks in conscious patients with stable VT, or patients with sinus or supraventricular tachycardia. Other physiological parameters, such as maximal positive and negative systolic right ventricular (RV) dP/dt (RV + dP/dtmax, RV - dP/dtmax, respectively), may be included in detection algorithms for future implantable defibrillators. We studied frequency band limited positive and negative RV dP/dtmax before, during, and after 13 episodes of VT lasting at least 40 beats in duration in nine male patients. The mean (+/- SEM) RV + dP/dtmax, dropped by 120 +/- 28 mmHg/sec (P less than 0.001) during the first five beats of VT. RV + dP/dtmax then slowly rose toward baseline levels until a significant overshoot occurred during the first ten beats following VT termination (delta = 234 +/- 58 mmHg/second, P less than 0.002). RV + dP/dtmax correlated poorly with mean arterial pressure (r = 0.32, P greater than 0.1), systolic blood pressure (r = 0.19, P greater than 0.1), and VT cycle length (r = 0.34, P greater than 0.1). Conversely, RV - dP/dtmax rose during the first ten beats of VT (74 +/- 27 mmHg/sec, P greater than 0.05) and then slowly drifted back toward baseline levels. Like RV + dP/dtmax, RV - dP/dtmax overshot baseline levels during the recovery phase (-108 +/- 48 mmHg/sec, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗

Utility of adenosine administration during intraoperative mapping in a patient with the Wolff-Parkinson-White syndrome.

Adenosine is an endogenous nucleoside that is administered intravenously and has potent chronotropic and dromotropic effects. This drug is distinguished from verapamil by its very short half-life. This makes it an ideal agent for use in the operating room where long lasting electrophysiological effects may not be desirable. A 61-year-old man with preexcited atrial fibrillation was referred for surgical ablation of his accessory pathway. Preexcitation was minimal or absent on arrival in the operating room. Intravenous adenosine was given causing AV nodal block, and resulted in marked preexcitation, thus allowing computerized mapping to localize the site of the accessory pathway. Adenosine may be a useful agent for rapid and precise localization of accessory pathway(s) in a select group of patients with minimal preexcitation at the time of surgery. Its short half-life allows additional mapping without sustained electrophysiological effects on the AV node, or accessory pathway.

Adenosine↗

Subnormal parasympathetic activity after cardiac transplantation.

Heart period variability (standard deviation of 120 consecutive RR or PP intervals) was used to assess baseline parasympathetic activity in 18 patients with congestive heart failure before and after orthotopic cardiac transplantation, and was compared to that of 16 age-matched control subjects. Mean heart period variability (+/- standard error of the mean) was significantly greater (p less than 0.05) in control subjects (58 +/- 5 ms) than in the patients at any time before or after transplantation. Heart period variability of innervated recipient atria did not change significantly early (1 to 4 weeks) after transplantation (16 +/- 2 to 24 +/- 5 ms; p = 0.11), but increased significantly between weeks 15 and 37 after transplantation (30 +/- 5 ms, p less than 0.002 versus before transplantation). A stepwise regression model (R2 = 0.35; p = 0.01) showed that heart period variability was directly related to time after transplantation and inversely related to systolic arterial pressure after transplantation and degree of rejection. Heart period variability of the denervated donor atria did not change from early to late periods after transplantation, suggesting that vagal reinnervation of the donor heart had not occurred. These data indicate that baseline parasympathetic activity does not increase significantly during the first month after transplantation but increases significantly between months 3 and 6.

Atrial Function↗

Arrhythmias in patients with CHF. Should they be treated?

Ventricular arrhythmias are a major cause of death in patients with congestive heart failure. Dr Ellenbogen and his associates discuss the current thinking, based on recent studies, concerning use of antiarrhythmic agents to prevent sudden cardiac death in these patients. As they point out, the proper antiarrhythmic therapy may be crucial to long-term survival.

Adult↗

Comparison of right ventricular impedance, pulse pressure and maximal dP/dt for determination of hemodynamic stability of ventricular arrhythmias associated with coronary artery disease.

By monitoring hemodynamic parameters, a future generation of automatic implantable defibrillators will provide tiered therapy of ventricular arrhythmias according to the associated hemodynamic compromise. Changes in intracardiac impedance permit beat-to-beat assessment of ventricular volumes and make this parameter attractive as a rapid discriminator of hemodynamic compromise during arrhythmias. Beat-to-beat changes in right ventricular (RV) impedance were measured before, during and after 27 episodes of ventricular tachyarrhythmias induced in 17 men (64 +/- 7 years, mean +/- standard deviation; left ventricular ejection fraction 41 +/- 11%). Impedance was measured using a tripolar lead system and was compared to ventricular tachycardia cycle length, RV pulse pressure and maximum systolic RV dP/dt as indicators of systemic hemodynamic compromise. The average decreases in systolic blood pressure and mean arterial pressure during ventricular tachycardia were 48 +/- 23% and 46 +/- 26%, respectively (mean +/- standard deviation; p less than 0.001 for each). Right ventricular impedance decreased an average 39 +/- 22% from its baseline value (p less than 0.001) during ventricular tachycardia. The percent change in impedance from baseline during ventricular tachycardia correlated significantly with the percent decrease in systolic and mean arterial pressure (r = 0.45 and 0.42, respectively; both p less than 0.05). Right ventricular dP/dt correlated the most poorly of all parameters with changes in blood pressure while impedance X RV pulse pressure correlated best with changes in mean and systolic pressure (r greater than or equal to 0.82, p less than 0.001).

Aged↗