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Biomedical subjects

K A Ellenbogen

Publications and source records attributed to K A Ellenbogen.

At least 145 records · Page 8Linked to original sources

Increased circulating atrial natriuretic factor (ANF) release during induced ventricular tachycardia.

During sustained ventricular tachycardia (VT), there is usually a rise in mean atrial pressure. Atrial natriuretic factor (ANF) is a peptide released by the atria in response to increased atrial pressure or distension. ANF causes arterial vasodilation and natriuresis in man, and may contribute to the polyuria noted during tachycardia. We hypothesized that induction of sustained VT would cause elevation of right atrial pressure and lead to increased release of ANF. We measured mean arterial pressure, right atrial pressure, VT cycle length, atrial cycle length, plasma norepinephrine, and central ANF in 11 patients during 20 episodes of VT. The mean cycle length of induced tachycardia was 335 +/- 15 msec, with a mean atrial cycle length of 547 +/- 43 msec. Baseline plasma ANF was 70 +/- 11 femtomoles per milliliter and increased to 133 +/- 22 fmol/ml (p less than 0.001) after 4 minutes of VT. There was a decrease in mean arterial pressure from 87 +/- 3 to 66 +/- 3 mm Hg, and a rise in mean right atrial pressure from 4.0 +/- 0.8 to 11 +/- 1 mm Hg (p less than 0.001). The change in plasma ANF was quite variable among individual patients and was correlated with changes in mean right atrial pressure but poorly correlated with changes in mean arterial pressure, plasma norepinephrine, and atrial cycle length. Our data demonstrate that significant increased in ANF levels occur during sustained VT and are associated with increased right atrial pressure.

Atrial Function↗

Atrial natriuretic factor release is enhanced by incremental atrial pacing.

There is ample evidence from animal models indicating that secretion of atrial natriuretic factor (ANF) can be induced by an increase in atrial contraction frequency or atrial distension. The influence of these stimulatory signals on ANF secretion in humans has not been fully elucidated. We assessed the responses to graded right atrial pacing in 28 patients (aged 33 to 70 years) at rates of 100, 125, and 150 beats/min on right atrial pressure, left atrial size (by two-dimensional echocardiography in 9 of 28 patients), and circulating plasma ANF levels. At pacing rates of 125 and 150 beats/min, ANF levels increased from a baseline value of 64 +/- 9 fmol/ml (mean +/- SEM) to 89 +/- 13 fmol/ml (pp less than 0.05) and to 132 +/- 17 fmol/ml, respectively (p less than 0.001). Right atrial pressure increased from a baseline value of 4.1 +/- 0.7 mm Hg to 4.5 +/- 0.6 mm Hg at a pacing rate of 125 beats/min (p less than 0.05) and to 6.1 +/- 0.8 mm Hg at a pacing rate of 150 beats/min (p less than 0.001). Left atrial dimension increased from a baseline value of 44.5 +/- 3 mm to 49.5 +/- 3 mm at a pacing rate of 125 beats/min (p less than 0.05) and increased further to 52.5 +/- 3 mm at a pacing rate of 150 beats/min (p less than 0.001). No significant changes in atrial pressure or size or in plasma ANF were observed at a pacing rate of 100 beats/min.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Electrophysiological observations during QRS alternans in a patient with incessant tachycardia.

Electrophysiological observations during preoperative and intraoperative study of a 46-year-old patient with incessant ventricular tachycardia and QRS alternans demonstrated a potential mechanism for this electrocardiographic finding. During QRS alternans, conduction delay (or block) was recorded from the site of origin of the tachycardia, high on the anterior septum to the His bundle: After procainamide infusion, the tachycardias slowed and, concurrent with the disappearance of QRS alternans, conduction from the site of tachycardia origin to the His bundle could no longer be demonstrated.

Electrocardiography↗

Frequency, diagnosis and clinical characteristics of patients with multiple accessory atrioventricular pathways.

Multiple accessory atrioventricular (AV) pathways were documented in 52 of 388 patients (13%) who underwent detailed electrophysiologic evaluation. Multiple AV pathways were identified during intraoperative mapping or electrophysiologic study by different patterns of ventricular preexcitation during atrial fibrillation, flutter or atrial pacing with different delta-wave morphologic and ventricular activation patterns; different sites of atrial activation during right ventricular pacing or orthodromic reciprocating tachycardia; or preexcited reciprocating tachycardia using a second pathway as the retrograde limb of the tachycardia. A logistic model was used to determine which clinical, electrocardiographic and electrophysiologic variables were associated with multiple AV pathways. Right free-wall and posteroseptal accessory AV pathways were more common in patients with multiple AV pathways and were frequently associated. Multivariate logistic regression identified Ebstein's anomaly, and a history of preexcited reciprocating tachycardia as significant variables (p less than 0.0001). Pathway location was not subjected to statistical analysis because of confounding variables.

Adolescent↗

Pharmacodynamics and pharmacokinetics of oral pirmenol.

The efficacy, pharmacokinetics, and pharmacodynamics of pirmenol, a class Ia antiarrhythmic agent, were studied in patients with frequent symptomatic premature ventricular complexes (PVCs). Pirmenol was given every 12 hours to eight patients in a dose-ranging protocol, and median PVC suppression of 94% (range 72% to 100%) was achieved. The median effective pirmenol dose was 300 mg/day (range 200 to 500 mg/day), and mean (+/- SD) trough plasma pirmenol concentration at the effective dose was 0.98 +/- 0.29 micrograms/ml. The mean half-life of elimination was 10.5 +/- 2 hours. There was considerable overlap among patients with respect to plasma pirmenol concentration and times at which PVC frequency returned to 25%, 50%, and 75% of baseline during drug washout trials. Altering pirmenol's dose interval (while maintaining a constant daily dose) from 12 to 6 hours did not improve drug efficacy. Pirmenol was given to seven patients for long-term therapy (24 to 44 months). Median PVC suppression at 24 months was 70%. Pirmenol is safe and well tolerated, and it can be administered twice daily for PVC suppression.

Administration, Oral↗

Effects of bolus injection of esmolol in healthy, exercising subjects.

Esmolol is an investigational ultra-short-acting beta-adrenergic blocker that has potential application in many clinical cardiology settings. The purpose of this study was to investigate the effect of a bolus dose of esmolol on heart rate, blood pressure, and PR interval in healthy, exercising male subjects. We gave a single esmolol bolus over 30 seconds to 13 men who exercised to a predetermined target heart rate. Each subject performed the exercise protocol twice, receiving a different dose between 10 and 300 mg each time. An additional eight subjects received two esmolol boluses 5 minutes apart while performing the same exercise protocol. Esmolol doses of 180 mg or greater caused a 13% to 18% decrease in heart rate, an 11% to 18% decrease in blood pressure, and a 13% to 22% prolongation of the PR interval. The median time to peak esmolol effect was 1 minute for heart rate, 2 minutes for blood pressure, and 4 minutes for PR interval. The median time required to recover 50%, 75%, and 90% of the decrement in heart rate was 8, 10, and 13 minutes, respectively. The rapid onset and disappearance of esmolol effects may make it an appealing drug in acute care settings.

Adult↗

Effects of sustained intravenous diltiazem infusion in healthy persons.

A 3-stage infusion of diltiazem was tested in 8 subjects for up to 48 hours: a bolus injection (10 mg over 3 minutes), a rapid loading infusion (20 mg over 30 minutes) and a maintenance infusion (10 mg/hour to the end of the study). This regimen produced stable median plasma diltiazem concentrations of approximately 150 ng/ml. The median half-life of elimination for diltiazem was 206 minutes (range 144 to 452) and median total clearance was 980 ml/min (range 665 to 1,907). The PR interval lengthened 10 to 18% during the maintenance infusion in 7 subjects; in 1 subject atrioventricular nodal Wenckebach conduction was recorded during the rapid loading infusion. Systolic blood pressure decreased from 124 +/- 7 mm Hg (mean +/- standard deviation) during the control period to 121 +/- 8 mm Hg during the rapid loading infusion (p = 0.03 compared with control) and to 117 +/- 7 mm Hg (p = 0.04 compared with control) during the maintenance infusion. Heart rate did not change. PR interval and blood pressure returned to control levels within 4 hours after the infusion was stopped. Loading and maintenance infusion may be an attractive method of administering diltiazem when stable drug concentrations are required for prolonged periods.

Adult↗

Characterization of retrograde conduction by direct endocardial recording from an accessory atrioventricular pathway.

Accessory pathway electrograms are rarely recorded in patients with Wolff-Parkinson-White syndrome. In one patient, during electrophysiologic study, simultaneous local ventricular (V) accessory pathway (AP) and atrial (A) deflections were recorded during bipolar catheter endocardial mapping over the pathway. Analysis of changes in electrographic intervals during performance of the ventricular extrastimulus technique allowed characterization of the retrograde conduction properties of the pathway. As coupling intervals were decreased, an initial increase was seen in the AP2A2 interval with subsequent ventriculoatrial block between the accessory pathway and atrium. When coupling intervals were further decreased, the V2AP2 interval lengthened with ultimate block between the ventricle and accessory pathway. These findings support the concept of impedance mismatch as the cause of conduction block in accessory pathways with the distal junction of the accessory pathway being the most vulnerable.

Adult↗

Cardiac function in patients on chronic amiodarone therapy.

Antiarrhythmic agents may depress cardiac contractility and worsen heart failure. Few data are available describing the chronic effects of amiodarone on myocardial function. To assess the effects of amiodarone on cardiac function, we studied 41 consecutive patients with first-pass or equilibrium radionuclide angiography prior to and 3 months after drug therapy was initiated. The mean heart rate, systolic blood pressure (BP), and diastolic BP were not significantly altered by treatment. The mean ejection fraction was 36% +/- 19 (mean +/- 1 SD) at the time of drug initiation and 36% +/- 17 3 months later (p less than 0.05). Nineteen patients had an ejection fraction greater than 30% and 16 had an ejection fraction less than 30%. The mean change in ejection fraction for these two subgroups showed no statistically significant difference, although a decrease in EF greater than 10% was seen in three patients (symptomatic in two), necessitating an increase in diuretic dose. No correlation between amiodarone dose and change in ejection fraction (r = -0.12, p greater than 0.05) was noted. There was no correlation between baseline ejection fraction and change in ejection fraction over this 3-month period (r = -0.36, p greater than 0.05). In summary, amiodarone does not depress left ventricular function and as a result can be used safely in patients with mild to moderate impairment of left ventricular function. In patients with stable left ventricular function, serial tests of left ventricular function may not be necessary.

Adult↗

Frequency-dependent effects of verapamil on atrioventricular nodal conduction in man.

We sought to determine if verapamil induces frequency-dependent prolongation of atrioventricular nodal conduction in 10 consecutive patients studied in the electrophysiology laboratory. We used a maintenance infusion of verapamil designed to produce plasma concentrations of verapamil in the "therapeutic" range and that did not alter heart rate or blood pressure significantly. Frequency-dependent prolongation of atrioventricular nodal conduction (AH interval) was demonstrated in all 10 patients (p less than .001), and no change in HV conduction time with decreasing cycle length was noted in any patients while receiving verapamil. Two patterns of use-dependent response were seen. In four patients frequency-dependent prolongation of the delta(AH) interval [delta(AH) = AHverapamil - AHcontrol at a given cycle length] was seen with each decrement in pacing cycle length. In six patients frequency-dependent prolongation of the delta(AH) interval was not manifest until the fifth to eighth pacing cycle length tested. There was no association between the pattern observed and the initial heart rate or AH interval. After an abrupt change in pacing cycle length, the kinetics of delta (AH) interval prolongation were rapid; equilibrium was achieved by five to eight pulses in all patients. There was no correlation between the magnitude of prolongation of the AH interval noted at a particular cycle length and the concentration of verapamil during the maintenance infusion. These results indicate that verapamil causes use-dependent prolongation of atrioventricular nodal conduction in man.

Atrioventricular Node↗

Life after pacemaker implantation: management of common problems and environmental interactions.

Patients with permanent pacemakers have become an increasingly common clinical entity for physicians. Many patients who receive pacemakers are active people who leave the hospital expecting to return to fully functional, normal lives. These patients need to be aware of potential pacemaker interactions at work and in other environments. One location in which many patients with pacemakers find themselves is the hospital environment, which is host to an abundant array of diagnostic and therapeutic sources of electromagnetic interference that are capable of disrupting normal pacemaker function. Previous studies have addressed issues ranging from these patients' use of cellular telephones to the dangers of magnetic resonance imaging. This article reviews the medical literature on the management of patients with permanent pacemakers and the problems that these patients may encounter because of electromagnetic interference.

Contraindications↗

Limitations of esophageal electrocardiography in recording atrial rhythms after orthotopic heart transplantation.

Esophageal electrocardiography is a commonly used tool for the differential diagnosis of arrhythmias. A 39-year-old man who underwent orthotopic heart transplantation developed a narrow complex tachycardia. Esophageal electrocardiography showed a junctional tachycardia (recording native atrial activity alone), whereas atrial intracavitary electrograms showed the correct diagnosis of atrial flutter. Esophageal recording in patients who undergo orthotopic heart transplantation is a useful technique for recording native atrial activity. For arrhythmia diagnosis in these patients it is frequently necessary to record donor atrial activity with intracavitary electrograms. The limitations of esophageal electrocardiography should be recognized by physicians who care for these patients.

Adult↗

Procainamide: a perspective on its value and danger.

Procainamide remains one of the most widely used antiarrhythmic agents in clinical practice. Currently, it is widely used alone or in combination with class I agents (eg, mexiletine or tocainide) to prevent recurrent ventricular tachycardia or symptomatic nonsustained ventricular tachycardia. Procainamide is also used for short-term treatment of ventricular tachycardia and a variety of supraventricular tachycardias, primarily atrial flutter and atrial fibrillation. Long-term procainamide therapy is limited by a number of systemic side effects, primarily lupus-like syndrome, gastrointestinal disturbances, and autoimmune blood dyscrasias. Procainamide levels can be useful in initial dose titrations; however, QRS and QT interval measurements help prevent drug toxicity. It is recommended that patients being started on antiarrhythmic therapy with procainamide be admitted to the hospital for monitoring to ensure that their QT interval is not excessively prolonged.

Anti-Arrhythmia Agents↗