Delivery of RF energy through a cooled catheter tip allows the creation of larger endomyocardial lesions by limiting the occurrence of impedance rise despite the delivery of greater energy. These observations suggest that, under certain conditions, resistive tissue heating at a distance from the site of current delivery may play an important role in RF ablation therapy.

The purpose of this study was to determine whether a quantitative relationship existed between a reduction in regional myocardial blood flow, measured by radiolabeled microspheres, and the degree and type of changes in myocardial activation recorded in bipolar left ventricular subepicardial and subendocardial electrograms, in open-chest dogs following acute coronary artery occlusion. We found that the degree of regional myocardial ischemia was related quantitatively to the reduction in amplitude recorded with bipolar electrograms in the subepicardium and subendocardium, and to the increase in duration of subepicardial electrograms. Other characteristics measured in electrograms did not relate to the degree of ischemia. Despite a comparable reduction in regional myocardial blood flow, subepicardial conduction delay exceeded that recorded in the subendocardium, which often exhibited accelerated conduction.

Electrophysiologic studies were performed on a 49 year old woman who had paroxysmal nonreentrant supraventricular tachycardia due to simultaneous anterograde conduction through dual atrioventricular (AV) node pathways. Slow pathway conduction was inversely related to the preceding sinus cycle length and fast pathway conduction was determined by the Hs-A interval (measured from the His potential due to slow pathway conduction to the onset of the subsequent atrial electrogram). Major determinants of sustained simultaneous anterograde fast and slow pathway conduction during sinus rhythm were 1) a retrograde unidirectional block in both fast and slow pathways, and 2) a critical conduction delay in the slow pathway and a long enough Hs-A interval to allow sequential conduction of impulse from both pathways. Flecainide was successful in preventing recurrences of the tachycardia by eliminating slow pathway conduction during long-term follow-up.

Biotherapeutic agents must be administered parenterally to obtain therapeutic blood concentrations, lowering patient compliance and complicating care. An oral delivery platform (ODP) was developed to deliver drugs into the small intestinal wall. This proof‐of‐concept study was performed in 17 anesthetized, laparotomized swine. In 8 swine weighing 17.4 ± 1.2 kg (mean ± SEM), 20 IU of recombinant human insulin (RHI) were auto‐injected into the jejunal wall by placing the ODP inside the jejunum via an enterotomy. In 9 control swine weighing 17.0 ± 0.4 kg, 20 IU of RHI were injected subcutaneously. In both groups, under a 60‐80 mg/dL euglycemic glucose clamp, blood glucose was measured with a handheld glucometer and serum insulin was measured using ELISA, at 10‐minute intervals between −20 and +420 minutes after RHI delivery. The peak serum concentration of RHI was 517 ± 109 pmol/L in the ODP and 342 ± 50 pmol/L in the subcutaneous group (ns). The areas under the insulin concentration curves (83 ± 18 and 81 ± 10 nmol/L·min) were also similar in both groups. The mean time to peak serum concentration of insulin was 139 ± 42 minutes in the ODP and 227 ± 24 minutes in the subcutaneous group (ns). In conclusion, (a) The bioactivity of RHI was preserved after its delivery into the jejunal wall, (b) the intrajejunal route delivered insulin as rapidly and physiologically as the subcutaneous route, and (c) these pharmacokinetic and pharmacodynamic characteristics of RHI after intrajejunal delivery suggest that drugs currently administered parenterally, such as basal insulin, could be successfully delivered into the proximal intestinal wall via the ingestible capsule.

Library of Congress Cataloging-in-Publication Data Fischer, Wilhelm. 1949-[Praxis der Herzschrittmachertherapie. English] Cardiac pacing in clinical practice / W. Fischer, Ph. Ritter; with a foreword by David Hayes ; [translator, Rodolphe Ruffy]. --ist ed. p. cm. "Translation of the second German edition 1997" -T.p. verso Includes bibliographical references and index.

Oral amiodarone therapy was given to seven patients already taking oral flecainide regularly. In one additional patient, administration of flecainide was temporarily discontinued when amiodarone therapy was begun, and then resumed. Amiodarone produced a rise in mean dose-adjusted flecainide plasma level (trough plasma level at steady state/daily dose) from 2.3 +/- 0.8 to 3.4 +/- 0.9 (ng/ml)(mg/day) (p less than 0.01). Accordingly, the mean dose of flecainide required to maintain similar plasma levels of the drug was one-third lower during combined treatment than during therapy with flecainide alone. This drug interaction must be accounted for when amiodarone and flecainide are used concomitantly.

SUMMARY Termination of ventricular tachycardia by low-energy shocks delivered during the ventricular refractory period has been reported. We describe a case of reproducible termination of multiple episodes of sustained ventricular tachycardia by a low-current extrastimulus delivered during the effective refractory period of the right ventricle, from the distal bipole of a quadripolar electrode catheter.NONPROPAGATED electrical activity of diseased myocardial cells has been well demonstrated, particularly in canine' and human ischemic myocardium.2 The role of such activity in the modulation of paroxysmal dysrhythmia in man, although strongly suspected, is undefined. We describe the reproducible termination of multiple episodes of sustained ventricular tachycardia (VT) by a single, nonpropagated pacing stimulus delivered during the effective refractory period of the right ventricle.Case Report GF was a 57-year-old man with ischemic heart disease, an old anterior myocardial infarction and severe left ventricular dysfunction. He had been treated for 2 years with various antiarrhythmic drugs for several episodes of VT and ventricular fibrillation that occurred within 1 month after the infarction. At the time of the study, the patient was receiving no antiarrhythmic therapy. An atrioventricular sequential permanent pacemaker had been implanted several months earlier, and amiodarone had been discontinued for 3 weeks because of severe neurotoxicity. The patient was taken to the electrophysiology laboratory unsedated and, after local anesthesia (1% lidocaine) of the right femoral area, a #7F (USCI) quadripolar electrode catheter was advanced into the right ventricle under fluoroscopic control. A #5F cannula was placed in the right femoral artery for monitoring the systemic blood pressure. The distal pair of poles of the electrode catheter was connected to a programmable stimulator (Bloom DTU-101), and the proximal pair was used for electrogram recording. Leads I, aVF and V, of the surface ECG, the right ventricular (RV) electrogram (filtered between 100 and 500 Hz), the stimulation artifact and the blood pressure tracing were displayed on an oscilloscope (Electronics for Medicine VR-16) and recorded on photographic paper at speeds of 25-100 mm/sec.

Catecholamines facilitate ventricular defibrillation in animals. We examined the effects of beta-adrenergic stimulation and blockade on ventricular defibrillation threshold in anesthetized dogs. Calibrated shocks were delivered between epicardial and superior vena caval electrodes, and defibrillation threshold was measured before and after administration of isoproterenol and propranolol. Eight dogs (group 1) received isoproterenol before propranolol. Nine dogs (group 2) received propranolol before isoproterenol. In group 1, the minimum energy required to defibrillate before isoproterenol was 10.6 +/- 1.7 (SE) J and decreased to 5.9 +/- 1.3 with isoproterenol (P less than 0.001). In group 2, the minimum energy required to defibrillate was 8.3 +/- 2.4 J before propranolol and increased to 10.7 +/- 2.2 after propranolol (P less than 0.001). In group 1, propranolol after isoproterenol increased defibrillation threshold (P less than 0.07), whereas in group 2 isoproterenol after propranolol produced no significant change in defibrillation threshold. Thus beta-stimulation decreased defibrillation threshold significantly in the anesthetized dog heart, an effect that was blocked by propranolol. Conversely, propranolol increased defibrillation threshold, an effect that occurred despite prior beta-stimulation, probably because of the short half-life of isoproterenol.