Influence of myocardial ischemia and reperfusion on beta-adrenoceptor subtype expression.

The effects of ischemic injury and reperfusion on myocardial beta-adrenoceptor expression were examined in dogs after 30 min of left anterior descending coronary artery (LAD) ligation. Three sets of six dogs were allocated to either sham ligation (group I), 30 min ischemia without reperfusion (group II), or ischemia with 1 h of reperfusion (group III). The density of total beta-adrenoceptors along with beta1- and beta2-adrenoceptor subtypes were compared in tissue from the ischemic LAD and nonischemic left lateral zones by using radioligand binding with 125-labeled iodocyanopindolol (ICYP). In the control animals, there was no difference between total beta-adrenoceptors (43.8 +/- 7.2 vs. 40.7 +/- 8.0 fmol/mg protein +/- SEM) or percentage beta-adrenoceptor subtypes between the two zones. In group II, total beta-adrenoceptors increased 19.9% (p = 0.03) in the LAD compared with the lateral zone after 30 min of ischemia. Both beta-adrenoceptor subtypes increased, but only the increase in beta2-adrenoceptor was significant (39.8%; p = 0.02). Animals in group III revealed no difference in total beta-adrenoceptors density between LAD and lateral zones (48.3 +/- 13.4 vs. 55.2 +/- 8.5 fmol/mg protein). Brief myocardial ischemia is associated with an increase in total beta-adrenoceptors, attributed predominantly to increased beta2-adrenoceptors density. The increase in beta-adrenoceptor density is reversible after 1 h of reperfusion.

The vanishing defibrillator syndrome: incidence, mechanism, and clinical relevance.

Intraperitoneal migration of an abdominally implanted cardioverter defibrillator is a complication not yet fully described. In a consecutive series of 195 patients, migration occurred between 1 and 20 months in 5 (8%) of the 63 patients in whom a subrectus abdomini placement of the generator was chosen. It was unrelated to the patients' clinical characteristics or the defibrillator model. Dysuria and inability to interrogate the device were present in every subject, and the diagnosis was confirmed by the characteristic abdominal x-ray appearance and the findings at the time of surgery. Adhesions involving the omentum, and in one case, the small bowels, were present in three patients and seem to be related to the length of intraabdominal permanence of the generator. Because this complication may be due to specific anatomical characteristics of the aponeurosis of the abdominal muscles, it is likely that its incidence will be unchanged by the use of smaller devices. A close follow-up of the generators implanted deep to the rectus fascia is therefore advisable.

Localization of accessory pathways in the Wolff-Parkinson-White syndrome.

Operative and ablative therapy in the Wolff-Parkinson-White syndrome requires accurate localization of accessory atrioventricular pathways. A reasonable first approximation to pathway location can be obtained by noninvasive techniques, the 12-lead electrocardiogram being the most readily available of these. Accurate characterization of the number and anatomic localization of accessory pathways still requires invasive electrophysiological assessment. The most useful technique for accessory pathway localization remains endocardial atrial mapping of the tricuspid and mitral (via the coronary sinus) ring during atrioventricular reciprocating tachycardia and ventricular pacing. Other techniques provide important confirmatory evidence and may be the only guides to accessory pathway location in selected individuals.

Usefulness of isoproterenol during atrial fibrillation in evaluation of asymptomatic Wolff-Parkinson-White pattern.

The asymptomatic individual with a Wolff-Parkinson-White (WPW) pattern is considered at risk for ventricular fibrillation if a rapid ventricular response (shortest RR interval less than or equal to 250 ms) is observed during induced atrial fibrillation (AF) in the laboratory. It has been suggested that isoproterenol administration during AF may more accurately define the patient at risk. Consequently, the effect of isoproterenol on ventricular response during AF was studied in 21 asymptomatic individuals with WPW pattern to assess the potential of isoproterenol to identify patients at risk for sudden death. An electrophysiologic study that included elective induction of AF was performed. The shortest and mean RR intervals between 2 consecutive preexcited and normal QRS complexes, the average RR interval and the proportion of preexcited QRS complexes were measured in the control state and after bolus injections of isoproterenol (0.5, 1.0, 2.0 and 4.0 micrograms) during AF. Both atrioventricular nodal and accessory pathway conductions were enhanced proportional to isoproterenol dose. Isoproterenol had a greater effect on the atrioventricular node, as reflected by significantly greater changes in the shortest RR between normal complexes (339 +/- 70 vs 255 +/- 21 ms, mean +/- standard deviation, p less than 0.001) than the shortest RR between preexcited complexes (264 +/- 39 vs 219 +/- 34 ms, p less than 0.001) and a decrease in percentage of preexcited complexes (65 +/- 37 vs 50 +/- 33%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Flecainide acetate does not alter the energy requirements for direct ventricular defibrillation using sequential pulse defibrillation in pigs.

Flecainide acetate is a recently approved class 1c antiarrhythmic agent indicated for patients with serious ventricular arrhythmias. Because flecainide may be used in patients with automatic implantable defibrillators, we assessed the effect of flecainide on ventricular defibrillation energy requirements in a pig model. Different doses of flecainide maintaining plasma levels in the "subtherapeutic" (six pigs), "therapeutic" (eight pigs), and "supratherapeutic" (eight pigs) range were administered to three groups of pigs. A fourth group (six pigs) served as a time control and was given normal saline only. Episodes of ventricular fibrillation were induced and then terminated using sequential truncated trapezoidal direct current shocks delivered by a tripolar internal defibrillator system. Energy requirements for defibrillation were assessed by measuring defibrillation threshold and also by comparing shifts in the curves relating energy with percent successful defibrillation. Flecainide failed to alter defibrillation requirements at any dose. We conclude that ventricular defibrillation energy requirements are not affected by flecainide in our pig model. Both the defibrillation threshold technique and the comparison of curves relating success of defibrillation to energy yielded similar results suggesting that either can be used to assess energy requirements for defibrillation.

Cryosurgical modification of the atrioventricular node: a closed heart approach in the dog.

Intraoperative modification of the atrioventricular (AV) node to prolong refractoriness could be an alternative to His bundle ablation in patients with refractory supraventricular arrhythmias. It was postulated that a cryosurgical lesion at the posterior interatrial septum in the closed heart could achieve this. An electrophysiologic study was performed in anesthetized dogs. The AV fat pad was mobilized to expose the posteroseptal region. A cryoprobe cooled to 0 to -10 degrees C was moved in the exposed region until reversible AV block indicated proximity of the AV node. The probe was then cooled to -70 degrees C for 30 seconds. Four weeks later, five dogs had a favorable result with a mean prolongation of Wenckebach cycle length of 45 +/- 7% (p less than 0.05). Two dogs had complete heart block. Decreased (one dog) or increased (one dog) duration of freezing resulted in no change and complete heart block, respectively. Histologic examination verified partial damage to the AV node with preservation of the His bundle. Thus, controlled cryoinjury to modify AV node function is feasible in the closed heart; preservation of AV conduction provides an advantage over His bundle ablation.