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The parasympathetic (P) nervous system is thought to contribute significantly to focal atrial fibrillation (AF). Thus we hypothesized that P nerve fibers [and related muscarinic ([M.sub.2]) receptors] are preferentially located in the posterior left atrium (PLA) and that selective cholinergic blockade in the PLA can be successfully performed to alter vagal AF substrate. The PLA, pulmonary veins (PVs), and left atrial appendage (LAA) from six dogs were immunostained for sympathetic (S) nerves, P nerves, and M2 receptors. Epicardial electrophysiological mapping was performed in seven additional dogs. The PLA was the most richly innervated, with nerve bundles containing P and S fibers (0.9 [+ or -] 1, 3.2 [+ or -] 2.5, and 0.17 [+ or -] 0.3/[cm.sup.2] in the PV, PLA, and LAA, respectively, P < 0.001); nerve bundles were located in fibrofatty tissue as well as in surrounding myocardium. P fibers predominated over S fibers within bundles (P-to-S ratio = 4.4, 7.2, and 5.8 in PV, PLA, and LAA, respectively). [M.sub.2] distribution was also most pronounced in the PLA (17.8 [+ or -] 8.3, 14.3 [+ or -] 7.3, and 14.5 [+ or -] 8 [M.sub.2]-stained cells/[cm.sup.2] in the PLA, PV, and LAA, respectively, P = 0.012). Left cervical vagal stimulation (VS) caused significant effective refractory period shortening in all regions, with easily inducible AF. Topical application of 1% tropicamide to the PLA significantly attenuated VS-induced effective refractory period shortening in the PLA, PV, and LAA and decreased AF inducibility by 92% (P < 0.001). We conclude that 1) P fibers and [M.sub.2] receptors are preferentially located in the PLA, suggesting an important role for this region in creation of vagal AF substrate and 2) targeted P blockade in the PLA is feasible and results in attenuation of vagal responses in the entire left atrium and, consequently, a change in AF substrate. nervous system; autonomic; immunohistochemistry

The association of minor and major baseline and incident electrocardiographic (ECG) abnormalities in asymptomatic postmenopausal women with long-term cardiovascular morbidity and mortality is investigated. It is found that in such women, clinically relevant baseline and incident ECG abnormalities are associated with increased risk of cardiovascular events and mortality, independent of established risk factors.

Ventricular tachycardia and ventricular fibrillation are both abnormalities of the heartbeat. In ventricular tachycardia, the ventricles contract with great rapidity; in fibrillation, the individual muscle cells are contracting with great rapidity but also with greatly reduced overall coordination within the heart muscle. The consequences of these conditions can vary greatly from patient to patient, so it would be valuable to establish what other aspects of these conditions might help distinguish between patients with a good prognosis and those at grave risk. For this reason, the cases of 121 patients ventricular tachycardia or fibrillation were reviewed. The cases suggested that cardiac arrest was an indicator of poor outcome and the patients who experienced cardiac arrest were more likely to die suddenly than those for whom palpitations and dizziness were the only symptoms to accompany the tachycardia or fibrillation. (Consumer Summary produced by Reliance Medical Information, Inc.)

Discusses the actuarial performance of implantable cardiac rhythm management devices. Equivalent survival rate for nuclear-powered units; Compilation of all documented cardiac pulse generator failures which occurred during 1988; Use of atrial radio frequency units.

Reports on the development of a training program in clinical electrophysiology by the North American Society of Pacing and Electrophysiology in the U.S. General objectives; Duration of the training program; Outline of the training course.

Evaluates the actuarial performance of implantable cardiac rhythm management devices (ICRMD) which may be used to control bradycardia, tachyarrhythmia. Comparison of the cumulative survival of the ICRMD between the lithium iodide and lithium cupric sulfide chemistries; Performance of the individual models of pulse generators; Summarization of the eight-center experience with rhythm control devices which includes a number of automatic implantable cardioverter-defibrillators and antitachycardia pulse generators.

We evaluated the frequency and type of electrophysiologic abnormalities in an unselected population of consecutive patients with unexplained syncope. Fifty patients were entered in the study; all had 24-hour dynamic electrocardiographic (Holter) recordings and underwent complete electrophysiological studies. An abnormal electrophysiologic study was found in 74% of the patients. Sinus node abnormality was observed in 30%, abnormal AV node function in 14%, long HV in 10%, block distal to H during rapid atrial pacing in 6%, paroxysmal supraventricular tachycardia in 12%, ventricular tachycardia/fibrillation in 8%, and hypersensitive carotid sinus syndrome in 24%. There was no correlation between Holter and electrophysiologic study findings except for the presence of paroxysmal sustained supraventricular tachycardia. Based on clinical, Holter monitoring, and electro- physiologic findings, 38% were treated by antiarrhythmic drugs, 40% received permanent pacemakers, and. 22% were not treated at all. During follow-up (23 ± 13 months), 9 patients (18%) experienced recurrent syncope or death. [ABSTRACT FROM AUTHOR]

The incidence of multiple, inducible sustained arrhythmius during electrophysiologic studies is unknown. We hove identified five patients who had several sustained tachycardias, some of which were not previously recognized clinically. Three patients had documented sustained supraventricular tachycordia (one of these also had nonsustained ventricular tachycardia) and two had documented sustained ventricular tachycardia. The clinically documented tachycardia was successfully reproduced in all cases; however, the three cases of supraventricular tachycardia also had sustained ventricular tachycardia initiated, and the two cases of ventricular tachycardia also had sustained supraventricular tachycardia, which had not previously been seen. The underlying common denominators for all five patients were poor left ventricular function due to ischemic heart disease and a history of syncope. In one case of clinical supraventricular tachycardia, the second sustained tachycardia appeared following drug therapy (procainamide), which seemed to convert nonsustained to sustained ventricular tachycardia. In another patient with clinical ventricular tachycardia, the supraventricular tachycardia was also initiated following drug therapy (indecainide). We conclude that: (II patients with syncope may have multiple arrhythmic etiologies and (2) complete electrophysiologic evaluation, during control studies as well as serial drug studies, are important in the management of these patients. [ABSTRACT FROM AUTHOR]