[Prevention of post-ERCP acute pancreatitis with octreotide]. / Profilassi della pancreatite acute post ERCP con octreotide.

Acute pancreatitis is one of the most serious complications in endoscopic cholangio-pancreatography (ERCP) and endoscopic sphincterotomy (EPT). Many attempts to avoid such complication have proved to be unsuccessful. The aim of this study was to evaluate the therapeutic effect of octreotide acetate in preventing acute pancreatitis following ERCP. The study was carried out over 100 patients, randomly allocated in two groups. The first group of patients (50 pt.) received 0.1 mg of octreotide acetate s.c. 45 minutes before the ERCP, followed by another dose given 6 hours later. The second group received placebo s.c.

Epicardial excitation during ventricular pacing. Relative independence of breakthrough sites from excitation sequence in canine right ventricle.

In a previous investigation, epicardial recordings with 1,124 closely spaced electrodes revealed 20-35 breakthrough (BKT) sites and an equal number of separate wave fronts on the ventricular surface of exposed dog hearts during normal sinus rhythm. In the present study we tried 1) to determine whether ventricular pacing also produced multiple BKTs and wave fronts and 2) to determine whether the number and location of BKTs were, to some degree, independent of pacing site. The study mainly focused on right ventricular BKTs observed during right ventricular pacing. To test hypotheses 1 and 2 we identified many breakthrough sites during sinus rhythm in seven exposed dog hearts and then paced the heart from several BKT and non-BKT sites on the right ventricle. Epicardial potential maps and excitation time maps were obtained by using 1,124 epicardial electrodes covering the anterior right ventricle and part of the anterior left ventricle. A primary wave front spread radially for several centimeters from the pacing site, and no BKTs appeared in the areas covered by the primary wave front. In the remaining areas (secondary areas), multiple BKTs appeared; their number was close to that observed during sinus rhythm in the same areas (113 versus 115, respectively, in 12 paced beats). The majority of paced BKTs (83 out of 115, or 72%) occurred exactly at the same locations where they appeared during sinus rhythm. However, 30 right ventricular BKTs observed during sinus rhythm disappeared in the secondary areas and were replaced by approximately the same number of new BKTs. Many areas without BKTs in normal beats remained so in paced beats.(ABSTRACT TRUNCATED AT 250 WORDS)

A new intracavitary probe for detecting the site of origin of ectopic ventricular beats during one cardiac cycle.

An olive-shaped probe (25 X 12 mm) with 41 evenly distributed recording electrodes on its surface was introduced into the left ventricles of seven open-chest dogs via the left atrium. In two other dogs a cylindrical probe (40 X 3 mm) was used. Electrical stimuli were delivered at 66 endocardial, midwall, or epicardial sites in the left and right ventricular walls and the septum. Mechanical stimuli were also applied at various epicardial sites. On-line mapping of equipotential contour lines on the surface of the probe invariably revealed a clear-cut potential minimum on the electrode that faced the pacing site. Time of appearance of potential minimum was 3 to 5 msec after endocardial stimuli, 10 to 25 msec for midwall and epicardial pacing, and 30 msec or more for right ventricular stimulation. Simultaneous stimulation at two sites 1.2 cm apart gave rise to two separate minima on the maps. "Pseudoisochrones" derived from electrograms recorded by the new probe were slightly less accurate in indicating the site of origin of extrasystoles. We conclude that equipotential and "isochrone" contour maps recorded from an array of semidirect electrodes, regularly distributed on the surface of an intraventricular probe, provide information on the site of origin (location and intramural depth) of ectopic paced beats in a normal dog heart.

The effect of cardiac electric anisotropy on epicardial potential fields during ventricular repolarization.

We tried to establish whether some of the manifestations of electrical anisotropy previously observed on the canine ventricular epicardium during the spread of excitation were also present during repolarization, with the appropriate polarity. To this end we determined the potential distribution on the ventricular surface of exposed dog hearts during ventricular excitation and repolarization. The ventricles were paced by means of epicardial or intramural electrodes. During the early stages of ventricular excitation following epicardial pacing we observed typical, previously described potential patterns, with negative, elliptical equipotential lines surrounding the pacing site, and two maxima aligned along the direction of subepicardial fibers. Intramural pacing gave rise to similar patterns. The axis joining the maxima, however, was oriented along the direction of intramural fibers. The repolarization potential pattern relating to epicardial excitation exhibited some features similar to those observed during the spread of excitation, namely the presence of families of elliptical equipotential lines around the pacing site, with pairs of potential extrema along the major or minor axes of the ellipses or both. The location of the extrema and the distribution of the epicardial potential gradients during repolarization suggested the presence of anisotropic current generators mainly oriented along the direction of deep myocardial fibers, with some contribution from more superficial sources which were oriented along the direction of subepicardial fibers. Deep stimulation elicited more complicated epicardial patterns whose interpretation is still obscure. We conclude that the electrical anisotropy of the heart affects the distribution of repolarization potentials and probably the strength of electrical generators during ventricular repolarization.

Potential fields on the ventricular surface of the exposed dog heart during normal excitation.

We studied the normal spread of excitation on the anterior and posterior ventricular surface of open-chest dogs by recording unipolar electrograms from an array of 1124 electrodes spaced 2 mm apart. The array had the shape of the ventricular surface of the heart. The electrograms were processed by a computer and displayed as epicardial equipotential maps at 1-msec intervals. Isochrone maps also were drawn. Several new features of epicardial potential fields were identified: (1) a high number of breakthrough points; (2) the topography, apparent widths, velocities of the wavefronts and the related potential drop; (3) the topography of positive potential peaks in relation to the wavefronts. Fifteen to 24 breakthrough points were located on the anterior, and 10 to 13 on the posterior ventricular surface. Some were in previously described locations and many others in new locations. Specifically, 3 to 5 breakthrough points appeared close to the atrioventricular groove on the anterior right ventricle and 2 to 4 on the posterior heart aspect; these basal breakthrough points appeared when a large portion of ventricular surface was still unexcited. Due to the presence of numerous breakthrough points on the anterior and posterior aspect of the heart which had not previously been described, the spread of excitation on the ventricular surface was "mosaic-like," with activation wavefronts spreading in all directions, rather than radially from the two breakthrough points, as traditionally described. The positive potential peaks which lay ahead of the expanding wavefronts moved along preferential directions which were probably related to the myocardial fiber direction.

[Experimental studies on the diffusion of excitation on the right ventricular surface in the dog, during normal and stimulated beats]. / Studio sperimentale sulla diffusione dell'eccitamento alla superficie ventricolare destra del cane, durante il battito normale e stimulato.

Previous work on the spread of excitation on the dog's ventricular surface enabled us to locate up to 30 breakthrough points (BKTPs) where excitation reaches the ventricular surface. In particular the equipotential contour maps enabled us to detect 3 to 5 BKTPs on the anterior right ventricular surface, near the a-v groove when a large part of ventricular surface was still at rest. With a view to investigating the mechanism underlying the early excitation of these basal regions, we stimulated the heart at several right ventricular BKTPs and in other points located at a distance from the BKTPs. The instantaneous equipotential maps showed that after stimulation most right ventricular BKTPs remained in the same position as observed the normal beats. The early appearance of epicardial wavefronts in the basal region and generally in other areas of the right ventricle was attributed to the rapid propagation of excitation waves through the Purkinje network, probably associated to a short transmural crossing time, due to a local thinness of the ventricular wall.