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Implantation of transvenous devices is a widespread procedure in clinical cardiology. It is well known that the presence of the electrodes in the cardiovascular system can induce fibrosis or fibrous adhesions between them and cause tricuspid regurgitation. Moreover there are suggestions that the placement of the electrode in the tricuspid orifice may also play a role in the development of tricuspid insufficiency because of the thickening of reactive leaflets and the impairment of their mobility in morphological studies. There are no papers regarding the topography of the electrode in the right ventricle judged by means of transthoracic echocardiography. Moreover in literature we did not meet reports comparing the localisation of the lead on the tricuspid valve function. Therefore we decided to describe the detailed topographic relations between the lead and the structures of the right ventricle in a larger population and we compared the influence of the lead location for tricuspid valve function. Research was carried out on a group of 86 patients (52 M, 34 F), with a mean age of 64.7 ± 14.9 years with permanent cardiac pacemaker or implantable cardioverter-defibrillator (ICD). On the basis of echocardiograms performed we assessed the position of the lead regarding the tricuspid valve leaflets or commissure, and judged the course of the lead beneath the tricuspid valve level. Moreover special attention was focused on the placement of the tip of the electrode. We qualified its position into three categories: apex of the right ventricle, right ventricle outflow tract, and “para-apex” position. The degree of the tricuspid valve insufficiency was assessed by means of semiquantitative method based on the Color-flow Doppler echocardiography. We measured the extension and the area of the tricuspid regurgitant jet using four-gradual scale. We compared the topography of the lead at the level of the valve with its function by means of the presence and degree of its regurgitation. We stated that in 35% of cases the pacing lead was located at the level of the anterior leaflet of the tricuspid valve, in 23% at the level of the septal leaflet and in 12% at the posterior one. Besides in 10% the electrode was placed between the leaflets just over the commissures. On the other hand in the remaining 20% the lead was positioned centrally in the right atrioventricular orifice without adherence to any leaflet. Next we assessed the course of the lead beneath the tricuspid valve level and stated that most frequently (45%) it run just across the centre of the right ventricle, and in other cases was lying along the interventricular septum (in 39% of cases) or along the anterior wall of the right ventricle (in 16%). The tip of the lead was positioned exactly in the apex of the right ventricle in 74%, in the right ventricular outflow tract in 9% and in 17% its position was “para-apical”. We did not see any statistically significant differences between the presence and intensification of valve regurgitation and topography of the lead. We concluded that at the level of the tricuspid valve the lead was positioned in the anteroseptal part of tricuspid annulus and the proper apical position of the electrode’s tip occurred in approximately 75% of cases. Localisation of the electrode at the level of the tricuspid orifice does not influence its insufficiency as detected by Doppler echocardiography.
Permanent cardiac pacing is a widely applied procedure in invasive cardiology. The aim of our study was the analysis of the localisation of the tip of the pacemaker lead and its course in the right ventricle. Research was carried out on a group of 12 patients (5F, 7M), from 40 to 93 years of age (average 70±15 yrs) with permanent cardiac pacing or implantable cardioverter-defibrillator (ICD). Subsequent echocardiographic views were applied: an apical four chamber view, a subcostal one and a parasternal right ventricular inflow tract view. At the level of the tricuspid annulus the electrode was positioned: the anterior leaflet – 41.7% (5 pts), the anteroseptal commissure 25% (3 pts), the posterior leaflet 8.3% (1 pt) and the septal one – 8.3% (1 pt). In 16.7% (2 patients) the lead was positioned centrally in the right atrioventricular orifice. Regarding the further positioning of the electrode in the ventricle, in 41.7% (5 pts) the leads were placed along the interventricular septum, in 16.7% (2 pts) along the anterior wall of right ventricle and in 41.7% (5 pts) across the centre of the right ventricle. The tip of the lead was positioned in the apex of the right ventricle in 83.4% (10 pts). In the remaining 16.7% (2 pts) the position was not apical — in 1 patient the anterior wall of the right ventricle and in 1 patient the interventricular septum. In the VVI pacing mode the electrode did not lie on the interventricular septum. In contrast to this in 80% of patients (4 pts) having the DDD pacing mode the lead was situated on the interventricular septum on its course downwards to the ventricle. Conclusions: 1) On the level of the leaflets of the tricuspid valve the lead most often was positioned at the level of the anterior leaflet and the anteroseptal commissure. 2) Most patients had an apical localisation of the tip of the lead. 3) Differences between morphological and echocardiographic studies are related to the intravital and the two-dimensional character of echocardiography, and probably to the small population of the group examined.
One of the hypotheses put forward concerning the mechanism of vasovagal syncope is that the vagal afferent fibres are activated during vigorous contractions against a partly empty left ventricle. The aim of the study was to confirm this hypothesis by using 2D echocardiography during a head-up tilt test. The study was carried out on 39 patients (17 male, 22 female, age range 21–64 years), all with a history of recurrent syncope. The patients were examined using a 2D echo to measure the end-diastolic and end-systolic volume before the head-up tilt test after the Westminster protocol (45min/60 grade) and every five minutes after tilting. T patients during head-up tilt test had a positive response and 32 proved negative. A reduction of both the end-diastolic and end-systolic volumes of the left ventricle was noticed. There was no significant difference in the degree of ejection fraction reduction. The difference in ejection fraction reduction between the two groups was similarly non-significant. It was also noticed that the patients with a positive response had more vigorous contractions than those with a negative test. The decision was therefore taken to use a different parameter for the left ventricle contraction, namely the LV posterior wall slope. As this parameter is partly dependent on time, its use in confirming the extremely vigorous nature of the contractions was considered appropriate. Only 6 patients were tested using this parameter. A tendency towards greater left ventricle posterior wall slope values, both before and during tilting was noticed in the group of patients with vasovagal reaction. Our data shows that vigorous contraction is probably less responsible for vasovagal syncope release than left ventricle volume reduction.
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