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Permanent cardiac pacing and its influence on tricuspid valve function.

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.