Clinical performance of steroid-eluting pacing leads with 1.2-mm2 electrodes

To raise pacing impedance and reduce battery current drain, new tined steroid-eluting leads were developed with 1.2-mm2 hemispherical electrodes, instead of conventional 5-8 mm2. Twenty-two unipolar J-shaped atrial leads and 25 unipolar ventricular leads (models 4533 and 4033, respectively) were implanted in 33 consecutive patients and followed for a mean of 25 months (range 18-29). Handling characteristics of atrial leads were found favorable. The leads slipped easily into the right atrial appendage and were easy to position. Handling characteristics of ventricular leads were satisfying, but more efforts had to be applied to cross the tricuspid valve. Special care was taken to avoid perforation of the myocardium due to the small lead tip. Following implantation, four ventricular and one atrial lead exhibited instability of pacing thresholds that resolved spontaneously within 1-3 days of implantation. Except for this, no lead malfunctioned. The reoperation rate was zero. The mean electrogram amplitudes of 15 mV (ventricle) and 4 mV (atrium), and the mean chronic pacing threshold of 0.085 ms at 1.6 V (app. 0.43 V at 0.5 ms) were comparable with the best values seen in the literature on passive fixation leads. The rest of the electrophysiological parameters were enhanced: mean pacing impedances were 984 omega (acute) and 900 Q (chronic), mean slew rates 3.26 V/s (ventricle) and 1.75 V/s (atrium), mean acute voltage threshold at 0.5 ms was 0.25 V, mean current and energy thresholds calculated at 0.5 ms were 260 microA and 32 nJ (acute) and 478 microA and 103 nJ (chronic). The electrical characteristics of these leads provide for increased pacemaker longevity in combination with substantial safety margins for pacing and sensing.     

A novel function of haptoglobin: haptoglobin-haemoglobin complex induces apoptosis of hepatocarcinomatous Hep 3B cells

Haptoglobin-haemoglobin complex (Cx) showed a cytotoxic effect on the growth of Hep 3B (human hepatocellular carcinoma) cells, dose dependently. The antiproliferative effect of Cx on the multiplication of Hep 3B cells was augmented by the presence of prostaglandin (PG) D2. Antihuman Hb IgG abolished the effect of Cx, dose-dependently, which indicates that the antiproliferative effect of Cx really is exerted by Cx. Hep 3B cells treated with Cx showed the characteristic biochemical changes of apoptosis, such as DNA fragmentation which was blocked by pretreatment with cycloheximide, and the increase of transglutaminase expression. Thus, the antiproliferative effect of Cx against Hep 3B cells occurs via the typical apoptotic pathway.