This multicentre study suggests that left atrial RFA is effective and safe in patients with chronic atrial fibrillation and mitral valve disease.

A bioprosthetic valve used for aortic valve IE replacement may be associated with lower overall 5-year survival than the use of a mechanical valve in patients up to 65 years old. Further studies are needed to explain these results.

No abstract

Some cases of heparin-induced thrombocytopenia (HIT) have been reported to be associated with antibodies against interleukin-8 (IL-8), a chemokine related to platelet factor 4. We found that sera from 5 HIT patients containing immunoglobulin G (IgG) or IgM antibodies to IL-8, as evidenced using surface plasmon resonance spectroscopy, were able to trigger IL-8-dependent activation of washed platelets, leading to procoagulant activity. This activation occurred at IL-8 concentrations achievable in vivo and was facilitated by heparin (0.1 U/mL). Activation was also induced by affinity-purified anti-IL-8 IgG and involved Fc␥RIIa. In the 2 patients who could be followed up, antibodies were no longer detectable 4 months after heparin withdrawal. One additional patient with paraneoplastic recurrent thrombosis without thrombocytopenia was found to have platelet-activating anti-IL-8 IgM, but in this case heparin was inhibitory. This is another example of potentially pathogenic platelet activation by antibodies. IntroductionIn most patients with heparin-induced thrombocytopenia (HIT), antibodies bind to complexes of heparin and platelet factor 4 (PF4). If these antibodies are immunoglobulin G (IgG), they interact with Fc␥RIIa receptors and trigger platelet activation. 1,2 However, previous investigators using enzyme-linked immunosorbent assay (ELISA) have reported that a few HIT patients have antibodies specific to another, PF4-related ␣-chemokine-interleukin-8 (IL-8), alone 3,4 or in combination with antibodies to heparin-PF4 complexes. 5 These antibodies were infrequently detected in patients with heparin exposure but no thrombocytopenia and in patients with thrombocytopenia from another etiology. 3 The main known property of IL-8 is to induce neutrophil activation, and anti-IL-8 autoantibodies have been shown to inhibit IL-8 interaction with its specific receptors on neutrophils. 6 IL-8 also binds to heparin, 7 and there may be IL-8 receptors on platelets. [8][9][10] This study was undertaken to investigate whether antibodies to IL-8 are able to induce platelet activation in vitro and whether they are dependent on heparin. Study designSera were obtained from 5 selected patients (P1-P5) who fulfilled the diagnostic criteria for HIT 1,11 (suggestive temporal pattern of platelet counts in relation to heparin therapy and evidence for heparin-dependent platelet-activating antibodies) but without IgG to heparin-PF4 complexes. 3 Patient 6 had typical HIT with IgG to heparin-PF4 only. One additional patient (P7), who had experienced fatal recurrent paraneoplastic thromboses while on heparin therapy without thrombocytopenia, 12 was also studied. Small volumes of blood were collected from samples required for routine patient management and were withdrawn after heparin therapy was stopped; heparin was no longer detectable with anti-Xa assay. ELISA (Asserachrom HPIA; Diagnostica Stago, Asnières, France) was used to detect antibodies to heparin-PF4. 13 IgG was purified by affinity chromatography on protein G-Sepharose (Pharmacia Bi...

Myocardial T2 determined using a black-blood MRI sequence, is sufficiently sensitive to identify most of the moderate acute rejections documented with biopsy at the same time, but is also a predictor of the subsequent occurrence of such biopsy-defined rejections.