Anticardiolipin antibodies are not associated with restenosis or endothelial activation after percutaneous transluminal angioplasty.
OBJECTIVE
Restenosis following percutaneous transluminal angioplasty (PTA) continues to be a major clinical problem. Anticardiolipin antibodies (aCL) have been established as risk factors for venous or arterial thrombosis. The aim of this study was to assess: a) the influence of positive aCL upon restenosis within 6 months after PTA, b) the possibility of a seroconversion from negative to positive aCL after PTA and c) a possible link between positive aCL and endothelial activation.


METHODS
71 patients (50 men and 21 women, age 68+/-13 years) with peripheral arterial occlusive disease (PAOD, Fontaine II-IV) undergoing a successful PTA entered the study and were prospectively followed for 3 and 6 months thereafter.


METHODS
PTA was carried out successfully and noninvasive grading was done with duplex scanning. Laboratory investigation included aCL, thrombin generation markers, such as thrombin-antithrombin III complexes and prothrombin fragments 1+2, as well as thrombomodulin, soluble P-selectin, E-selectin and the vascular cell adhesion molecule-1, as endothelial activation markers.


RESULTS
30/71 (42.3%) patients developed restenosis (>50% reduction of the lumen diameter) within 6 months after PTA. 9/71(12.7%), had positive aCL IgG (19-35 GPL) and/or IgM (14-103 MPL) at all three measurements. 2/9 (22.2%) of aCL positive and 28/62 (45.2%) of aCL negative patients had restenosis at 6 months after PTA (relative risk RR=0.51, 95%-Cl: 0.14-1.78, chi2 non-significant). All other parameters did not differ between aCL positive and -negative groups.


CONCLUSIONS
Our findings suggest that: a) patients with PAOD have a slightly higher prevalence of positive aCL compared to the general population, but no association is evident between positive aCL and restenosis within 6 months after PTA, b) no seroconversion from negative to positive aCL occurred within 6 months after PTA, c) no association of aCL with endothelial activation markers or thrombin generation markers was found.
Tsakiris
D A
DA
Department of Central Laboratory, University Hospital Basel, Switzerland.
Tschöpl
M
M
Jäger
K
K
Wolf
F
F
Marbet
G A
GA
D000368:Aged; D000800:Angioplasty, Balloon; D017153:Antibodies, Anticardiolipin / Q000032:analysis*; D001157:Arterial Occlusive Diseases / Q000276:immunology / Q000628:therapy*; D004730:Endothelium, Vascular / Q000276:immunology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D016491:Peripheral Vascular Diseases / Q000276:immunology / Q000628:therapy*; D011446:Prospective Studies; D012008:Recurrence; D013997:Time Factors
D017153:Antibodies, Anticardiolipin