IgA anticardiolipin antibody is associated with the extent of daily-life ischaemia in patients with chronic coronary artery disease.

Abstract

Circulating anticardiolipin antibodies (aCL) may cause endothelial dysfunction. We investigated whether aCL are related to platelet activation, thrombin generation and daily-life ischaemia in patients with chronic coronary artery disease (CAD). We measured (medians 25th-75th percentile) IgG, IgM, IgA aCL serum levels (Arbitrary Elisa Units, AEU), prothrombin fragments (F1+2, nmol/l), 24 h urine excretion of 11-dehydrothromboxane B2 (11-DHTXB2, ng/mg creatinine) creatine kinase (CK) and its cardiac isoenzyme CK-MB (IU/l) in 60 patients with angiographically documented CAD and in 40 age and sex matched controls. Patients underwent a 48 h Holter monitoring for assessment of the number and duration of ischaemic episodes. Patients had higher IgA-aCL levels than controls (3.2 vs 2.4 AEU, p = 0.002). Increased IgA-ACA levels were related to increased number and duration of ischaemic episodes (p<0.01). By ANOVA, patients with >or=10 ischaemic episodes (3rd tertile) or duration of ischaemia >or=32min (3rd tertile) had higher IgA-aCL than those with lower ischaemic burden (4.95 vs 3 vs 2.5 AEU, p = 0.002 and 4.9 vs 3 vs 2.5 AEU, p = 0.001 respectively). Patients with >or=2 ischaemic episodes (2nd and 3rd tertile) had higher 11-DHTXB2, than those with minimal ischaemia (2< episodes, 1st tertile) (p = 0.001). CK and CK-MB were within normal range after Holter monitoring. Receiver operating curve analysis showed a greater area under the curve for IgA-aCL than for 11-DHTXB2 in predicting severe ischaemia (>or=10 ischemic episodes or >or=32 min duration of ischaemia). Increasing IgA-aCL levels are associated with increasing ischemic burden in patients with CAD.