BACKGROUND: 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). METHODS: 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. RESULTS: 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). CONCLUSION: Increasing IgA-aCL levels are associated with increasing ischemic burden in patients with CAD.
BACKGROUND: 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). METHODS: 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. RESULTS: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). CONCLUSION: Increasing IgA-aCL levels are associated with increasing ischemic burden in patients with CAD.
Authors: M Sorice; A Circella; I M Cristea; T Garofalo; L Di Renzo; C Alessandri; G Valesini; M Degli Esposti Journal: Cell Death Differ Date: 2004-10 Impact factor: 15.828