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

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 ⩾10 ischaemic episodes (3rd tertile) or duration of ischaemia ⩾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 ⩾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 (⩾10 ischemic episodes or ⩾32 min duration of ischaemia).

Conclusion

Increasing IgA‐aCL levels are associated with increasing ischemic burden in patients with CAD.While cardiac enzymes are sensitive markers of myocardial necrosis, there are no reliable biomarkers for myocardial ischaemia. Increased production of anticardiolipin antibodies (aCL) has been linked to lipid peroxidation and may cause endothelial dysfunction favouring vasoconstriction.¹ In this study we examined the relationship between aCL, platelet activation and ischaemia during daily‐life activities as assessed by 48 h Holter monitoring in chronic coronary artery disease (CAD).