Clinical Management
Fujito Numano, MD, Ph.D
Lecturer
Department of Pediatrics, Niigata University Graduate School of Medical and Dental Sciences
Niigata, Niigata, Japan
BACKGROUND/
Aim: Warfarin is the main anticoagulant used to prevent ischemic cardiac events due to thrombotic occlusion of coronary artery aneurysms (CAAs) after KD. However, since warfarin administration results in accelerated calcification of the vascular wall as well as the serious complication of bleeding complications, direct oral anticoagulants (DOACs) have begun to be offered to patients with giant CAAs after KD as an option for systemic anticoagulation therapy.
The aim of our study is to evaluate whether warfarin treatment is involved in promoting vascular wall calcification in giant CAAs after KD using CT calcium scores (CTCS).
Methods: We measured CTCS for a total of 17 cases with a history of KD with giant CAAs (maximal luminal diameter ≥ 8 mm or Z-score ≥ +10 at 30 days and later after KD onset) .
Enrolled cases were divided into two cohorts based on warfarin administration and evaluate the CTCS for each cohort. WF(+): Cohort using warfarin at the time of CTCS measurement (n=7), WF(-): cohort without warfarin (n=10). For 11 cases with multiple CTCS measurements, we calculated the annual increase rate of CTCS as the rate of rise.
Results: CTCS in the WF(+) cohort showed a clear and consistent increase over time compared to the WF(-) (Figure). The median rate of rise was 210.33 for WF(+) and 7.67 for WF(-) (p=0.026, Welch Two Sample t-test).
A case of warfarin resistance did not show an increase in CTCS despite the use of warfarin.
Conclusion: There is a possibility that the administration of warfarin is involved in promoting vascular wall calcification in giant coronary artery aneurysms following Kawasaki disease. The exacerbation of stenotic lesions with calcification poses a risk of ischemic cardiovascular events, suggesting that the administration of DOACs may be preferable. Biomarker studies are needed to elucidate the role of warfarin in promoting vascular wall calcification.