Objective: To compare the safety and efficacy of warfarin plus aspirin versus aspirin alone for the treatment of children with giant coronary artery aneurysm (CAA) secondary to Kawasaki disease (KD). Methods: We searched the PubMed, EMBASE, Cochrane Library, CNKI, WANFAN and VIP databases. We selected case-controlled trials of warfarin plus aspirin versus aspirin alone for the treatment of children with giant CAA secondary to KD. Results: Six retrospective studies met our inclusion criteria. There was no significant difference between the warfarin plus aspirin and aspirin alone groups in the rate of CAA regression (OR 1.38, 95% CI 0.52-3.68, p = 0.52) or the incidence of persistent CAA (OR 2.34, 95% CI 0.16-33.50, p = 0.53), coronary artery stenosis (OR 0.55, 95% CI 0.18-1.72, p = 0.30) or thrombus formation (OR 0.50, 95% CI 0.15-1.69, p = 0.26). There was evidence that warfarin plus aspirin reduced the incidence of coronary artery occlusion (OR 0.08, 95% CI 0.02-0.29, p < 0.0001), cardiac infarction (OR 0.27, 95% CI 0.11-0.63, p = 0.003) and death (OR 0.18, 95% CI 0.04-0.88, p = 0.03). Conclusion: Warfarin plus aspirin therapy reduced the incidence of occlusion, cardiac infarction and death in children with giant CAA secondary to KD.

Calcium-activated chloride channels (CaCCs) play a vital role in regulating pulmonary artery tone during pulmonary arterial hypertension (PAH) induced by high blood flow. The role of CaCCs inhibitor niflumic acid (NFA) in vivo during this process requires further investigation. We established the PAH model by abdominal shunt surgery and treated with NFA in vivo. Fifty rats were randomly divided into normal, sham, shunt, NFA group 1 (0.2 mg/kg), and NFA group 2 (0.4 mg/kg). Pathological changes, right ventricle hypertrophy index, arterial wall area/vessel area, and arterial wall thickness/vessel external diameter were analyzed. Then contraction reactions of pulmonary arteries were measured. Finally, the electrophysiological characteristics of pulmonary arterial smooth muscle cells were investigated using patch-clamp technology. After 11 weeks of shunting, PAH developed, accompanied with increased right ventricle hypertrophy index, arterial wall area/vessel area, and arterial wall thickness/vessel external diameter. In the NFA treatment groups, the pressure and pathological changes were alleviated. The pulmonary artery tone in the shunt group increased, whereas it decreased after NFA treatment. The current density of CaCC was higher in the shunt group, and it was decreased in the NFA treatment groups. In conclusion, NFA attenuated pulmonary artery tone and structural remodeling in PAH induced by high pulmonary blood flow in vivo. CaCCs were involved and the augmented current density was alleviated by NFA treatment.

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