Does Abciximab enhance regression of coronary aneurysms resulting from Kawasaki disease?
OBJECTIVE
Acute Kawasaki disease can result in the development of large coronary artery aneurysms that may persist. Abciximab, a platelet glycoprotein IIb/IIIa receptor inhibitor, is associated with resolution of thrombi and vascular remodeling in adults with acute coronary syndromes. The purpose of this study was to compare changes in aneurysm diameter at early follow-up in patients who had Kawasaki disease and received abciximab in addition to standard therapy with those who were treated with standard therapy alone.


METHODS
Patients with Kawasaki disease and large aneurysms were divided into 2 groups on the basis of acute therapy: 1) abciximab in addition to standard therapy and 2) standard therapy alone. Echocardiograms were reviewed for coronary aneurysms (lumen diameter 1.5 times that of the adjacent vessel). Maximum aneurysm diameter was determined during the acute/subacute phase of Kawasaki disease (<6 weeks) and at early follow-up (4-6 months). Regression of the aneurysm was defined as a decrease in lumen diameter, and resolution was defined as normalization of the vessel.


RESULTS
Six patients had 20 aneurysms in the abciximab group, and 9 patients had 30 aneurysms in the standard therapy group. Early follow-up data were available for 19 of the 20 aneurysms in the abciximab group and 19 of the 30 aneurysms in the standard therapy group. Patients who were treated with abciximab demonstrated greater regression in aneurysm size at early follow-up than patients who were treated with standard therapy alone (percentage decrease: 41 +/- 19% vs 17 +/- 27%). In the abciximab group, 68% (13 of 19) of aneurysms resolved at early follow-up compared with 35% (7 of 19) in the standard therapy group.


CONCLUSIONS
Patients who were treated with abciximab demonstrated greater regression in aneurysm diameter at early follow-up than patients who received standard therapy alone. These findings suggest that treatment with abciximab may promote vascular remodeling in this population and warrants further study.
Williams
Richard V
RV
Division of Cardiology, Department of Pediatrics, Primary Children's Medical Center, and the University of Utah, Salt Lake City, Utah, USA. pcrwilli@ihc.com
Wilke
Venus M
VM
Tani
Lloyd Y
LY
Minich
L LuAnn
LL
D000077284:Abciximab; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D002648:Child; D002675:Child, Preschool; D003323:Coronary Aneurysm / Q000175:diagnosis / Q000188:drug therapy* / Q000209:etiology; D017023:Coronary Angiography; D004452:Echocardiography; D005500:Follow-Up Studies; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use*; D007223:Infant; D007275:Injections, Intravenous; D009080:Mucocutaneous Lymph Node Syndrome / Q000150:complications*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D012074:Remission Induction
D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D000077284:Abciximab