FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |   Search Term  Advanced Search

Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe

Previous Volume 321:1639-1642 December 14, 1989 Number 24 Next

	Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited PubMed Citation

Abstract

It has been hypothesized that the ingestion of aspirin by women during pregnancy increases their infants' risk of certain congenital heart defects. Using data from a large program of case-control surveillance of congenital malformations, we evaluated this hypothesis. The case groups were made up of infants with any structural cardiac defect (n = 1381) and five selected cardiac defects (the subgroups were not mutually exclusive): aortic stenosis (n = 43), coarctation of the aorta (n = 123), hypoplastic left ventricle (n = 98), transposition of the great arteries (n = 210), and conotruncal defects (n = 791). First-trimester aspirin use among the mothers of these infants was compared with that among the mothers of a control group of infants with other malformations (n = 6966). The prevalence of any maternal aspirin use was similar for cases (25 to 33 percent) and controls (27 percent). The relative risks (and 95 percent confidence interval) among infants whose mothers were aspirin users as compared with those whose mothers did not use aspirin, adjusted for potential confounding factors, were 0.9 (0.8 to 1.1) for any cardiac defect, 1.2 (0.6 to 2.3) for aortic stenosis, 1.0 (0.6 to 1.4) for coarctation, 0.9 (0.6 to 1.4) for hypoplastic left ventricle, 0.9 (0.6 to 1.2) for transposition of the great arteries, and 1.0 (0.8 to 1.2) for conotruncal defects. Furthermore, no dose-effect pattern was identified. The findings of this study indicate that aspirin use during the first trimester of pregnancy does not increase the risk of congenital heart defects in relation to that of other structural malformations.

Source Information

Slone Epidemiology Unit, School of Public Health, Boston University School of Medicine, Brookline, MA 02146.

This article has been cited by other articles:

• Jenkins, K. J., Correa, A., Feinstein, J. A., Botto, L., Britt, A. E., Daniels, S. R., Elixson, M., Warnes, C. A., Webb, C. L. (2007). Noninherited Risk Factors and Congenital Cardiovascular Defects: Current Knowledge: A Scientific Statement From the American Heart Association Council on Cardiovascular Disease in the Young: Endorsed by the American Academy of Pediatrics. Circulation 115: 2995-3014 [Abstract] [Full Text]  
• Li, D.-K., Liu, L., Odouli, R. (2003). Exposure to non-steroidal anti-inflammatory drugs during pregnancy and risk of miscarriage: population based cohort study. BMJ 327: 368- [Abstract] [Full Text]  
• Coomarasamy, A., Honest, H., Papaioannou, S., Gee, H., Khan, K. S. (2003). Aspirin for Prevention of Preeclampsia in Women With Historical Risk Factors: A Systematic Review. Obstet Gynecol 101: 1319-1332 [Abstract] [Full Text]  
• Nielsen, G. L., Sørensen, H. T., Larsen, H., Pedersen, L. (2001). Risk of adverse birth outcome and miscarriage in pregnant users of non-steroidal anti-inflammatory drugs: population based observational study and case-control study. BMJ 322: 266-270 [Abstract] [Full Text]  
• Siu, S.S.N., Yeung, J.H.K., Lau, T.K. (2000). A study on placental transfer of diclofenac in first trimester of human pregnancy. Hum Reprod 15: 2423-2425 [Abstract] [Full Text]  
• Koren, G., Pastuszak, A., Ito, S. (1998). Drugs in Pregnancy. NEJM 338: 1128-1137 [Full Text]  
• Badui, E., Enciso, R. (1996). Acute Myocardial Infarction During Pregnancy and Puerperium Review. ANGIOLOGY 47: 739-756 [Abstract]