Genetics of Ultrasonographic Carotid Atherosclerosis

Arteriosclerosis, Thrombosis, and Vascular Biology - Tập 24 Số 9 - Trang 1567-1577 - 2004
Teri A. Manolio1,2,3,4, Eric Boerwinkle1,2,3,4, Christopher J. O’Donnell1,2,3,4, Alexander F. Wilson1,2,3,4
1From the Division of Epidemiology and Clinical Applications (T.A.M., C.J.O.), National Heart, Lung, and Blood Institute, Bethesda, Md; the Human Genetics Center (E.B.), University of Texas Health Science Center at Houston, Houston, Tex; the National Heart, Lung, and Blood Institute Framingham Heart Study (C.J.O.), Framingham, Mass; and the Inherited Disease Research Branch (A.F.W.), National Human Genome Research Institute, Baltimore, Md.
2the Human Genetics Center (E.B.), University of Texas Health Science Center at Houston, Houston, Tex
3the Inherited Disease Research Branch (A.F.W.), National Human Genome Research Institute, Baltimore, Md.
4the National Heart, Lung, and Blood Institute Framingham Heart Study (C.J.O.), Framingham, Mass

Tóm tắt

The search for genes related to the cause of common complex disorders such as cardiovascular disease has been frustrating, partly because of the many factors known to contribute to cardiovascular disease and the potential “distance” of cardiovascular disease as a phenotype from genes and gene products. Linkage and association studies for phenotypes more proximal in the pathway from DNA sequence variation to overt clinical disease, such as ultrasound-defined carotid atherosclerosis, may potentially be more enlightening. Only one genetic variant previously reported to be associated with atherosclerosis or clinically evident cardiovascular disease, matrix metalloproteinase (MMP) 3, has shown consistently positive associations with carotid disease, although it has not been studied widely. Another, PON1 L55M, is weakly associated in subgroups only, and 2, ApoE and MTHFR, are equivocal. Genetic variants reported to be associated with clinical cardiovascular disease show weak or no relationship to carotid atherosclerosis. This may reflect the known inconsistency in associations of genetic variants with clinical cardiovascular disease itself. Alternatively, genetic determinants of ultrasound-defined carotid atherosclerosis may differ from those of clinically manifest cardiovascular disease and may require pursuit through large-scale genomic studies of carotid atherosclerosis as a distinct phenotype.

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Arteriosclerosis, Thrombosis, and Vascular Biology

Tập 24 Số 9

1567-1577

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