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A multilocus genetic risk score for coronary heart disease: case-control and prospective cohort analyses.

Ripatti S, Tikkanen E, Orho-Melander M, Havulinna AS, Silander K, Sharma A, Guiducci C, Perola M, Jula A, Sinisalo J, Lokki ML, Nieminen MS, Melander O, Salomaa V, Peltonen L, Kathiresan S - Lancet (2010)

Bottom Line: Adjustment for family history did not change these estimates.Genetic risk score did not improve C index over traditional risk factors and family history (p=0·19), nor did it have a significant effect on net reclassification improvement (2·2%, p=0·18); however, it did have a small effect on integrated discrimination index (0·004, p=0·0006).The Wellcome Trust; Academy of Finland Center of Excellence for Complex Disease Genetics; US National Institutes of Health; the Donovan Family Foundation.

View Article: PubMed Central - PubMed

Affiliation: Institute for Molecular Medicine Finland FIMM, University of Helsinki, Helsinki, Finland. samuli.ripatti@fi mm.fi

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Distributions at baseline of genetic risk score, LDL cholesterol, systolic blood pressure, and log-transformed C-reactive protein by 10-year incident coronary heart disease event status in FINRISK 1992 and 1997 cohortsData for C-reactive protein only available in FINRISK 1997. CHD=coronary heart disease.
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f10: Distributions at baseline of genetic risk score, LDL cholesterol, systolic blood pressure, and log-transformed C-reactive protein by 10-year incident coronary heart disease event status in FINRISK 1992 and 1997 cohortsData for C-reactive protein only available in FINRISK 1997. CHD=coronary heart disease.

Mentions: The genetic risk score conferred risk comparable to other established risk factors such as plasma LDL cholesterol (HR 2·08, 95% CI 1·57–2·76, for top vs bottom quintile of LDL cholesterol in FINRISK studies), systolic blood pressure (HR 1·66, 95% CI 1·19–2·30, for top vs bottom quintile of systolic blood pressure in FINRISK studies), or plasma C-reactive protein (HR 1·79, 95% CI 1·15–2·80, for top vs bottom quintile in FINRISK studies). Although the group means were statistically different, the distribution of each quantitative risk factor between those who went on to develop coronary heart disease and those who did not was broadly overlapping (figure).


A multilocus genetic risk score for coronary heart disease: case-control and prospective cohort analyses.

Ripatti S, Tikkanen E, Orho-Melander M, Havulinna AS, Silander K, Sharma A, Guiducci C, Perola M, Jula A, Sinisalo J, Lokki ML, Nieminen MS, Melander O, Salomaa V, Peltonen L, Kathiresan S - Lancet (2010)

Distributions at baseline of genetic risk score, LDL cholesterol, systolic blood pressure, and log-transformed C-reactive protein by 10-year incident coronary heart disease event status in FINRISK 1992 and 1997 cohortsData for C-reactive protein only available in FINRISK 1997. CHD=coronary heart disease.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2965351&req=5

f10: Distributions at baseline of genetic risk score, LDL cholesterol, systolic blood pressure, and log-transformed C-reactive protein by 10-year incident coronary heart disease event status in FINRISK 1992 and 1997 cohortsData for C-reactive protein only available in FINRISK 1997. CHD=coronary heart disease.
Mentions: The genetic risk score conferred risk comparable to other established risk factors such as plasma LDL cholesterol (HR 2·08, 95% CI 1·57–2·76, for top vs bottom quintile of LDL cholesterol in FINRISK studies), systolic blood pressure (HR 1·66, 95% CI 1·19–2·30, for top vs bottom quintile of systolic blood pressure in FINRISK studies), or plasma C-reactive protein (HR 1·79, 95% CI 1·15–2·80, for top vs bottom quintile in FINRISK studies). Although the group means were statistically different, the distribution of each quantitative risk factor between those who went on to develop coronary heart disease and those who did not was broadly overlapping (figure).

Bottom Line: Adjustment for family history did not change these estimates.Genetic risk score did not improve C index over traditional risk factors and family history (p=0·19), nor did it have a significant effect on net reclassification improvement (2·2%, p=0·18); however, it did have a small effect on integrated discrimination index (0·004, p=0·0006).The Wellcome Trust; Academy of Finland Center of Excellence for Complex Disease Genetics; US National Institutes of Health; the Donovan Family Foundation.

View Article: PubMed Central - PubMed

Affiliation: Institute for Molecular Medicine Finland FIMM, University of Helsinki, Helsinki, Finland. samuli.ripatti@fi mm.fi

Show MeSH
Related in: MedlinePlus