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Association of Plasma γ' Fibrinogen With Incident Cardiovascular Disease: The Atherosclerosis Risk in Communities (ARIC) Study.

TitleAssociation of Plasma γ' Fibrinogen With Incident Cardiovascular Disease: The Atherosclerosis Risk in Communities (ARIC) Study.
Publication TypeJournal Article
Year of Publication2015
AuthorsAppiah D, Schreiner PJ, Maclehose RF
Secondary AuthorsFolsom AR
JournalArterioscler Thromb Vasc Biol
Volume35
Issue12
Pagination2700-6
Date Published2015 Dec
ISSN1524-4636
KeywordsAged, Atherosclerosis, Biomarkers, C-Reactive Protein, Coronary Disease, Female, Fibrinogens, Abnormal, Heart Failure, Humans, Incidence, Inflammation Mediators, Kaplan-Meier Estimate, Male, Middle Aged, Peripheral Arterial Disease, Prognosis, Proportional Hazards Models, Prospective Studies, Risk Assessment, Risk Factors, Stroke, Time Factors, United States
Abstract

OBJECTIVES: To prospectively examine the association of plasma γ' fibrinogen with the incidence of multiple cardiovascular disease (CVD) end points, independent of established CVD risk factors, total fibrinogen, and other inflammatory markers.

APPROACH AND RESULTS: The Atherosclerosis Risk in Communities (ARIC) study measured γ' fibrinogen by enzyme-linked immunosorbent assay in stored plasma samples from 1993 to 1995 and related levels in 10 601 adults to incident CVD end points (coronary heart disease [n=1603], ischemic stroke [n=548], peripheral artery disease [n=599], heart failure [n=1411], and CVD mortality [n=705]) through 2012 (median follow-up, 18 years). In Cox models accounting for established CVD risk factors and total fibrinogen levels, γ' fibrinogen was associated positively with peripheral artery disease (hazard ratio [HR] per 1-SD [8.80 mg/dL] increment, 1.14 [1.04-1.24]), heart failure (HR, 1.06 [1.01-1.13]), and CVD deaths (HR, 1.12 [1.04-1.21]) but not with incident coronary heart disease (HR, 1.01 [0.96-1.07]) or ischemic stroke (HR, 0.98 [0.89-1.07]). Additional adjustment for C-reactive protein, however, eliminated the associations with peripheral artery disease and heart failure.

CONCLUSIONS: These findings do not lend support to the hypothesis that γ' fibrinogen influences CVD events through its prothrombotic properties. Rather, γ' fibrinogen concentrations seem to reflect general inflammation that accompanies and may contribute to atherosclerotic CVD, instead of γ' fibrinogen being a causal risk factor.

DOI10.1161/ATVBAHA.115.306284
Alternate JournalArterioscler Thromb Vasc Biol
PubMed ID26494231
PubMed Central IDPMC4662615
Grant ListHHSN268201100012C / HL / NHLBI NIH HHS / United States
HHSN268201100009I / HL / NHLBI NIH HHS / United States
HHSN268201100010C / HL / NHLBI NIH HHS / United States
HHSN268201100008C / HL / NHLBI NIH HHS / United States
HHSN268201100005G / HL / NHLBI NIH HHS / United States
HHSN268201100008I / HL / NHLBI NIH HHS / United States
HHSN268201100005C / / PHS HHS / United States
R01 HL059367 / HL / NHLBI NIH HHS / United States
HHSN268201100007C / HL / NHLBI NIH HHS / United States
HHSN268201100009C / / PHS HHS / United States
HHSN268201100011I / HL / NHLBI NIH HHS / United States
HHSN268201100011C / HL / NHLBI NIH HHS / United States
HHSN268201100010C / / PHS HHS / United States
T32 HL007779 / HL / NHLBI NIH HHS / United States
HHSN268201100006C / HL / NHLBI NIH HHS / United States
HHSN268201100008C / / PHS HHS / United States
HHSN268201100012C / / PHS HHS / United States
HHSN268201100005I / HL / NHLBI NIH HHS / United States
HHSN268201100007C / / PHS HHS / United States
HHSN268201100009C / HL / NHLBI NIH HHS / United States
HHSN268201100011C / / PHS HHS / United States
HHSN268201100005C / HL / NHLBI NIH HHS / United States
HHSN268201100007I / HL / NHLBI NIH HHS / United States
HHSN268201100006C / / PHS HHS / United States
T32HL007779 / HL / NHLBI NIH HHS / United States