Platelet function as a risk factor for venous thromboembolism in the Framingham Heart Study.
BACKGROUND
The relationship of venous thromboembolism (VTE) with platelet reactivity is unclear. Platelet function plays a key role in arterial thrombosis. Evidence suggests antiplatelet agents also effects in reducing VTE. Our aim is to describe the role of baseline platelet function in development of VTE in the community-based Framingham Heart Study (FHS) cohort.


METHODS
Participants in the Framingham Offspring cohort fifth examination and Omni cohort first examination were eligible. We used light transmission aggregometry to measure platelet aggregation in response to collagen and a range of ADP and epinephrine doses. The study population consisted of 2831 participants [average age 54.3years; 57% female].


CONCLUSIONS
During a median follow-up of 20.4years, we observed 138 incident VTE events. In age-, sex- and cohort-adjusted analysis an increase in collagen lag time was associated with increased risk for incident VTE (HR 1.01 [1.00-1.02]; p=0.049). Increased maximal aggregation to low dose epinephrine (1.0μM) was associated with lower VTE risk (HR 0.84 [0.71-0.99]; p=0.042]). However, additional multivariable analyses attenuated the collagen-VTE and epinephrine-VTE associations to trends, primarily due to adjustment for baseline body mass index (BMI), a VTE risk factor and potential modifier of platelet function. Secondary analyses considering varying follow-up periods, cancer incidence and interim aspirin use did not dramatically affect the collagen and epinephrine trends observed. Baseline platelet aggregability was only weakly associated with incident VTE, and in a paradoxical direction, in a community-based population. Other markers of platelet function and hemostasis could prove to be more useful predictors.
Framingham Heart Study of Boston University School of Medicine and NHLBI, Framingham, MA, USA.
Marja K
MK
Puurunen
Framingham Heart Study of Boston University School of Medicine and NHLBI, Framingham, MA, USA; Population Sciences Branch, Division of Intramural Research, NHLBI, NIH, Bethesda, MD, USA.
Shih-Jen
SJ
Hwang
Framingham Heart Study of Boston University School of Medicine and NHLBI, Framingham, MA, USA; Population Sciences Branch, Division of Intramural Research, NHLBI, NIH, Bethesda, MD, USA; Cardiology Section, Department of Medicine, Boston Veteran's Administration Healthcare, Boston, MA, USA.
Chris J
CJ
O'Donnell
Department of Cardiology, Royal North Shore Hospital, University of Sydney, Australia.
Geoffrey
G
Tofler
Framingham Heart Study of Boston University School of Medicine and NHLBI, Framingham, MA, USA; Population Sciences Branch, Division of Intramural Research, NHLBI, NIH, Bethesda, MD, USA. Electronic address: johnsonad2@nhlbi.nih.gov.
Andrew D
AD
Johnson
D000328:Adult; D001792:Blood Platelets / Q000473:pathology*; D005260:Female; D006487:Hemostasis; D006801:Humans; D015994:Incidence; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation; D010979:Platelet Function Tests; D012307:Risk Factors; D054556:Venous Thromboembolism / Q000097:blood / Q000209:etiology* / Q000473:pathology
Deep vein thrombosis; Platelet aggregation; Platelet function tests; Platelets; Pulmonary embolism; Venous thromboembolism