Abstract
Abstract 3178
HMG CoA reductase inhibitors (statins) were recently reported to reduce the rate of venous thromboembolism (VTE) in healthy people. Statins reduce levels of inflammation biomarkers, however the mechanism for a reduction in VTE risk is unknown. We studied cross-sectional associations of statin use with hemostatic factors related to venous thrombosis risk in a large cohort of healthy people.
Cross-sectional analyses were performed in the Multi-Ethnic Study of Atherosclerosis (MESA), a cohort study of 6814 healthy men and women age 45–84, free of clinical cardiovascular disease at baseline; 1001 were using statins. Twenty three warfarin users were excluded. Age, race, and sex-adjusted mean hemostatic factor levels were compared between statin users and nonusers, and multivariable linear regression models were used to assess associations of statin use with hemostasis factors, adjusted for age, race/ethnicity, education, income, hormone replacement therapy (in women) and major cardiovascular risk factors.
The table shows that those using statins had significantly lower levels of D-dimer, C-reactive protein and factor VIII than non-users. Homocysteine and von Willebrand factor did not differ by statin use. Specific adjustment for LDL and triglycerides did not attenuate the observed differences in these factors by statin use.
Findings of lower D-dimer, factor VIII and C-reactive protein levels with statin use suggest mechanisms whereby statins might lower VTE risk. These associations were not explained by lipid levels on treatment. A prospective study linking these biochemical differences to VTE outcomes is warranted.
Adjusted mean hemostatic factor levels by statin use
| Factor . | Nonuse . | Statin use . | P . |
|---|---|---|---|
| D–dimer* | |||
| Model 1 | 0.22 | 0.21 | 0.05 |
| Model 2 | 0.22 | 0.20 | 0.002 |
| Factor VIII | |||
| Model 1 | 163 | 164 | 0.90 |
| Model 2 | 164 | 158 | 0.02 |
| Homocysteine* | |||
| Model 1 | 8.85 | 8.79 | 0.54 |
| Model 2 | 8.87 | 8.71 | 0.08 |
| CRP* | |||
| Model 1 | 1.94 | 1.67 | <.0001 |
| Model 2 | 1.97 | 1.55 | <0.001 |
| vWF | |||
| Model 1 | 141 | 138 | 0.66 |
| Model 2 | 140 | 135 | 0.33 |
| Factor . | Nonuse . | Statin use . | P . |
|---|---|---|---|
| D–dimer* | |||
| Model 1 | 0.22 | 0.21 | 0.05 |
| Model 2 | 0.22 | 0.20 | 0.002 |
| Factor VIII | |||
| Model 1 | 163 | 164 | 0.90 |
| Model 2 | 164 | 158 | 0.02 |
| Homocysteine* | |||
| Model 1 | 8.85 | 8.79 | 0.54 |
| Model 2 | 8.87 | 8.71 | 0.08 |
| CRP* | |||
| Model 1 | 1.94 | 1.67 | <.0001 |
| Model 2 | 1.97 | 1.55 | <0.001 |
| vWF | |||
| Model 1 | 141 | 138 | 0.66 |
| Model 2 | 140 | 135 | 0.33 |
Model 1 = Adjusted for age, sex, education, individual income, race.
Model 2 = Model 1 + adjustment for smoking, current alcohol use, body–mass index, diabetes, hypertension, low density lipoprotein cholesterol, triglycerides, insulin, postmenopausal hormone use (in women) and regular aspirin use.
Geometric means reported.
No relevant conflicts of interest to declare.
Author notes
Asterisk with author names denotes non-ASH members.
