BackgroundRed cell distribution width (RDW), a measure of the variability in size of circulating erythrocytes, is associated with mortality and adverse outcome in selected populations with cardiovascular disease. It is scarcely known whether RDW is associated with incident myocardial infarction (MI). We aimed to investigate whether RDW was associated with risk of first‐ever MI in a large cohort study with participants recruited from a general population.Methods and ResultsBaseline characteristics, including RDW, were collected for 25 612 participants in the Tromsø Study in 1994–1995. Incident MI during follow‐up was registered from inclusion through December 31, 2010. Cox regression models were used to calculate hazard ratios with 95% confidence intervals for MI, adjusted for age, sex, body mass index, smoking, hemoglobin, white blood cells, platelets, and other traditional cardiovascular risk factors. A total of 1779 participants experienced a first‐ever MI during a median follow‐up time of 15.8 years. There was a linear association between RDW and risk of MI, for which a 1% increment in RDW was associated with a 13% increased risk (hazard ratio 1.13; 95% CI, 1.07 to 1.19). Participants with RDW above the 95th percentile had 71% higher risk of MI compared with those with RDW in the lowest quintile (hazard ratio 1.71; 95% CI, 1.34 to 2.20). All effect estimates were essentially similar after exclusion of participants with anemia (n=1297) from the analyses.ConclusionRDW is associated with incident MI in a general population independent of anemia and cardiovascular risk factors.
Red cell distribution width (RDW), a measure of the variability in size of the circulating erythrocytes, is associated with cardiovascular morbidity and mortality. We aimed to investigate whether RDW was associated with incident stroke and case fatality in subjects recruited from the general population. Baseline characteristics were obtained from 25,992 subjects participating in the fourth survey of the Tromsø Study, conducted in 1994/95. Incident stroke was registered from inclusion until December 31, 2010. Cox regression models were used to calculate hazard ratios (HR) with 95% confidence intervals (95% CI) for stroke, adjusted for age, sex, body mass index, smoking, haemoglobin level, white blood cell count, thrombocyte count, hypertension, total cholesterol, triglycerides, self-reported diabetes, and red blood cell count. During a median follow-up of 15.8 years, 1152 participants experienced a first-ever stroke. A 1% increment in RDW yielded a 13% higher risk of stroke (multivariable HR: 1.13, 95% CI: 1.07-1.20). Subjects with RDW in the highest quintile compared to the lowest had a 37% higher risk of stroke in multivariable analysis (HR: 1.37, 95% CI: 1.11-1.69). Subjects with RDW above the 95-percentile had 55% higher risk of stroke compared to those in the lowest quintile (HR: 1.55, 95% CI: 1.16-2.06). All risk estimates remained unchanged after exclusion of subjects with anaemia (n=1102). RDW was not associated with increased risk of death within one year or during the entire follow-up after an incident stroke. RDW is associated with incident stroke in a general population, independent of anaemia and traditional atherosclerotic risk factors.
Recent studies suggest an association between red cell distribution width (RDW) and incident venous thromboembolism (VTE). We aimed to investigate the impact of RDW on risk of incident and recurrent VTE, and case-fatality, in a general population. RDW was measured in 26,223 participants enrolled in the Tromsø Study in 1994-1995. Incident and recurrent VTE events and deaths during follow-up were registered until January 1, 2012. Multivariate Cox proportional hazards regression models were used to calculate hazard ratios (HR) with 95% confidence intervals (CI). There were 647 incident VTE events during a median of 16.8 years of follow-up. Individuals with RDW in the highest quartile (RDW≥13.3%) had 50% higher risk of an incident VTE than those in the lowest quartile (RDW≤12.3%). The association was strongest for unprovoked deep-vein thrombosis (HR highest vs lowest quartile of RDW: 1.8, 95% CI 1.1-3.1). VTE patients with baseline RDW≥13.3% had 30% higher risk of all-cause mortality after the initial VTE event than VTE patients with RDW<13.3%. There were no association between RDW and risk of recurrent VTE. Our findings suggest that high RDW is a risk factor of incident VTE, and that RDW is a predictor of all-cause mortality in VTE patients.
Key Points• Iron deficiency may explain the association between RDW and risk of VTE.• Contrary to the hypothesis, increasing plasma levels of hepcidin, a biomarker of iron stores, were associated with increased risk of VTE.Red cell distribution width (RDW) is associated with venous thromboembolism (VTE), but the underlying mechanism(s) is unclear. Iron deficiency is associated with high RDW, and studies suggest an association between iron deficiency and VTE. To assess whether iron deficiency is a risk factor for VTE that explains the association between RDW and VTE, we conducted a nested case-control study of 390 patients with VTE and 802 age-and sex-matched controls selected from the population-based cohort of the Tromsø Study. Physical measurements and blood samples were collected from 1994 to 1995. Logistic regression models were used to calculate odds ratios (ORs) with 95% confidence intervals (CIs) for VTE by RDW, hepcidin, and ferritin light chain (FtL). RDW was inversely associated with hepcidin, FtL, and hemoglobin. The risk of VTE increased linearly across categories of higher plasma hepcidin levels. Participants with hepcidin in the highest quartile had an OR for VTE of 1.32 (95% CI, 1.00-2.42), and those in the .90% percentile had an OR for VTE of 1.66 (95% CI, 1.14-2.42) compared with the reference group (quartiles 2 and 3).The risk estimates remained similar after adjustment for C-reactive protein. The risk of VTE increased by categories of higher RDW and was strengthened after inclusion of hepcidin and FtL in the multivariable model. Our findings reject the hypothesis that iron deficiency explains the association between RDW and VTE and suggest, in contrast, that high body iron levels might increase the risk of VTE.
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