RESUMO
BACKGROUND: There is an independent association between white blood cell (WBC) and coronary heart disease (CHD) risk. However, the relationship between WBC and Framingham Risk Score (FRS) remains unclear. METHODS: This is a cross-sectional study on a consecutive sample of 520 white asymptomatic men (mean age 46 +/- 7 years) without CHD. The study population was divided into WBC quartiles (x10(9) cells/L): 1(st) quartile: 3.1-5.3 (n = 139), 2(nd) quartile: 5.4-6.1 (n = 129), 3(rd) quartile: 6.2-7.1 (n = 131), 4(th) quartile: >/=7.2 (n = 121), and into tertiles according to the 10-year FRS: 1(st) tertile (low risk <5%, n = 180, 35%), 2(nd) tertile (intermediate risk 5-12%, n = 210, 40%), 3(rd) tertile (high risk: >/=13%, n = 130, 25%). RESULTS: WBC correlated only weakly with FRS (r = 0.18, p = 0.001). Among individual components of FRS, WBC correlated minimally with smoking (r = 0.12, p = 0.003), systolic blood pressure (r = 0.07, p = 0.1), and high-density lipoprotein cholesterol (r = -0.06, p = 0.1). However, no correlation was observed with age (p = 0.3) and total cholesterol (p = 0.5). Nearly one third (31%) of men in the low-risk (FRS <5%) had WBC count in the 1(st) quartile compared to 20% of those classified as high risk (FRS >/=13%). The prevalence of WBC in the 4(th) quartile increased across FRS tertiles (18, 22, 32%) (p = 0.09). CONCLUSIONS: WBC correlates weakly with FRS or its individual components. Since WBC count is strongly related to CHD, WBC may reflect different components of cardiovascular risk, which might not be captured by traditional cardiovascular risk factors used in calculating FRS. Inflammatory biomarkers afford adjunctive value to FRS and may be used to improve CHD risk stratification.
Assuntos
Doença das Coronárias/epidemiologia , Contagem de Leucócitos , Adulto , Biomarcadores/sangue , Brasil/epidemiologia , Colesterol/sangue , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de RiscoRESUMO
The objective of this study was to evaluate whether uric acid (UA) levels were associated with coronary artery calcium (CAC) in white men asymptomatic for coronary heart disease. We also evaluated whether this relation was dependent or not on the presence of the metabolic syndrome (MS). The study population consisted of 371 asymptomatic Brazilian men (48 +/- 7 years of age) who underwent a routine evaluation. The average 10-year total risk of coronary heart disease calculated by Framingham risk score was 10.8 +/- 7.8%. The age-adjusted prevalence of CAC in patients with a high UA level (fourth quartile > or =7.1 mg/dl, n = 91) was significantly higher than that in those with a normal UA level (58% vs 44%, p = 0.02). With respect to age, smoking, physical activity, and components of MS-adjusted analyses, a high UA level was independently associated with the presence of CAC (p = 0.043) and with increasing levels of CAC (p = 0.028). Prevalence of MS showed a graded increase according to serum UA values. In patients with the MS, after adjusting for age, smoking, physical activity, and white blood cell count, high levels of UA were strongly associated with the presence of any CAC (odds ratio 3.47, 95% confidence interval 1.26 to 9.53, p = 0.01) and with increasing levels of CAC (odds ratio 2.74, 95% confidence interval 1.15 to 6.50, p = 0.02). Conversely, there was no significant association of high UA levels in patients without the MS. However, the interaction between high UA level and the MS did not achieve statistical significance for the presence of CAC (p = 0.11) or higher levels of CAC (p = 0.16). In conclusion, our study suggests that, among asymptomatic moderate-risk men, high UA levels were independently associated with CAC in subjects with the MS.