In whites, the mean ± SD, median and inter-quartile range for sICAM-1 (ng/ml) are 246.7 ± 78.6, 231.3, and 195.1~281.6, respectively, and for MCP-1 (pg/ml) were 189.1 ± 60.5, 180.2, and 149.9~218.9, respectively. In African Americans, the mean ± SD, median and inter-quartile range for MCP-1 (pg/ml) were 174.3 ± 68.3, 168.2, and 136.5~195.0, respectively. The mean level of MCP-1 was significantly lower in African Americans than in whites, and this difference persisted after adjusting for age, gender, BMI, SBP, diabetes, HDL and LDL cholesterol, triglycerides, physical activity index (met-min/week), hours of television watched/day, smoking status (current, former, never), pack-years of smoking, current alcohol consumption, and hormone replacement therapy (p < 0.01). The prevalence of hypertension was 39.3% in whites and 75.1% in African Americans.
Table shows demographic and clinical characteristics of subjects by CAC status. Compared to subjects with zero calcium score, subjects with detectable calcium were older and more likely to be males, current or former smokers, and have hypertension and diabetes. All of the other risk factors, except race, LDL cholesterol, current alcohol consumption, and aspirin use, were also significantly associated with CAC status.
Demographic and clinical characteristics by CAC status: mean ± SD or percentage
Table presents partial Spearman correlation coefficients of MCP-1 and sICAM-1 with continuous covariates. Due to smaller sample size, the correlations between MCP-1 and the continuous covariates were generally less significant in African Americans than in whites. However, the pattern of correlations agreed between the two racial groups for most of the covariates except that MCP-1 was less strongly associated with BMI, SBP, and physical activity index in African Americans.
Adjusted* spearman correlation coefficients of sICAM-1 and MCP-1 with continuous covariates
Table presents adjusted geometric means of MCP-1 and sICAM-1 by categorical covariates. The pattern of associations between MCP-1 and the categorical covariates were consistent between the two racial groups. It is interesting to note that at each level of the categorical variables, mean MCP-1 was consistently lower in African Americans than in whites, further confirming our earlier observation that African Americans had lower levels of MCP-1 compared to whites.
Adjusted geometric means* (95% confidence interval) of sICAM-1 and MCP-1 by categorical covariates
Tables and present ORs of presence of CAC by quintiles of sICAM-1 and MCP-1, respectively, in whites. Based on a criterion of CAC score > 0, coronary calcification was present in 55% (1239) of subjects. When the cut point was raised to CAC ≥ 10, the prevalence of CAC was 37%. There was a significant and positive association between the presence of CAC, sICAM-1 and MCP-1 before and after adjusting for age and gender (Tables and ). This association was consistent for both the CAC > 0 and CAC ≥ 10 criteria. However, after additionally adjusting for other CHD risk factors, the association between CAC and sICAM-1 was no longer significant whether CAC > 0 or CAC ≥ 10 were analyzed as an outcome (Table ). In the multivariable adjustment models, the association between CAC and MCP-1 was borderline significant for CAC > 0 and not significant for CAC ≥ 10 (Table ).
Odds ratios (95% Confidence Interval) of CAC > 0 or CAC ≥ 10 by sICAM-1 quintile in whites
Odds ratios (95% confidence interval) of CAC > 0 or CAC ≥ 10 by MCP-1 quintile in whites
Table presents ORs of presence of CAC by tertiles of MCP-1 in African Americans, in which the percentage of CAC > 0 and CAC ≥ 10 was 48% and 31%, respectively. Similar to whites, MCP-1 was positively associated with the presence of CAC in unadjusted models. This association was no longer significant after adjustment for age and gender or additional adjustment for other CHD risk factors. Figure shows prevalence of CAC (%) across MCP-1 tertiles in African Americans in comparison to whites, in which MCP-1 tertile cutpoints from African Americans were used to group participants. As shown in Figure , the prevalence of CAC > 0 or CAC ≥ 10 increased with MCP-1 in a similar fashion between African Americans and whites; consistent with this observation, tests of interactions did not detect significant interactions of race on the associations between MCP-1 and CAC in raw (no adjustment), partial or multivariate adjustment models (p > 0.05).
Odds ratios (95% Confidence Interval) of CAC > 0 or CAC ≥ 10 by MCP-1 tertile in African Americans
Figure 1 Prevalence of CAC (%) across MCP-1 tertiles by race. The three bar pairs on the left hand side are for CAC > 0 and those on the right hand side are for CAC ≥ 10. The tertile cutpoints for MCP-1 were based on the African-American sample (more ...)
Among whites with CAC > 0, there was a positive trend between the amount of CAC and levels of sICAM-1 and MCP-1. However, this association did not reach statistical significance in either partial or multivariable adjustment models (data not shown).
The above results did not change materially after we substituted hypertension for SBP, waist circumference for BMI, and fasting glucose for diabetes in the multivariable adjustment models. Finally, since it is of concern that measurement errors in the estimated LDL cholesterol for those with triglycerides > 400 mg/dL may affect our ability to control for confounding, we replaced LDL cholesterol by total cholesterol in the multivariable analyses and all results were similar (data not shown).