Figure 1.
Figure 1. Elevation of ECP serves as a marker for CVD in humans. (A and B) Forest plots of the prospective association of baseline ECP with events of CVD (A) and early and advanced atherosclerosis (B) in the Bruneck Study (follow-up 2000 to 2010). All analyses were adjusted for age, sex, and prior CVD. Analyses focusing on ultrasound endpoints were adjusted to the extent of baseline atherosclerosis (log-transformed atherosclerosis summation score). Squares and lines represent hazard ratios of events and 95% confidence intervals (CI). Hazard ratios were derived from Cox regression models and calculated for a 1-SD–higher level of ECP. Composite CVD events considered ischemic strokes, medical record–confirmed TIAs, myocardial infarctions, and vascular deaths. Mean and median follow-ups were 8.6 and 10 yr. The extended CVD events additionally considered revascularization procedures. *, This analysis is confined to 277 individuals free of atherosclerosis at baseline and focused on the manifestation of first carotid plaques. †, This analysis considers all 558 individuals with ultrasound follow-up and focused on the manifestation of new carotid plaques. ‡, This analysis considers all 558 individuals with ultrasound follow-up and focused on both the manifestation of new carotid plaques and extension of existing ones. §, This analysis considers all 558 individuals with ultrasound follow-up and focused on the development of advanced complicated plaques (stenosis >40%). The second line is confined to 269 subjects with manifest baseline atherosclerosis. (C) Odds ratios/hazard ratios and 95% confidence intervals derived from logistic regression and Cox regression models and calculated for a 1-SD–higher level of ECP. The composite CVD endpoint included ischemic strokes, medical record–confirmed TIAs, myocardial infarctions, and vascular deaths. *, Multivariable models were additionally adjusted for hypertension, smoking (pack-years), diabetes, log-transformed C-reactive protein, body-mass index, and LDL and HDL cholesterol. †, Models with extended adjustment additionally included HbA1c, platelet, and lymphocyte counts. (D) Correlation pattern of ECP level with blood cell counts and demographic and vascular risk factors in the Bruneck Study (evaluation 2000; n = 682 including 354 women and 328 men). BP, blood pressure; GFR, glomerular filtration rate; HbA1c, glycated hemoglobin; HDL-C, HDL cholesterol; hs-CRP, high-sensitivity C-reactive protein; LDL-C, LDL cholesterol. Spearman correlation coefficients are given for all variables. Correlations that are statistically significant after correction for multiple comparisons (Bonferroni-corrected p-value <0.05) are in bold, and corresponding squares have covering colors.

Elevation of ECP serves as a marker for CVD in humans. (A and B) Forest plots of the prospective association of baseline ECP with events of CVD (A) and early and advanced atherosclerosis (B) in the Bruneck Study (follow-up 2000 to 2010). All analyses were adjusted for age, sex, and prior CVD. Analyses focusing on ultrasound endpoints were adjusted to the extent of baseline atherosclerosis (log-transformed atherosclerosis summation score). Squares and lines represent hazard ratios of events and 95% confidence intervals (CI). Hazard ratios were derived from Cox regression models and calculated for a 1-SD–higher level of ECP. Composite CVD events considered ischemic strokes, medical record–confirmed TIAs, myocardial infarctions, and vascular deaths. Mean and median follow-ups were 8.6 and 10 yr. The extended CVD events additionally considered revascularization procedures. *, This analysis is confined to 277 individuals free of atherosclerosis at baseline and focused on the manifestation of first carotid plaques. †, This analysis considers all 558 individuals with ultrasound follow-up and focused on the manifestation of new carotid plaques. ‡, This analysis considers all 558 individuals with ultrasound follow-up and focused on both the manifestation of new carotid plaques and extension of existing ones. §, This analysis considers all 558 individuals with ultrasound follow-up and focused on the development of advanced complicated plaques (stenosis >40%). The second line is confined to 269 subjects with manifest baseline atherosclerosis. (C) Odds ratios/hazard ratios and 95% confidence intervals derived from logistic regression and Cox regression models and calculated for a 1-SD–higher level of ECP. The composite CVD endpoint included ischemic strokes, medical record–confirmed TIAs, myocardial infarctions, and vascular deaths. *, Multivariable models were additionally adjusted for hypertension, smoking (pack-years), diabetes, log-transformed C-reactive protein, body-mass index, and LDL and HDL cholesterol. †, Models with extended adjustment additionally included HbA1c, platelet, and lymphocyte counts. (D) Correlation pattern of ECP level with blood cell counts and demographic and vascular risk factors in the Bruneck Study (evaluation 2000; n = 682 including 354 women and 328 men). BP, blood pressure; GFR, glomerular filtration rate; HbA1c, glycated hemoglobin; HDL-C, HDL cholesterol; hs-CRP, high-sensitivity C-reactive protein; LDL-C, LDL cholesterol. Spearman correlation coefficients are given for all variables. Correlations that are statistically significant after correction for multiple comparisons (Bonferroni-corrected p-value <0.05) are in bold, and corresponding squares have covering colors.

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