The association of c-reactive protein with arterial compliance in asymptomatic young adults: the bogalusa heart study

Atherogeneis is a chronic progressive syndrome caused by endothelial dysfunction, vascular inflammation, vessel wall remodeling and eventual vascular flow compromise. Emerging data suggest that arterial compliance inversely correlates with atherogenesis and cardiovascular (CV) events. However, infor...

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Published inJournal of human hypertension Vol. 27; no. 4; pp. 256 - 260
Main Authors Sharma, D, DasMahapatra, P, Fernandez, C, Chen, W, Srinivasan, S R, Xu, J, Berenson, G S
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.04.2013
Nature Publishing Group
Subjects
631/443/1338/243
692/420/256
692/499
692/699/75/593/2100
Adult
Age Factors
Aorta
Arteries - physiopathology
Asymptomatic
Asymptomatic Diseases
Atherogenesis
Atherosclerosis - blood
Atherosclerosis - ethnology
Atherosclerosis - immunology
Atherosclerosis - physiopathology
Biomarkers - blood
Black or African American
Blood pressure
C-reactive protein
C-Reactive Protein - analysis
Cardiovascular diseases
Compliance
Development and progression
Epidemiology
Female
Females
Genetic aspects
Health Administration
Humans
Inflammation
Inflammation Mediators - blood
Insulin
Insulin resistance
Least-Squares Analysis
Linear Models
Louisiana - epidemiology
Male
Males
Medicine
Medicine & Public Health
Multivariate Analysis
original-article
Physiological aspects
Public Health
Pulse Wave Analysis
Risk Assessment
Risk Factors
Sex differences
Vascular Stiffness
Veins & arteries
White People
Young adults
Louisiana
United States
hsCRP
vascular
compliance
Online AccessGet full text
ISSN0950-9240
1476-5527
1476-5527
DOI10.1038/jhh.2012.34

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Abstract Atherogeneis is a chronic progressive syndrome caused by endothelial dysfunction, vascular inflammation, vessel wall remodeling and eventual vascular flow compromise. Emerging data suggest that arterial compliance inversely correlates with atherogenesis and cardiovascular (CV) events. However, information is scant on the association of chronic systemic inflammation with arterial elasticity in young asymptomatic adults. The association of hsC-reactive protein (CRP) and central-vascular compliance was studied in 641 individuals (45.2% males; 71.8% whites), aged 31–43 years enrolled in the Bogalusa Heart Study. The measured variables included large-artery compliance (capacitive, C1), representative of the aorta and its major branches; and small-artery compliance (oscillatory, C2), representative of the distal part of the circulation; hsCRP, as a measure of systemic inflammation; along with traditional CV risk factor variables. Significant race and sex differences were noted for C1 (white males>black males P -value <0.0001; males>females P -value 0.04), C2 (whites>blacks P -value 0.0004; males>females P -value<0.0001) and hsCRP (blacks>whites P -value 0.03; females>males P -value 0.002). Mean values of C1 in subjects with high hsCRP levels (>3 mg l −1 ) were significantly lower than those with average (1–3 mg l −1 ) and low levels (<1 mg l −1 ) (14.2 ml per mmHg × 10 versus 15.2 ml per mm Hg × 10 versus 15.7 ml per mmHg × 10, P for trend=0.02), after adjusting for age, race, sex and body surface area (BSA). hsCRP showed a trend toward inverse correlation with C1 (−0.07, P =0.07) but no such trend for C2, after adjusting for race and sex. In the multivariate linear regression model, adding age, race, sex, BSA, mean arterial pressure, insulin resistance, lipoprotein variables and smoking status, the effect persisted between C1 and hsCRP ( β =−0.35, P =0.01). In an asymptomatic population of young adults, hsCRP predicts reduced large-artery compliance (C1). These findings support the role of systemic inflammation in early pathological changes in artery wall in atherogenesis. Small-artery compliance (C2) however did not correlate with hsCRP.
AbstractList Atherogeneis is a chronic progressive syndrome caused by endothelial dysfunction, vascular inflammation, vessel wall remodeling and eventual vascular flow compromise. Emerging data suggest that arterial compliance inversely correlates with atherogenesis and cardiovascular (CV) events. However, information is scant on the association of chronic systemic inflammation with arterial elasticity in young asymptomatic adults. The association of hsC-reactive protein (CRP) and central-vascular compliance was studied in 641 individuals (45.2% males; 71.8% whites), aged 31-43 years enrolled in the Bogalusa Heart Study. The measured variables included large-artery compliance (capacitive, C1), representative of the aorta and its major branches; and small-artery compliance (oscillatory, C2), representative of the distal part of the circulation; hsCRP, as a measure of systemic inflammation; along with traditional CV risk factor variables. Significant race and sex differences were noted for C1 (white males>black males P-value <0.0001; males>females P-value 0.04), C2 (whites>blacks P-value 0.0004; males>females P-value<0.0001) and hsCRP (blacks>whites P-value 0.03; females>males P-value 0.002). Mean values of C1 in subjects with high hsCRP levels (>3 mg l(-1)) were significantly lower than those with average (1-3 mg l(-1)) and low levels (<1 mg l(-1)) (14.2 ml per mmHg × 10 versus 15.2 ml per mm Hg × 10 versus 15.7 ml per mmHg × 10, P for trend=0.02), after adjusting for age, race, sex and body surface area (BSA). hsCRP showed a trend toward inverse correlation with C1 (-0.07, P=0.07) but no such trend for C2, after adjusting for race and sex. In the multivariate linear regression model, adding age, race, sex, BSA, mean arterial pressure, insulin resistance, lipoprotein variables and smoking status, the effect persisted between C1 and hsCRP (β=-0.35, P=0.01). In an asymptomatic population of young adults, hsCRP predicts reduced large-artery compliance (C1). These findings support the role of systemic inflammation in early pathological changes in artery wall in atherogenesis. Small-artery compliance (C2) however did not correlate with hsCRP.
Atherogeneis is a chronic progressive syndrome caused by endothelial dysfunction, vascular inflammation, vessel wall remodeling and eventual vascular flow compromise. Emerging data suggest that arterial compliance inversely correlates with atherogenesis and cardiovascular (CV) events. However, information is scant on the association of chronic systemic inflammation with arterial elasticity in young asymptomatic adults. The association of hsC-reactive protein (CRP) and central-vascular compliance was studied in 641 individuals (45.2% males; 71.8% whites), aged 31–43 years enrolled in the Bogalusa Heart Study. The measured variables included large-artery compliance (capacitive, C1), representative of the aorta and its major branches; and small-artery compliance (oscillatory, C2), representative of the distal part of the circulation; hsCRP, as a measure of systemic inflammation; along with traditional CV risk factor variables. Significant race and sex differences were noted for C1 (white males>black males P -value <0.0001; males>females P -value 0.04), C2 (whites>blacks P -value 0.0004; males>females P -value<0.0001) and hsCRP (blacks>whites P -value 0.03; females>males P -value 0.002). Mean values of C1 in subjects with high hsCRP levels (>3 mg l −1 ) were significantly lower than those with average (1–3 mg l −1 ) and low levels (<1 mg l −1 ) (14.2 ml per mmHg × 10 versus 15.2 ml per mm Hg × 10 versus 15.7 ml per mmHg × 10, P for trend=0.02), after adjusting for age, race, sex and body surface area (BSA). hsCRP showed a trend toward inverse correlation with C1 (−0.07, P =0.07) but no such trend for C2, after adjusting for race and sex. In the multivariate linear regression model, adding age, race, sex, BSA, mean arterial pressure, insulin resistance, lipoprotein variables and smoking status, the effect persisted between C1 and hsCRP ( β =−0.35, P =0.01). In an asymptomatic population of young adults, hsCRP predicts reduced large-artery compliance (C1). These findings support the role of systemic inflammation in early pathological changes in artery wall in atherogenesis. Small-artery compliance (C2) however did not correlate with hsCRP.
Atherogeneis is a chronic progressive syndrome caused by endothelial dysfunction, vascular inflammation, vessel wall remodeling and eventual vascular flow compromise. Emerging data suggest that arterial compliance inversely correlates with atherogenesis and cardiovascular (CV) events. However, information is scant on the association of chronic systemic inflammation with arterial elasticity in young asymptomatic adults. The association of hsC-reactive protein (CRP) and central-vascular compliance was studied in 641 individuals (45.2% males; 71.8% whites), aged 31–43 years enrolled in the Bogalusa Heart Study. The measured variables included large-artery compliance (capacitive, C1), representative of the aorta and its major branches; and small-artery compliance (oscillatory, C2), representative of the distal part of the circulation; hsCRP, as a measure of systemic inflammation; along with traditional CV risk factor variables. Significant race and sex differences were noted for C1 (white males>black males P-value <0.0001; males>females P-value 0.04), C2 (whites>blacks P-value 0.0004; males>females P-value<0.0001) and hsCRP (blacks>whites P-value 0.03; females>males P-value 0.002). Mean values of C1 in subjects with high hsCRP levels (>3 mg l−1) were significantly lower than those with average (1–3 mg l−1) and low levels (<1 mg l−1) (14.2 ml per mmHg × 10 versus 15.2 ml per mm Hg × 10 versus 15.7 ml per mmHg × 10, P for trend=0.02), after adjusting for age, race, sex and body surface area (BSA). hsCRP showed a trend toward inverse correlation with C1 (−0.07, P=0.07) but no such trend for C2, after adjusting for race and sex. In the multivariate linear regression model, adding age, race, sex, BSA, mean arterial pressure, insulin resistance, lipoprotein variables and smoking status, the effect persisted between C1 and hsCRP (β=−0.35, P=0.01). In an asymptomatic population of young adults, hsCRP predicts reduced large-artery compliance (C1). These findings support the role of systemic inflammation in early pathological changes in artery wall in atherogenesis. Small-artery compliance (C2) however did not correlate with hsCRP.
Atherogeneis is a chronic progressive syndrome caused by endothelial dysfunction, vascular inflammation, vessel wall remodeling and eventual vascular flow compromise. Emerging data suggest that arterial compliance inversely correlates with atherogenesis and cardiovascular (CV) events. However, information is scant on the association of chronic systemic inflammation with arterial elasticity in young asymptomatic adults. The association of hsC-reactive protein (CRP) and central-vascular compliance was studied in 641 individuals (45.2% males; 71.8% whites), aged 31-43 years enrolled in the Bogalusa Heart Study. The measured variables included large-artery compliance (capacitive, C1), representative of the aorta and its major branches; and small-artery compliance (oscillatory, C2), representative of the distal part of the circulation; hsCRP, as a measure of systemic inflammation; along with traditional CV risk factor variables. Significant race and sex differences were noted for C1 (white males > black males P-value <0.0001; males > females P-value 0.04), C2 (whites > blacks P-value 0.0004;males>females P-value<0.0001) and hsCRP (blacks > whites P-value 0.03;females> males P-value 0.002). Mean values of C1 in subjects with high hsCRP levels (>3 mg [l.sup.-1]) were significantly lower than those with average (1-3 mg [l.sup.-1]) and low levels (<1 mg [l.sup.-1]) (14.2 ml per mmHg x 10 versus 15.2 ml per mm Hg x 10 versus 15.7 ml per mmHg x 10, P for trend = 0.02), after adjusting for age, race, sex and body surface area (BSA). hsCRP showed a trend toward inverse correlation with C1 (-0.07, P = 0.07) but no such trend for C2, after adjusting for race and sex. In the multivariate linear regression model, adding age, race, sex, BSA, mean arterial pressure, insulin resistance, lipoprotein variables and smoking status, the effect persisted between C1 and hsCRP (β = 0.35, P = 0.01). In an asymptomatic population of young adults, hsCRP predicts reduced large-artery compliance (C1). These findings support the role of systemic inflammation in early pathological changes in artery wall in atherogenesis. Small-artery compliance (C2) however did not correlate with hsCRP. Journal of Human Hypertension (2013) 27, 256-260; doi: 10.1038/jhh.2012.34; published online 15 November 2012 Keywords: hsCRP; vascular; compliance
Atherogeneis is a chronic progressive syndrome caused by endothelial dysfunction, vascular inflammation, vessel wall remodeling and eventual vascular flow compromise. Emerging data suggest that arterial compliance inversely correlates with atherogenesis and cardiovascular (CV) events. However, information is scant on the association of chronic systemic inflammation with arterial elasticity in young asymptomatic adults. The association of hsC-reactive protein (CRP) and central-vascular compliance was studied in 641 individuals (45.2% males; 71.8% whites), aged 31-43 years enrolled in the Bogalusa Heart Study. The measured variables included large-artery compliance (capacitive, C1), representative of the aorta and its major branches; and small-artery compliance (oscillatory, C2), representative of the distal part of the circulation; hsCRP, as a measure of systemic inflammation; along with traditional CV risk factor variables. Significant race and sex differences were noted for C1 (white males > black males P-value <0.0001; males > females P-value 0.04), C2 (whites > blacks P-value 0.0004;males>females P-value<0.0001) and hsCRP (blacks > whites P-value 0.03;females> males P-value 0.002). Mean values of C1 in subjects with high hsCRP levels (>3 mg [l.sup.-1]) were significantly lower than those with average (1-3 mg [l.sup.-1]) and low levels (<1 mg [l.sup.-1]) (14.2 ml per mmHg x 10 versus 15.2 ml per mm Hg x 10 versus 15.7 ml per mmHg x 10, P for trend = 0.02), after adjusting for age, race, sex and body surface area (BSA). hsCRP showed a trend toward inverse correlation with C1 (-0.07, P = 0.07) but no such trend for C2, after adjusting for race and sex. In the multivariate linear regression model, adding age, race, sex, BSA, mean arterial pressure, insulin resistance, lipoprotein variables and smoking status, the effect persisted between C1 and hsCRP (β = 0.35, P = 0.01). In an asymptomatic population of young adults, hsCRP predicts reduced large-artery compliance (C1). These findings support the role of systemic inflammation in early pathological changes in artery wall in atherogenesis. Small-artery compliance (C2) however did not correlate with hsCRP.
Atherogeneis is a chronic progressive syndrome caused by endothelial dysfunction, vascular inflammation, vessel wall remodeling and eventual vascular flow compromise. Emerging data suggest that arterial compliance inversely correlates with atherogenesis and cardiovascular (CV) events. However, information is scant on the association of chronic systemic inflammation with arterial elasticity in young asymptomatic adults. The association of hsC-reactive protein (CRP) and central-vascular compliance was studied in 641 individuals (45.2% males; 71.8% whites), aged 31-43 years enrolled in the Bogalusa Heart Study. The measured variables included large-artery compliance (capacitive, C1), representative of the aorta and its major branches; and small-artery compliance (oscillatory, C2), representative of the distal part of the circulation; hsCRP, as a measure of systemic inflammation; along with traditional CV risk factor variables. Significant race and sex differences were noted for C1 (white males>black males P-value <0.0001; males>females P-value 0.04), C2 (whites>blacks P-value 0.0004; males>females P-value<0.0001) and hsCRP (blacks>whites P-value 0.03; females>males P-value 0.002). Mean values of C1 in subjects with high hsCRP levels (>3mgl(-1)) were significantly lower than those with average (1-3mgl(-1)) and low levels (<1mgl(-1)) (14.2ml per mmHg × 10 versus 15.2ml per mm Hg × 10 versus 15.7ml per mmHg × 10, P for trend=0.02), after adjusting for age, race, sex and body surface area (BSA). hsCRP showed a trend toward inverse correlation with C1 (-0.07, P=0.07) but no such trend for C2, after adjusting for race and sex. In the multivariate linear regression model, adding age, race, sex, BSA, mean arterial pressure, insulin resistance, lipoprotein variables and smoking status, the effect persisted between C1 and hsCRP ([beta]=-0.35, P=0.01). In an asymptomatic population of young adults, hsCRP predicts reduced large-artery compliance (C1). These findings support the role of systemic inflammation in early pathological changes in artery wall in atherogenesis. Small-artery compliance (C2) however did not correlate with hsCRP.
Atherogeneis is a chronic progressive syndrome caused by endothelial dysfunction, vascular inflammation, vessel wall remodeling and eventual vascular flow compromise. Emerging data suggest that arterial compliance inversely correlates with atherogenesis and cardiovascular (CV) events. However, information is scant on the association of chronic systemic inflammation with arterial elasticity in young asymptomatic adults. The association of hsC-reactive protein (CRP) and central-vascular compliance was studied in 641 individuals (45.2% males; 71.8% whites), aged 31-43 years enrolled in the Bogalusa Heart Study. The measured variables included large-artery compliance (capacitive, C1), representative of the aorta and its major branches; and small-artery compliance (oscillatory, C2), representative of the distal part of the circulation; hsCRP, as a measure of systemic inflammation; along with traditional CV risk factor variables. Significant race and sex differences were noted for C1 (white males>black males P-value <0.0001; males>females P-value 0.04), C2 (whites>blacks P-value 0.0004; males>females P-value<0.0001) and hsCRP (blacks>whites P-value 0.03; females>males P-value 0.002). Mean values of C1 in subjects with high hsCRP levels (>3 mg l(-1)) were significantly lower than those with average (1-3 mg l(-1)) and low levels (<1 mg l(-1)) (14.2 ml per mmHg × 10 versus 15.2 ml per mm Hg × 10 versus 15.7 ml per mmHg × 10, P for trend=0.02), after adjusting for age, race, sex and body surface area (BSA). hsCRP showed a trend toward inverse correlation with C1 (-0.07, P=0.07) but no such trend for C2, after adjusting for race and sex. In the multivariate linear regression model, adding age, race, sex, BSA, mean arterial pressure, insulin resistance, lipoprotein variables and smoking status, the effect persisted between C1 and hsCRP (β=-0.35, P=0.01). In an asymptomatic population of young adults, hsCRP predicts reduced large-artery compliance (C1). These findings support the role of systemic inflammation in early pathological changes in artery wall in atherogenesis. Small-artery compliance (C2) however did not correlate with hsCRP.Atherogeneis is a chronic progressive syndrome caused by endothelial dysfunction, vascular inflammation, vessel wall remodeling and eventual vascular flow compromise. Emerging data suggest that arterial compliance inversely correlates with atherogenesis and cardiovascular (CV) events. However, information is scant on the association of chronic systemic inflammation with arterial elasticity in young asymptomatic adults. The association of hsC-reactive protein (CRP) and central-vascular compliance was studied in 641 individuals (45.2% males; 71.8% whites), aged 31-43 years enrolled in the Bogalusa Heart Study. The measured variables included large-artery compliance (capacitive, C1), representative of the aorta and its major branches; and small-artery compliance (oscillatory, C2), representative of the distal part of the circulation; hsCRP, as a measure of systemic inflammation; along with traditional CV risk factor variables. Significant race and sex differences were noted for C1 (white males>black males P-value <0.0001; males>females P-value 0.04), C2 (whites>blacks P-value 0.0004; males>females P-value<0.0001) and hsCRP (blacks>whites P-value 0.03; females>males P-value 0.002). Mean values of C1 in subjects with high hsCRP levels (>3 mg l(-1)) were significantly lower than those with average (1-3 mg l(-1)) and low levels (<1 mg l(-1)) (14.2 ml per mmHg × 10 versus 15.2 ml per mm Hg × 10 versus 15.7 ml per mmHg × 10, P for trend=0.02), after adjusting for age, race, sex and body surface area (BSA). hsCRP showed a trend toward inverse correlation with C1 (-0.07, P=0.07) but no such trend for C2, after adjusting for race and sex. In the multivariate linear regression model, adding age, race, sex, BSA, mean arterial pressure, insulin resistance, lipoprotein variables and smoking status, the effect persisted between C1 and hsCRP (β=-0.35, P=0.01). In an asymptomatic population of young adults, hsCRP predicts reduced large-artery compliance (C1). These findings support the role of systemic inflammation in early pathological changes in artery wall in atherogenesis. Small-artery compliance (C2) however did not correlate with hsCRP.
Audience Academic
Author DasMahapatra, P
Srinivasan, S R
Xu, J
Fernandez, C
Sharma, D
Chen, W
Berenson, G S
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vascular
compliance
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Snippet Atherogeneis is a chronic progressive syndrome caused by endothelial dysfunction, vascular inflammation, vessel wall remodeling and eventual vascular flow...
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SubjectTerms 631/443/1338/243
692/420/256
692/499
692/699/75/593/2100
Adult
Age Factors
Aorta
Arteries - physiopathology
Asymptomatic
Asymptomatic Diseases
Atherogenesis
Atherosclerosis - blood
Atherosclerosis - ethnology
Atherosclerosis - immunology
Atherosclerosis - physiopathology
Biomarkers - blood
Black or African American
Blood pressure
C-reactive protein
C-Reactive Protein - analysis
Cardiovascular diseases
Compliance
Development and progression
Epidemiology
Female
Females
Genetic aspects
Health Administration
Humans
Inflammation
Inflammation Mediators - blood
Insulin
Insulin resistance
Least-Squares Analysis
Linear Models
Louisiana - epidemiology
Male
Males
Medicine
Medicine & Public Health
Multivariate Analysis
original-article
Physiological aspects
Public Health
Pulse Wave Analysis
Risk Assessment
Risk Factors
Sex differences
Vascular Stiffness
Veins & arteries
White People
Young adults
Title The association of c-reactive protein with arterial compliance in asymptomatic young adults: the bogalusa heart study
URI https://link.springer.com/article/10.1038/jhh.2012.34
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Volume 27
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