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Updated: Jun 25, 2026
A Methodological Approach to Non-invasive Assessments of Vascular Function and Morphology
Published on: February 7, 2015
Multimarker approach to evaluate correlates of vascular stiffness: the Framingham Heart Study
Wolfgang Lieb1, Martin G Larson, Emelia J Benjamin
1Framingham Heart Study, Framingham, MA, USA.
Insights
Biomarkers like aldosterone and C-reactive protein are linked to arterial stiffness in older adults. These findings highlight distinct biological pathways influencing vascular health and aging.
Area of Science:
- Cardiovascular Science
- Aging Research
- Biomarker Discovery
Background:
- Arterial stiffness increases with age, contributing to systolic hypertension and cardiovascular disease in the elderly.
- Understanding the pathophysiological drivers of arterial stiffness is crucial for developing targeted therapeutic strategies.
Purpose of the Study:
- To investigate the associations between specific circulating biomarkers and various measures of arterial stiffness.
- To explore how distinct biological pathways relate to different aspects of vascular function.
Main Methods:
- Cross-sectional analysis of 2000 participants from the Framingham Offspring Study (mean age 61).
- Measured 7 circulating biomarkers (e.g., C-reactive protein, aldosterone-to-renin ratio) and 5 vascular function measures (e.g., pulse pressure, pulse-wave velocity).
- Utilized multivariable linear regression models, adjusting for relevant covariates.
Main Results:
- A panel of biomarkers was significantly associated with all measured vascular stiffness indices (P<0.003).
- Aldosterone-to-renin ratio showed positive associations with all stiffness measures (P≤0.002).
- C-reactive protein correlated with augmented pressure (P=0.0003), and plasminogen activator inhibitor-1 with mean arterial pressure and central stiffness measures (P≤0.01).
Conclusions:
- Distinct patterns of association exist between biomarkers and vascular stiffness measures.
- Biomarkers of renin-angiotensin-aldosterone system activation link to pan-arterial stiffness.
- C-reactive protein relates to wave reflection, and PAI-1 to central stiffness, supporting differential pathway influences.
Background:
Arterial stiffness increases with age and contributes to the pathogenesis of systolic hypertension and cardiovascular disease in the elderly. Knowledge about the pathophysiological processes that determine arterial stiffness may help guide therapeutic approaches.
Methods And Results:
We related 7 circulating biomarkers representing distinct biological pathways (C-reactive protein, aldosterone-to-renin ratio, N-terminal proatrial natriuretic peptide and B-type natriuretic peptide, plasminogen activator inhibitor-1, fibrinogen, and homocysteine) to 5 vascular function measures (central pulse pressure, carotid-femoral pulse-wave velocity, mean arterial pressure, forward pressure wave amplitude [all measures of conduit artery stiffness], and augmented pressure, an indicator of wave reflection) in 2000 Framingham Offspring Study participants (mean age, 61 years; 55% women). Tonometry measures were obtained on average 3 years after the biomarkers were measured. In multivariable linear regression models adjusting for covariates, the biomarker panel was significantly associated with all 5 vascular measures (P<0.003 for all). On backward elimination, the aldosterone-to-renin ratio was positively associated with each stiffness measure (P< or =0.002 for all). In addition, C-reactive protein was positively related to augmented pressure (P=0.0003), whereas plasminogen activator inhibitor-1 was positively associated with mean arterial pressure (P=0.003), central pulse pressure (P=0.001), and forward pressure wave (P=0.01).
Conclusions:
Our cross-sectional data on a community-based sample suggest a distinctive pattern of positive associations of biomarkers of renin-angiotensin-aldosterone system activation with pan-arterial vascular stiffness, plasminogen activator inhibitor-1 with central vascular stiffness indices, and C-reactive protein with wave reflection. These observations support the notion of differential influences of biological pathways on vascular stiffness measures.
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