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Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
Soluble Vascular Cell Adhesion Molecules May be Protective of Future Cardiovascular Disease Risk: Findings from the
Setor K Kunutsor1, Stephan J L Bakker2,3, Robin P F Dullaart4
1School of Clinical Sciences, University of Bristol.
Insights
Plasma vascular cell adhesion molecule-1 (VCAM-1) is inversely associated with cardiovascular disease (CVD) risk. However, VCAM-1 does not improve CVD risk prediction beyond established factors.
Area of Science:
- Cardiovascular Disease Research
- Biomarker Discovery
- Preventive Cardiology
Background:
- Soluble cell adhesion molecules (sCAMs) are implicated in cardiovascular disease (CVD) risk.
- The specific role of vascular cell adhesion molecule-1 (VCAM-1) in CVD risk and prediction remains uncertain.
Purpose of the Study:
- To evaluate the association between plasma VCAM-1 concentrations and CVD risk.
- To determine if VCAM-1 can enhance the prediction of CVD events.
Main Methods:
- Prospective study (PREVEND) with 2,638 participants.
- Baseline plasma VCAM-1 measured; CVD events tracked over 9.9 years.
- Hazard ratios and risk reclassification metrics calculated.
Main Results:
- Plasma VCAM-1 showed an inverse association with CVD risk, independent of established risk factors.
- Higher VCAM-1 levels were associated with a reduced hazard of CVD events.
- VCAM-1 did not significantly improve CVD risk prediction models.
Conclusions:
- Plasma VCAM-1 is independently and inversely linked to cardiovascular disease.
- VCAM-1 does not offer added value for CVD risk assessment beyond conventional factors.
Aim:
Soluble cell adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1, E-selectin, and P-selectin, have been suggested to be associated with cardiovascular disease (CVD) risk; however, the nature and magnitude of the association between VCAM-1 and CVD risk is uncertain. We aimed to assess the association of VCAM-1 with CVD risk and determine its potential utility for CVD risk prediction.
Methods:
VCAM-1 concentrations were measured at baseline in the PREVEND prospective study of 2,638 participants. Hazard ratios (95% confidence intervals [CI]) and measures of risk discrimination for CVD (e.g., C-index) and reclassification (i.e., net reclassification improvement) of participants were assessed.
Results:
During a median follow-up of 9.9 years, 614 CVD events occurred. Plasma VCAM-1 was weakly associated with several cardiovascular risk markers. In analyses adjusted for established cardiovascular risk factors, the hazard ratio (95% CI) for CVD per 1 standard deviation increase in loge VCAM-1 was 0.91 (0.84-0.99; P =0.020), which remained consistent after additional adjustment for body mass index, alcohol consumption, triglycerides, renal function, and C-reactive protein; hazard ratio (95% CI) 0.89 (0.82-0.97; P =0.006). Comparing the top versus bottom quintiles of VCAM-1 levels, the corresponding adjusted hazard ratios were 0.74 (0.57-0.96; P =0.023) and 0.70 (0.54-0.91; P =0.007) respectively. Adding VCAM-1 to a CVD risk prediction model containing conventional risk factors did not improve the C-index or net reclassification.
Conclusions:
Plasma VCAM-1 is inversely and independently associated with CVD. However, VCAM-1 provides no significant improvement in CVD risk assessment beyond conventional CVD risk factors.
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