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Published on: February 7, 2015
Relationship between Circulating Inflammatory Monocytes and Cardiovascular Disease Measures of Carotid Intimal
Ivo N SahBandar1,2, Lishomwa C Ndhlovu1,2, Katelyn Saiki1
1Hawai'i Center for AIDS, Department of Medicine, University of Hawaii John A. Burns School of Medicine.
Insights
Higher intermediate monocyte counts correlate with increased carotid intima-media thickness, a cardiovascular disease risk marker. This suggests inflammatory monocytes may play a role in atherosclerosis development and metabolic diseases.
Area of Science:
- Immunology
- Cardiovascular Science
- Atherosclerosis Research
Background:
- Cardiovascular disease (CVD) is a leading global cause of death, with atherosclerosis as a primary driver.
- Monocytes, key innate immune cells, are implicated in CVD progression, but distinct subset associations with risk remain unclear.
- Carotid intima-media thickness (cIMT) is a validated marker for subclinical atherosclerosis and CVD risk.
Purpose of the Study:
- To investigate the association between peripheral monocyte subpopulation numbers and cIMT in a general adult population.
- To determine if specific monocyte subsets correlate with subclinical atherosclerosis as measured by cIMT.
Main Methods:
- Utilized clinical data and peripheral blood mononuclear cell (PBMC) specimens from 67 individuals.
- Measured cIMT using high-resolution ultrasound of the carotid artery.
- Defined monocyte subpopulations (classical, intermediate/inflammatory, non-classical) via CD14 and CD16 co-expression.
Main Results:
- A higher count of intermediate monocytes showed a significant correlation with increased cIMT in the right common carotid artery (RCCA) and right carotid bifurcation (RBIF).
- This association remained significant after adjusting for CVD-associated clinical data.
- p-values for the correlations were 0.004 and 0.006 for RCCA and RBIF, respectively.
Conclusions:
- Demonstrated a strong correlation between inflammatory (intermediate) monocyte counts and cIMT.
- Suggests intermediate monocyte expansion is linked to elevated CVD risk predictors in the general population.
- Highlights potential roles for intermediate monocytes in atherosclerosis and metabolic diseases, indicating possible therapeutic targets.
Aims:
Cardiovascular disease (CVD) remains the leading cause of death worldwide despite improvements in the treatment of atherosclerosis, an inflammatory disease and major underlying cause of CVD. Monocytes, an innate immune cell type, are linked to CVD progression; however, given their heterogeneity, the association between distinct monocyte subsets and increased risk of CVD remains unclear. This study investigated the association between peripheral monocyte subpopulation numbers and carotid intima-media thickness (cIMT), a sensitive measure of CVD risk, in a cohort of adults recruited from the general population.
Methods:
We used clinical data and peripheral blood mononuclear cell (PBMC) specimens from 67 individuals. cIMT was measured by high-resolution, B-mode, ultrasound images of the right carotid artery. PBMCs were stained with conjugated monoclonal antibodies to define monocyte subpopulations based on CD14 and CD16 co-expressions into classical (CD14++CD16-), intermediate/inflammatory (CD14++CD16+), and non-classical/patrolling (CD14low/+CD16++) monocytes.
Results:
We found a higher intermediate monocyte count was significantly correlated with increased right common carotid artery (RCCA) and right carotid bifurcation (RBIF) intima-media thickness (IMT) (p=0.004 and 0.006,respectively), even after adjusting for CVD-associated clinical data (p=0.006 and 0.004, respectively).
Conclusion:
Our study demonstrated a strong correlation between inflammatory monocyte counts and cIMT. These results suggest that, in the general population, there is a relationship between intermediate monocyte expansion and elevated predictors for CVD risk, and intermediate monocytes may be involved in the development of atherosclerosis and metabolic diseases. Strategies targeting inflammatory monocytes may be needed to slow CVD progression.
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