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In hypercholesterolemia, lower peripheral monocyte count is unique among the major predictors of atherosclerosis
1Department of Internal Medicine, College of Medicine, National Taiwan University, Taipei, ROC.
Insights
High cholesterol may lower monocyte counts by increasing their adherence to blood vessel walls, potentially initiating atherosclerosis. Smoking, however, was linked to higher monocyte counts in this study.
Area of Science:
- Cardiovascular Research
- Immunology
- Epidemiology
Background:
- Enhanced monocyte adherence is a key factor in atherosclerosis initiation.
- Limited research exists on the link between circulating monocyte count and atherosclerosis predictors.
Purpose of the Study:
- To investigate the relationship between circulating monocyte count and atherosclerosis.
- To clarify the association between monocyte count and major atherosclerosis predictors.
Main Methods:
- Carotid artery duplex study and white blood cell analysis were performed on 409 participants.
- Data analysis adjusted for age and sex.
Main Results:
- No correlation was found between existing carotid atherosclerosis and monocyte count.
- Hypercholesterolemia correlated with lower monocyte count and percentage (P < .001, P < .0001).
- Smoking correlated with higher monocyte count (P < .001).
Conclusions:
- Hypercholesterolemia may reduce peripheral monocyte levels by enhancing endothelial adhesion, initiating atherosclerosis.
- Atherosclerosis mechanisms may differ based on predictors like hypercholesterolemia.
- Inverse correlation suggests decreased monocytes might lead to hypercholesterolemia via reduced cholesterol uptake.
Abstract:
Many studies have shown that enhanced monocyte adherence is an important factor in the initiation of atherosclerosis. Because the relationships between circulating monocyte count and atherosclerosis or its major predictors have received little attention, we conducted this study with the aim of clarifying these relationships. The study included 409 men and women who underwent a carotid artery duplex study and white blood cell analysis (Sysmex Cell Counter) during a 2-day health check at our hospital in 1994. We found no correlation between preexisting carotid atherosclerosis and monocyte count. After adjustment for age and sex, hypercholesterolemia, among the major predictors of atherosclerosis, showed a unique correlation with both lower monocyte count and percentage (P < .001, P < .0001, respectively), whereas smoking was correlated with a higher monocyte count (P < .001). There was a slight but nonsignificant increase in monocyte count in hypertension, diabetes, and hypertriglyceridemia. Our results imply that: (1) hypercholesterolemia has a strong, peripheral monocyte-reducing effect, probably due to direct enhancement of monocyte adhesion to the endothelium, which subsequently initiates the atherosclerotic process, and (2) the mechanisms of other predictor(s)-induced atherosclerosis may be quite different from that of hypercholesterolemia. Another possible explanation for the inverse correlation between monocyte count and serum cholesterol level is that decreased monocyte levels might lead to hypercholesterolemia because of decreased uptake of cholesterol from the plasma by less monocyte-derived macrophages. The reasons why preexisting carotid atherosclerosis did not correlate with monocyte count are also discussed.