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Protective effect of high density lipoprotein on endothelium-dependent vasodilatation
1Departments of Cardiology, Second Affiliated Hospital, Human Medical University, 410011, Changsha, PR China.
Insights
Low high-density lipoprotein cholesterol (HDL-C) is linked to coronary heart disease (CHD) risk. This study shows HDL-C protects against impaired blood vessel function, crucial for heart health.
Area of Science:
- Cardiovascular Research
- Vascular Biology
- Biochemistry
Background:
- Low high-density lipoprotein cholesterol (HDL-C) is a risk factor for coronary heart disease (CHD), even with normal total cholesterol (TC).
- The protective mechanisms of HDL-C against atherosclerosis are not fully understood.
- Endothelial dysfunction is a key factor in atherosclerosis development.
Purpose of the Study:
- To investigate the relationship between HDL-C levels and brachial artery vasodilatation in patients with established CHD.
- To assess both endothelium-dependent (flow-mediated dilatation, FMD) and endothelium-independent (glyceryl trinitrate-induced, GTN) vasodilatation.
- To identify predictors of impaired vascular function in a population with normal TC.
Main Methods:
- High-resolution ultrasound was used to measure brachial artery diameter changes.
- Measurements were taken during reactive hyperemia (FMD) and after sublingual glyceryl trinitrate (GTN).
- 63 patients with CHD and 45 controls with normal TC were studied.
Main Results:
- Patients with CHD exhibited significantly reduced FMD and GTN-induced dilatation compared to controls.
- HDL-C levels were positively related to FMD in both CHD patients and controls.
- HDL-C and age were independent predictors of FMD, while baseline diameter predicted GTN-induced dilatation.
Conclusions:
- Endothelium-dependent and independent vasodilatation are impaired in patients with CHD.
- HDL-C plays a protective role in endothelium-dependent vasodilatation, even in individuals with normal TC.
- These findings highlight the importance of HDL-C in maintaining vascular health and preventing atherosclerosis.
Abstract:
Low concentrations of high-density lipoprotein cholesterol (HDL-C) have been associated with increased risk of coronary heart disease (CHD) even when the total cholesterol (TC) and triglyceride (TG) levels are not elevated. The mechanism by which HDL confers protection against atherosclerosis remains speculative. Using high-resolution ultrasound, we measured the dilatation changes of brachial arteries during reactive hyperemia and after sublingual glyceryl trinitrate (GTN) in 63 patients with established (CHD) and 45 controls, in which the serum TC level was normal. The results showed that both flow-mediated dilatation (FMD) and GTN-induced dilatation of brachial arteries in patients with CHD were much reduced compared with control group (2.31+/-2.46% vs. 7.43+/-4.10% and 16.41+/-6.15% vs. 22.44+/-8.63%, respectively, P<0.001 for all). Univariate analysis indicated that FMD of brachial arteries was inversely related to age (r=-0.226, P<0.05), hypertension (r=-0.229, P<0.05), baseline diameter (r=-0.299, P<0.01) and LDL-C (r=-0.237, P<0.05) and positively related to HDL-C (r=0.491, P<0.01). GTN induced vasodilatation was inversely related to age (r=-0.216, P<0. 05) and baseline diameter (-0.476, P<0.01). Multiple stepwise regression analyses in two groups taken together showed that HDL-C and age were the independent predictors of the FMD of brachial arteries (beta=0.466, P=0.000 and beta=-0.184, P=0.020, respectively). Baseline diameter was significant predictor of GTN-induced vasodilatation (beta=-0.390, P=0.000). The analysis in the group of CHD patients showed that only HDL-C was significantly relate to the FMD of brachial arteries (beta=0.295, P=0.018 ) and in controls that hypertension and HDL-C were significantly relate to the FMD of brachial arteries (beta=-0.395, P=0.004 and beta=0.344, P=0.011, respectively). These finding suggest that endothelium-dependent and endothelium-independent vasodilatation are impaired in the patients with CHD. HDL exerts a protective effect on endothelium-dependent vasodilatation in TC being relatively normal population.