Abstract
Background Central arterial stiffness is a surrogate of cardiovascular risk and predicts cardiovascular mortality. Apolipoprotein B lipoproteins are also established cardiovascular risk factors. It is not known whether specific lipoprotein subclasses measured in the Malmö Diet and Cancer Study and previously shown to be associated with coronary heart disease also predict arterial stiffening after a mean period of 17 years. Methods Lipoprotein particle analysis was performed on 2,505 men and women from Malmö, Sweden, from 1991 to 1994, and arterial stiffness was assessed by carotid-femoral pulse wave velocity (c-fPWV) on this same cohort from 2007 to 2012. Associations between c-fPWV and lipoprotein particles were determined with multiple linear regression, controlling for sex, presence of diabetes, waist-to-hip circumference, and smoking status at baseline, as well as heart rate (measured at the carotid artery), mean arterial pressure, antihypertensive and lipid-lowering medications, C-reactive protein (CRP), and age at the time of c-fPWV measurement. Results The results confirm that triglycerides (TG) and high-density lipoprotein cholesterol (HDL-c) but not low-density lipoprotein cholesterol (LDL-c) predict c-fPWV. We identify a positive predictive association for very small, small, and medium (high risk), but not large LDL particles. There was a negative association for large HDL particles. The relationships between c-fPWV and high-risk LDL particles were unaffected by adjusting for LDL-c or CRP and were only mildly attenuated by adjusting for the homeostatic model for insulin resistance (HOMA-IR). Due to the collinearity of very small, small, and medium LDL particles and dyslipidemia (elevated TG and decreased HDL-c), the observed relationship between c-fPWV and high-risk LDL particles became insignificant after controlling for the concentration of HDL-c, large cholesterol-rich HDL particles, and TG. Conclusions The development of central arterial stiffness previously associated with combined dyslipidemia may be mediated in part by LDL particles, particularly the very small-, small-, and medium-sized LDL particles.
Highlights
The infiltration of apolipoprotein B containing lipoproteins within the vessel wall, release of inflammatory cholesterol crystals, and the development of fatty streaks are features of early atherosclerosis [1], but their influence on central arterial stiffening is not known
A recent analysis using data from the Malmö Diet and Cancer Study found that hyperglycemia and insulin resistance, central adiposity, hypertriglyceridemia, and decreased high-density lipoprotein cholesterol (HDL-c), but not elevated low-density lipoprotein cholesterol (LDL-c), were associated with increased central arterial stiffness measured by carotidfemoral pulse wave velocity (c-fPWV) [11]
There were no significant relationships between carotid-femoral pulse wave velocity (c-fPWV) and particle concentrations of very low-density lipoprotein (VLDL) or large intermediate-density lipoprotein (IDL) subfractions, while there was an inverse association with small IDL particles (IDL-2, β = −0:042, p = 0:02)
Summary
The infiltration of apolipoprotein B (apoB) containing lipoproteins within the vessel wall, release of inflammatory cholesterol crystals, and the development of fatty streaks are features of early atherosclerosis [1], but their influence on central arterial stiffening is not known. A recent analysis using data from the Malmö Diet and Cancer Study found that hyperglycemia and insulin resistance, central adiposity, hypertriglyceridemia, and decreased HDL-c, but not elevated LDL-c, were associated with increased central arterial stiffness measured by carotidfemoral pulse wave velocity (c-fPWV) [11]. The same combination of risk factors associated with c-fPWV in the Malmö cohort correlates with the presence of increased concentrations of small and total LDL particles across the lifespan. This relationship has been described in school-aged children [18] and in adults [19]. The development of central arterial stiffness previously associated with combined dyslipidemia may be mediated in part by LDL particles, the very small-, small-, and medium-sized LDL particles
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