Low‐grade systemic inflammation impairs arterial stiffness in newly diagnosed hypercholesterolaemia

Abstract
Background Excess of cardiovascular risk among patients with chronic inflammatory diseases has been attributed to increased arterial stiffness. Hypercholesterolaemia has been demonstrated to promote a low‐grade inflammatory status. The objective of the present study was to define, in hypercholesterolaemia, the influence of plasma lipids, low‐grade inflammation, and indices of adiposity on aortic pulse wave velocity, a measure of arterial stiffness and cardiovascular risk. Materials and methods Anthropometric characteristics, plasma lipids, C‐reactive protein and aortic pulse wave velocity were measured in 85 subjects (60 patients with newly diagnosed never‐treated hypercholesterolaemia and 25 age‐ and sex‐matched normocholesterolaemic controls). Results Plasma C‐reactive protein and aortic pulse wave velocity were significantly higher among hypercholesterolaemic patients than in controls (P < 0·05 for both). Aortic pulse wave velocity was associated with age (r = 0·24, P = 0·04), body mass index (r = 0·33, P = 0·006), waist (r = 0·42, P < 0·001) and hip (r = 0·32, P = 0·007) circumferences, as well as with systolic (r = 0·34, P = 0·003) and diastolic (r = 0·30, P = 0·01) blood pressures, plasma C‐reactive protein (r = 0·51, P < 0·001), total cholesterol (r = 0·45, P < 0·001), and low‐density lipoprotein cholesterol (r = 0·46, P < 0·001). In the multivariate analysis, waist circumference and C‐reactive protein levels predicted increased aortic stiffness, independently of traditional cardiovascular risk factors. The degree of independent association between cholesterol, systolic blood pressure and aortic stiffness increased when indices of adiposity and inflammation were excluded from the multivariate analysis. Comparable results were obtained when the analyses were restricted to hypercholesterolaemic patients. Conclusions Low‐grade systemic inflammation and abdominal fat, more than traditional risk factors, are major determinants of reduced arterial distensibility in hypercholesterolaemia.

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