Central and Brachial Blood Pressures, Statins, and Low-Density Lipoprotein Cholesterol: A Mediation Analysis.

Hypertension

From the Hôpital du Sacré-Cœur de Montréal (F.L., F.M., R.G.) and Hôpital Maisonneuve-Rosemont (A.-C.N.-F.), Université de Montréal, Canada; and CHU de Québec, Hôtel-Dieu de Québec, Université Laval, Canada (M.A.).

Published: March 2018

Central blood pressure may be a better predictor of cardiovascular disease than brachial pressure. Although statins reduce brachial pressure, their impact on central pressure remains unknown. Furthermore, whether this effect is mediated through a decrease in low-density lipoprotein cholesterol (LDL-c) is unknown. This study aims to characterize the association of statins and LDL-c with central and brachial blood pressures and to quantify their respective effects. Of the 20 004 CARTaGENE participants, 16 507 had available central blood pressure, LDL-c, and Framingham risk score. Multivariate analyses were used to evaluate the association between central pressure and LDL-c in subjects with or without statins. The impact of LDL-c on the association between statin and pressure parameters was determined through mediation analyses. LDL-c was positively associated with systolic and diastolic central pressure in nonusers (β=0.077 and 0.106; <0.001) and in participants with statins for primary (β=0.086 and 0.114; <0.001) and secondary prevention (β=0.120 and 0.194; <0.003). Statins as primary prevention were associated with lower central systolic, diastolic, and pulse pressures (-3.0, -1.6, and -1.3 mm Hg; <0.001). Mediation analyses showed that LDL-c reduction contributed to 15% of central systolic and 44% of central diastolic pressure changes associated with statins and attenuated 22% of the effects on central pulse pressure. Similar results were found with brachial pressure components. In conclusion, reduction of LDL-c was associated with only a fraction of the lower blood pressures in statin user and seemed to be mostly associated with improvement of steady (diastolic) pressure, whereas non-LDL-c-mediated pathways were mostly associated with changes in pulsatile pressure components.

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http://dx.doi.org/10.1161/HYPERTENSIONAHA.117.10476DOI Listing

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