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

• Published in: Hypertension (Dallas, Tex. 1979) Vol. 71; no. 3; pp. 415 - 421
• Main Authors: Lamarche, Florence, Agharazii, Mohsen, Nadeau-Fredette, Annie-Claire, Madore, François, Goupil, Rémi
• Format: Journal Article
• Language: English
• Published: United States American Heart Association, Inc 01.03.2018
• Subjects: blood pressure; cardiovascular disease; secondary prevention; cholesterol, LDL
• DOI: 10.1161/HYPERTENSIONAHA.117.10476
• ISSN: 0194-911X; 1524-4563

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; P<0.001) and in participants with statins for primary (β=0.086 and 0.114; P<0.001) and secondary prevention (β=0.120 and 0.194; P<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; P<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.