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LDL cholesterol is associated with systemic vascular resistance and wave reflection in subjects naive to cardiovascular drugs

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journal contribution
posted on 29.10.2018 by Manoj Kumar Choudhary, Arttu Eräranta, Antti J. Tikkakoski, Jenni Koskela, Elina J. Hautaniemi, Mika Kähönen, Jukka Mustonen, Ilkka Pörsti

Background and aim: Low density lipoprotein cholesterol (LDL-C) is a primary risk factor for atherosclerosis, but it is also associated with elevated blood pressure (BP) and future development of hypertension. We examined the relationship between LDL-C and haemodynamic variables in normotensive and never-treated hypertensive subjects.

Methods: We recruited 615 volunteers (19–72 years) without lipid-lowering and BP-lowering medication. Supine haemodynamics were recorded using continuous radial pulse wave analysis, whole-body impedance cardiography, and single channel electrocardiogram. The haemodynamic relations of LDL-C were examined using linear regression analyses with age, sex, body mass index (BMI) (or height and weight as appropriate), smoking status, alcohol use, and plasma C-reactive protein, sodium, uric acid, high density lipoprotein cholesterol (HDL-C), triglycerides, estimated glomerular filtration rate, and quantitative insulin sensitivity check index as the other included variables.

Results: The mean (SD) characteristics of the subjects were: age 45 (12) years, BMI 27 (4) kg/m2, office BP 141/89 (21/13) mmHg, creatinine 74 (14) µmol/l, total cholesterol 5.2 (1.0), LDL-C 3.1 (0.6), triglycerides 1.2 (0.8), and HDL-C 1.6 (0.4) mmol/l. LDL-C was an independent explanatory factor for aortic systolic and diastolic BP, augmentation index, pulse wave velocity (PWV), and systemic vascular resistance index (p < 0.05 for all). When central BP was included in the model for PWV, LDL-C was no longer an explanatory factor for PWV.

Conclusions: LDL-C is independently associated with BP via systemic vascular resistance and wave reflection. These results suggest that LDL-C may play a role in the pathogenesis of primary hypertension.

Funding

This work was financially supported by Aarne Koskelo Foundation, Competitive State Research Financing of the Expert Responsibility Area of Tampere University Hospital, Finnish Foundation for Cardiovascular Research, Paavo Nurmi Foundation, Päivikki and Sakari Sohlberg Foundation, Sigrid Jusélius Foundation, and Pirkanmaa Regional Fund of the Finnish Cultural Foundation.

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