Abstract

BackgroundLow-density lipoprotein cholesterol (LDL-c) has been proven to be a risk factor for atherosclerotic cardiovascular disease (CVD), while lipoprotein (a) (Lp(a)) is a residual risk factor for CVD, even though LDL-c is well controlled by statin use. Importantly, the role of Lp(a) in atherosclerotic renal artery stenosis (ARAS) is still unknown.MethodsFor this hospital-based cross-sectional study, patients who simultaneously underwent coronary and renal angiography were examined. ARAS was defined as a 50% reduction in the cross-sectional (two-dimensional plane) area of the renal artery. Data were collected and compared between ARAS and non-ARAS groups, including clinical history and metabolite profiles. Univariate analysis, three tertile LDL-c-based stratified analysis, and multivariate-adjusted logistic analysis were conducted, revealing a correlation between Lp(a) and ARAS.ResultsA total of 170 hypertensive patients were included in this study, 85 with ARAS and 85 with non-RAS. Baseline information indicated comparability between the two groups. In the univariate and multivariate analysis, common risk factors for atherosclerosis were not significantly different. Stratified analysis of LDL-c revealed a significant increase in the incidence of ARAS in patients who had high Lp(a) concentrations at low LDL-c levels (odds ratio (OR): 4.77, 95% confidence interval (CI): 1.04–21.79, P = 0.044). Further logistic analysis with adjusted covariates also confirmed the result, indicating that high Lp(a) levels were independently associated with ARAS (adjusted OR (aOR): 6.14, 95%CI: 1.03–36.47, P = 0.046). This relationship increased with increasing Lp(a) concentration based on a curve fitting graph. These results were not present in the low and intermediate LDL-c-level groups.ConclusionIn hypertensive patients who present low LDL-c, high Lp(a) was significantly associated with atherosclerotic renal artery stenosis and thus is a residual risk factor.

Highlights

  • Low-density lipoprotein cholesterol (LDL-c) has been proven to be a risk factor for atherosclerotic cardiovascular disease (CVD), while lipoprotein (a) (Lp(a)) is a residual risk factor for CVD, even though LDL-c is well controlled by statin use

  • Mendelian randomization studies and RCTs have consistently demonstrated that low-density lipoprotein cholesterol (LDL-c) is causally associated with the risk of arteriosclerotic cardiovascular disease (ASCVD) [2,3,4,5,6,7]

  • Definitions and laboratory examination In all patients, hypertension was diagnosed according to the European Society of Cardiology guidelines as Systolic blood pressure (SBP) ≥ 140 and/or Diastolic blood pressure (DBP) ≥ 90 mmHg, which is equivalent to a 24-h ambulatory blood pressure monitoring average of ≥130/80 mmHg, or a home blood pressure monitoring average of ≥135/85 mmHg for two measurements at least 3 days [27]

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Summary

Introduction

Low-density lipoprotein cholesterol (LDL-c) has been proven to be a risk factor for atherosclerotic cardiovascular disease (CVD), while lipoprotein (a) (Lp(a)) is a residual risk factor for CVD, even though LDL-c is well controlled by statin use. Mendelian randomization studies and RCTs have consistently demonstrated that low-density lipoprotein cholesterol (LDL-c) is causally associated with the risk of ASCVD [2,3,4,5,6,7]. Studies from the past few decades have revealed that populations with well-regulated LDL-c levels still had a considerably high residual cardiovascular risk, and that Lp(a) is responsible for this phenomena [9,10,11,12,13,14]

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