A synergistic relationship of elevated low-density lipoprotein cholesterol levels and systolic blood pressure with coronary artery calcification
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- 作者：Kiran Musunuru ; Khurram Nasir ; Shivda P ; ey ; Catherine C. Campbell ; Jose A.M. Carvalho ; Romeu Meneghello ; Matthew J. Budoff ; Roger S. Blumenthal ; Raul D. Santos
- 关键词：Coronary calcification ; Systolic blood pressure ; LDL-cholesterol ; Electron beam tomography ; Risk factors ; Subclinical atherosclerosis
- 刊名：Atherosclerosis
- 出版年：2008
- 出版时间：October 2008
- 年：2008
- 卷：200
- 期：2
- 页码：368-373
- 全文大小：195 K
文摘
We sought to evaluate this “response-to-injury” hypothesis of atherosclerosis by studying the interaction between systolic blood pressure (SBP) and LDL- cholesterol (LDL-C) in predicting the presence of coronary artery calcification (CAC) in asymptomatic men. We studied 526 men (46 ± 7 years of age) referred for electron-beam tomography (EBT) exam. The prevalence of CAC was determined across LDL-C tertiles (low: <115 mg/dl; middle: 115–139 mg/dl; high: ≥140 mg/dl) within tertiles of SBP (low: <121 mmHg; middle: 121–130 mmHg; high: ≥131 mmHg). CAC was found in 220 (42 % ) men. There was no linear trend in the presence of CAC across LDL-C tertiles in the low (p = 0.6 for trend) and middle (p = 0.3 for trend) SBP tertile groups, respectively. In contrast, there was a significant trend for increasing CAC with increasing LDL-C (1st: 44 % ; 2nd: 49 % ; 3rd: 83 % ; p < 0.0001 for trend) in the high SBP tertile group. In multivariate logistic analyses (adjusting for age, smoking, triglyceride levels, HDL-cholesterol levels, body mass index, and fasting glucose levels), the odds ratio for any CAC associated with increasing LDL-C was significantly higher in those with highest SBP levels, whereas no such relationship was observed among men with SBP in the lower two tertiles. An interaction term (LDL-C × SBP) incorporated in the multivariate analyses was statistically significant (p = 0.038). The finding of an interaction between SBP and LDL-C relation to CAC in asymptomatic men support the response-to-injury model of atherogenesis.