Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota, USA.
Am J Hypertens. 2012 Feb;25(2):145-51. doi: 10.1038/ajh.2011.193. Epub 2011 Oct 20.
Pulse pressure (an indirect measure of arterial stiffness) is a robust predictor of cardiovascular events, but its pathophysiology remains poorly understood. To gain insight into the pathophysiology of arterial stiffness we conducted an exploratory investigation of the associations of 47 circulating biomarkers in etiologic pathways of arteriosclerosis with brachial artery pulse pressure.
Participants included 1,193 African-Americans and 1,145 non-Hispanic whites belonging to hypertensive sibships. Blood pressure (BP) was measured with a random-zero sphygmomanometer. Multivariable linear regression was employed to assess the associations of biomarkers with pulse pressure after adjustment for age, sex, conventional risk factors, mean arterial pressure, heart rate, and use of aspirin, statins, estrogens, and antihypertensives. Statistical significance was set at P ≤ 0.001 (Bonferroni correction for multiple testing).
Log N-terminal probrain natriuretic peptide (NT-proBNP) (African-Americans: β = 2.11 ± 0.52, non-Hispanic whites: β = 2.65 ± 0.55), log midregional proatrial natriuretic peptide (African-Americans: β = 4.83 ± 0.70, non-Hispanic whites: β = 3.70 ± 0.67), and log osteoprotegerin (African-Americans: β = 4.64 ± 1.02, non-Hispanic whites: β = 4.19 ± 0.99) were independently associated with pulse pressure (P < 0.001 for all) in both ethnicities. Log C-reactive protein (CRP) (β = 1.56 ± 0.35), log midregional proadrenomedullin (MR-proADM) (β = 5.53 ± 1.19) and log matrix metalloproteinase-2 (β = 3.89 ± 1.06) were associated with greater pulse pressure in African-Americans only (P ≤ 0.001 for all), whereas higher fibrinogen was associated with pulse pressure in non-Hispanic whites only (β = 0.02 ± 0.004. P < 0.001).
Our results suggest that hemodynamic stress, vascular inflammation and calcification, and matrix remodeling may have a role in the pathogenesis and/or adverse consequences of increased pulse pressure.
脉压（动脉僵硬度的间接测量值）是心血管事件的强有力预测因子，但对其病理生理学仍知之甚少。为了深入了解动脉僵硬度的病理生理学，我们对动脉粥样硬化发病机制中 47 种循环生物标志物与肱动脉脉压的相关性进行了探索性研究。
参与者包括 1193 名非裔美国人和 1145 名非西班牙裔白人，他们均属于高血压同卵双胞胎。血压（BP）用随机零汞柱血压计测量。采用多元线性回归评估在调整年龄、性别、传统危险因素、平均动脉压、心率以及阿司匹林、他汀类药物、雌激素和抗高血压药物的使用后，生物标志物与脉压的相关性。统计显著性设为 P≤0.001（多重检验的 Bonferroni 校正）。
N 端脑利钠肽前体（NT-proBNP）的对数值（非裔美国人：β=2.11±0.52，非西班牙裔白人：β=2.65±0.55）、中区域 proatrial 利钠肽（非裔美国人：β=4.83±0.70，非西班牙裔白人：β=3.70±0.67）和骨保护素（非裔美国人：β=4.64±1.02，非西班牙裔白人：β=4.19±0.99）的对数值与脉压独立相关（在两个种族中 P＜0.001）。C 反应蛋白（CRP）的对数值（β=1.56±0.35）、中区域 proadrenomedullin（MR-proADM）的对数值（β=5.53±1.19）和基质金属蛋白酶-2（β=3.89±1.06）与非裔美国人的脉压增加相关（均 P≤0.001），而非西班牙裔白种人仅与纤维蛋白原相关（β=0.02±0.004，P＜0.001）。
我们的研究结果表明，血流动力学应激、血管炎症和钙化以及基质重塑可能在脉压增加的发病机制和/或不良后果中起作用。
