Olsen M H, Christensen M K, Wachtell K, Tuxen C, Fossum E, Bang L E, Wiinberg N, Devereux R B, Kjeldsen S E, Hildebrandt P, Dige-Petersen H, Rokkedal J, Ibsen H
Department of Clinical Physiology and Nuclear Medicine, Glostrup Hospital, University of Copenhagen, Denmark.
J Hum Hypertens. 2005 Apr;19(4):301-7. doi: 10.1038/sj.jhh.1001819.
Cardiac fibrosis and high levels of circulating collagen markers has been associated with left ventricular (LV) hypertrophy. However, the relationship to vascular hypertrophy and blood pressure (BP) load is unclear. In 204 patients with essential hypertension and electrocardiographic LV hypertrophy, we measured sitting BP, serum collagen type I carboxy-terminal telopeptide (ICTP) reflecting degradation, procollagen type I carboxy-terminal propeptide (PICP) reflecting synthesis and LV mass by echocardiography after 2 weeks of placebo treatment and after 1 year of antihypertensive treatment with a losartan- or an atenolol-based regimen. Furthermore, we measured intima-media thickness of the common carotid arteries (IMT), minimal forearm vascular resistance (MFVR) by plethysmography and ambulatory 24-h BP in around half of the patients. At baseline, PICP/ICTP was positively related to IMT (r=0.24, P<0.05), MFVR(men) (r=0.35, P<0.01), 24-h systolic BP (r=0.24, P<0.05) and 24-h diastolic BP (r=0.22, P<0.05), but not to LV mass. After 1 year of treatment with reduction in systolic BP (175+/-15 vs 151+/-17 mmHg, P<0.001) and diastolic BP (99+/-8 vs 88+/-9 mmHg, P<0.001), ICTP was unchanged (3.7+/-1.4 vs 3.8+/-1.4 microg/l, NS) while PICP (121+/-39 vs 102+/-29 microg/l, P<0.001) decreased. The reduction in PICP/ICTP was related to the reduction in sitting diastolic BP (r=0.31, P<0.01) and regression of IMT (r=0.37, P<0.05) in patients receiving atenolol and to reduction in heart rate in patients receiving losartan (r=0.30, P<0.01). In conclusion, collagen markers reflecting net synthesis of type I collagen were positively related to vascular hypertrophy and BP load, suggesting that collagen synthesis in the vascular wall is increased in relation to high haemodynamic load in a reversible manner.
心脏纤维化和循环中高水平的胶原蛋白标志物与左心室（LV）肥厚相关。然而，其与血管肥厚和血压（BP）负荷的关系尚不清楚。在204例原发性高血压且有心电图左心室肥厚的患者中，我们在安慰剂治疗2周后以及使用基于氯沙坦或阿替洛尔的方案进行抗高血压治疗1年后，通过超声心动图测量了静息血压、反映降解的血清I型胶原羧基末端肽（ICTP）、反映合成的I型前胶原羧基末端前肽（PICP）以及左心室质量。此外，我们在大约一半的患者中测量了颈总动脉内膜中层厚度（IMT）、通过体积描记法测量的最小前臂血管阻力（MFVR）以及动态24小时血压。在基线时，PICP/ICTP与IMT呈正相关（r = 0.24，P < 0.05）、与MFVR（男性）呈正相关（r = 0.35，P < 0.01）、与24小时收缩压呈正相关（r = 0.24，P < 0.05）以及与24小时舒张压呈正相关（r = 0.22，P < 0.05），但与左心室质量无关。经过1年治疗，收缩压降低（175±15 vs 151±17 mmHg，P < 0.001），舒张压降低（99±8 vs 88±9 mmHg，P < 0.001），ICTP无变化（3.7±1.4 vs 3.8±1.4 μg/l，无显著性差异），而PICP降低（121±39 vs 102±29 μg/l，P < 0.001）。在接受阿替洛尔治疗的患者中，PICP/ICTP的降低与静息舒张压的降低相关（r = 0.31，P < 0.01）以及与IMT的消退相关（r = 0.37，P < 0.05），在接受氯沙坦治疗的患者中与心率降低相关（r = 0.30，P < 0.01）。总之，反映I型胶原净合成的胶原蛋白标志物与血管肥厚和血压负荷呈正相关，提示血管壁中胶原蛋白合成随着高血流动力学负荷以可逆方式增加。
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