Systemic Vascular Dysfunction in Patients With Chronic Mountain Sickness
Systemic Vascular Dysfunction in Patients With Chronic Mountain Sickness
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DOI：
10.1378/chest.11-0342
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发表时间：
2012-01-01
期刊：
影响因子：
9.6
通讯作者：
Sartori, Claudio
中科院分区：
文献类型：
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作者：
Rimoldi, Stefano F.;Rexhaj, Emrush;Sartori, Claudio
背景：慢性高山病（CMS）是一个主要的公共卫生问题，其特征是严重的低氧血症和红细胞增多。在更晚期阶段，CMS患者经常出现肺循环的功能和结构变化，但有关体循环的信息很少。患有低海拔慢性低氧血症相关疾病的患者，全身血管功能会发生改变。我们假设 CMS 患者存在全身血管功能障碍，这可能会使他们增加全身心血管发病率。方法：为了检验这一假设，我们评估了全身内皮功能（通过血流介导的扩张 [FMD]）、动脉僵硬度；颈动脉内膜中层厚度和动脉血氧饱和度 (Sao(2)) 对 23 名没有其他典型心血管危险因素的 CMS 患者和 27 名出生并永久生活在 3,600 英寸的年龄匹配的健康山区居民进行了研究。对于某些分析，受试者根据基线 Sao(2) 四分位数进行分类；最高四分位数亚组 (Sao(2) >= 90%) 的 FMD 被用作事后比较的参考值。 结果：CMS 患者有明显的全身血管功能障碍，表现为 FMD 受损（CMS，4.6% +/- 1.2%；对照受试者，7.6% +/- 1.9%；P < .0001），脉搏波速度更大（10.6 +/- 2.1 m/s vs 8.4 +/- 1.0 m/s，P < .001），颈动脉内膜中层厚度更大（690 +/- 1.20 μm vs 570 +/- 110 μm，P = .001）。 Sao(2) 和 FMD 之间存在正相关关系 (r = 0.62, P < .0001)。吸氧改善了 (P < .001)，但并未使 CMS 患者的 FMD 正常化，尽管它使低氧血症对照受试者 (Sao(2) < 90%) 的 FMD 正常化，并且在血氧正常对照受试者 (Sao(2) >= 90%) 中没有可检测到的效果。 结论：CMS 患者表现出明显的全身血管功能障碍。结构和功能的改变导致了这个问题，可能使这些患者容易患上过早的心血管疾病。
Background: Chronic mountain sickness (CMS) is a major public health problem characterized by exaggerated hypoxemia and erythrocytosis. In more advanced stages, patients with CMS often present with functional and structural changes of the pulmonary circulation, but there is little information on the systemic circulation. In patients with diseases associated with chronic hypoxemia at low altitude, systemic vascular function is altered. We hypothesized that patients with CMS have systemic vascular dysfunction that may predispose them to increased systemic cardiovascular morbidity.Methods: To test this hypothesis, we assessed systemic endothelial function (by flow-mediated dilation [FMD]), arterial stiffness; and carotid intima-media thickness and arterial oxygen saturation (Sao(2)) in 23 patients with CMS without additional classic cardiovascular risk factors and 27 age-matched healthy mountain dwellers born and permanently living at 3,600 in. For some analyses, subjects were classified according to baseline Sao(2) quartiles; FMD of the highest quartile subgroup (Sao(2) >= 90%) was used as a reference value for post hoc comparisons.Results: Patients with CMS had marked systemic vascular dysfunction as evidenced by impaired FMD (CMS, 4.6% +/- 1.2%; control subjects, 7.6% +/- 1.9%; P < .0001), greater pulse wave velocity (10.6 +/- 2.1 m/s vs 8.4 +/- 1.0 m/s, P < .001), and greater carotid intima-media thickness (690 +/- 1.20 mu m vs 570 +/- 110 mu m, P = .001). A positive relationship existed between Sao(2) and FMD (r = 0.62, P < .0001). Oxygen inhalation improved (P < .001) but did not normalize FMD in patients with CMS, although it normalized FMD in hypoxemic control subjects (Sao(2) < 90%) and had no detectable effect in normoxemic control subjects (Sao(2) >= 90%).Conclusions: Patients with CMS show marked systemic vascular dysfunction. Structural and functional alterations contribute to this problem that may predispose these patients to premature cardiovascular disease.