Zanoli Luca, Rastelli Stefania, Inserra Gaetano, Castellino Pietro
Luca Zanoli, Stefania Rastelli, Gaetano Inserra, Pietro Castellino, Department of Internal Medicine, Policlinico Universitario, University of Catania, 95123 Catania, Italy.
World J Gastroenterol. 2015 Oct 28;21(40):11304-11. doi: 10.3748/wjg.v21.i40.11304.
Inflammatory bowel disease (IBD) is the result of a combination of environmental, genetic and immunologic factors that trigger an uncontrolled immune response within the intestine, which results in inflammation among genetically predisposed individuals. Several studies have reported that the prevalence of classic cardiovascular risk factors is lower among subjects with IBD than in the general population, including obesity, dyslipidaemia, diabetes and hypertension. Therefore, given the risk profile of IBD subjects, the expected cardiovascular morbidity and mortality should be lower in these patients than in the general population. However, this is not the case because the standardized mortality ratio is not reduced and the risk of coronary heart disease is increased in patients with IBD. It is reasonable to hypothesize that other factors not considered in the classical stratification of cardiovascular risk may be involved in these subjects. Therefore, IBD may be a useful model with which to evaluate the effects of chronic low-grade inflammation in the development of cardiovascular diseases. Arterial stiffness is both a marker of subclinical target organ damage and a cardiovascular risk factor. In diseases characterized by chronic systemic inflammation, there is evidence that the inflammation affects arterial properties and induces both endothelial dysfunction and arterial stiffening. It has been reported that decreasing inflammation via anti tumor necrosis factor alpha therapy decreases arterial stiffness and restores endothelial function in patients with chronic inflammatory disorders. Consistent with these results, several recent studies have been conducted to determine whether arterial properties are altered among patients with IBD. In this review, we discuss the evidence pertaining to arterial structure and function and present the available data regarding arterial stiffness and endothelial function in patients with IBD.
炎症性肠病（IBD）是环境、遗传和免疫因素共同作用的结果，这些因素会引发肠道内不受控制的免疫反应，从而在具有遗传易感性的个体中导致炎症。多项研究报告称，IBD患者中经典心血管危险因素的患病率低于普通人群，包括肥胖、血脂异常、糖尿病和高血压。因此，鉴于IBD患者的风险特征，这些患者的预期心血管发病率和死亡率应低于普通人群。然而，实际情况并非如此，因为IBD患者的标准化死亡率并未降低，冠心病风险反而增加。有理由推测，心血管风险经典分层中未考虑的其他因素可能与这些患者有关。因此，IBD可能是一个有用的模型，可用于评估慢性低度炎症在心血管疾病发展中的作用。动脉僵硬度既是亚临床靶器官损伤的标志物，也是心血管危险因素。在以慢性全身炎症为特征的疾病中，有证据表明炎症会影响动脉特性，并导致内皮功能障碍和动脉僵硬度增加。据报道，通过抗肿瘤坏死因子α治疗减轻炎症可降低慢性炎症性疾病患者的动脉僵硬度并恢复内皮功能。与这些结果一致，最近进行了多项研究以确定IBD患者的动脉特性是否发生改变。在本综述中，我们讨论了与动脉结构和功能相关的证据，并展示了IBD患者动脉僵硬度和内皮功能的现有数据。
