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首页> 外文期刊>Heart, lung & circulation >Right Ventricular Epicardial Vascularisation in Patients With Pulmonary Arterial Hypertension
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Right Ventricular Epicardial Vascularisation in Patients With Pulmonary Arterial Hypertension

机译：肺动脉高压患者的右心室心外膜血管体

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BackgroundPulmonary arterial hypertension (PAH) leads to a haemodynamic overload and ischaemia of the right ventricle (RV), which are important triggers of an arterial growth. Thus, we aimed to assess whether patients with PAH have altered epicardial vasculature of the RV, and how it corresponds to RV haemodynamic stress. MethodsWe enrolled consecutive patients with PAH diagnosed in a single pulmonary hypertension centre, who underwent coronary angiography. The control group consisted of patients with normal coronary arteries. Artery branches from segments I–III of the right coronary artery (RCAB) and branches of the left coronary artery (LCAB) were assessed. The sum of the diameters of RCABs (RCAB_sum) was used as a marker of RV epicardial vascularisation. Linear regression models were used to investigate associations between the RCAB_sum and markers of RV dysfunction. ResultsWe recruited 37 PAH patients (idiopathic, n=25; associated with connective tissue disease, n=12) and 37 control subjects of similar age (56±18 vs. 56±13 years, p=0.99) and sex (73% vs. 73% of women, p=0.99). Pulmonary arterial hypertension patients as compared with control subjects had more RCABs (7 [6–8] vs. 6 [5–7], p<0.001) and increased RCAB_sum (9.4 [8.2–10.5] vs. 7.3 [6.6–7.40] mm; p<0.001) although comparable LCAB count (4 [4–5] vs. 4 [4–5]; p=0.50). In a stepwise multivariable linear regression model, RA area (β=0.152 [0.062–0.242]; p=0.002) and diastolic wall stress (β=0.025 [0.005–0.045]; p=0.02) were significant predictors of RCAB_sum (model R2=0.65; p<0.0001). ConclusionsRight ventricular epicardial vasculature is more extensive in PAH patients as compared with control subjects, and it is in linear relation to potential markers of RV diastolic dysfunction.
机译：背景暴动动脉高血压（PAH）导致右心室（RV）的血液动力学过载和缺血性，这是动脉增长的重要触发。因此，我们的目标是评估PAH患者是否已改变RV的心外膜脉管系统，以及它如何对应于RV血液动力学应激。方法载有患有冠状动脉造影的单一肺动脉高压中心诊断的PAH的连续患者。对照组由患有正常冠状动脉的患者组成。评估来自右冠状动脉（RCAB）的段I-III的动脉分支，左冠状动脉（LCAB）的分支。 RCABs（RCAB_SUM）的总和用作RV心外膜血管分子的标志物。线性回归模型用于研究RCAB_SUM和RV功能障碍标记之间的关联。结果我们招募了37例PAH患者（特发性，n = 25;与结缔组织疾病相关，N = 12）和37个类似年龄的对照组织（56±18与56±13岁，P = 0.99）和性别（73％VS 。73％的女性，P = 0.99）。肺动脉高压患者与对照受试者相比具有更多的RCAB（7 [6-8] Vs.6 [5-7]，P <0.001）和增加的RCAB_SUM（9.4 [8.2-10.5]，7.3 [6.6-7.40] mm; p <0.001）尽管可比较的LCAB计数（4 [4-5]与4 [4-5]; p = 0.50）。在逐步多变量的线性回归模型中，RA面积（β= 0.152 [0.062-0.242]; p = 0.002）和舒张壁应力（β= 0.025 [0.005-0.045]; p = 0.02）是rcab_sum的显着预测因子（模型R2 = 0.65; p <0.0001）。结论与对照对象相比，PAH患者的血管性心外膜脉管系统更广泛，并且与RV舒张功能障碍的潜在标志物是线性的关系。

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