Magoń Wojciech, Stępniewski Jakub, Miszalski-Jamka Tomasz, Urbańczyk-Zawadzka Małgorzata, Podolec Piotr, Kopeć Grzegorz
Department of Cardiac and Vascular Diseases, Jagiellonian University Medical College at John Paul II Hospital in Kraków, Poland.
Department of Radiology and Diagnostic Imaging, John Paul II Hospital in Krakow, Prądnicka 80, Kraków, Poland.
Heart Lung Circ. 2018 Dec;27(12):1428-1436. doi: 10.1016/j.hlc.2017.08.023. Epub 2017 Sep 28.
Pulmonary 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.
We 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.
We 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 R=0.65; p<0.0001).
Right 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.
肺动脉高压（PAH）会导致血流动力学负荷过重以及右心室（RV）缺血，这是动脉生长的重要触发因素。因此，我们旨在评估PAH患者的右心室心外膜血管系统是否发生改变，以及它与右心室血流动力学应激之间的关系。
我们纳入了在单一肺动脉高压中心诊断为PAH且接受冠状动脉造影的连续患者。对照组由冠状动脉正常的患者组成。评估右冠状动脉（RCAB）I-III段的动脉分支以及左冠状动脉（LCAB）的分支。RCAB直径总和（RCAB_sum）用作右心室心外膜血管化的标志物。使用线性回归模型研究RCAB_sum与右心室功能障碍标志物之间的关联。
我们招募了37例PAH患者（特发性，n = 25；与结缔组织病相关，n = 12）和37例年龄相仿（56±18岁 vs. 56±13岁，p = 0.99）且性别相同（女性分别占73% vs. 73%，p = 0.99）的对照受试者。与对照受试者相比，PAH患者的RCAB更多（7 [6 - 8] vs. 6 [5 - 7]，p < 0.001）且RCAB_sum增加（9.4 [8.2 - 10.5] vs. 7.3 [6.6 - 7.40] mm；p < 0.001），尽管LCAB数量相当（4 [4 - 5] vs. 4 [4 - 5]；p = 0.50）。在逐步多变量线性回归模型中，右心房面积（β = 0.152 [0.062 - 0.242]；p = 0.002）和舒张期壁应力（β = 0.025 [0.005 - 0.045]；p = 0.02）是RCAB_sum的显著预测因子（模型R = 0.65；p < 0.0001）。
与对照受试者相比，PAH患者的右心室心外膜血管系统更广泛，且与右心室舒张功能障碍的潜在标志物呈线性关系。
