Plasma proteoglycan prolargin in diagnosis and differentiation of pulmonary arterial hypertension.

Plasma proteoglycan prolargin in diagnosis and differentiation of pulmonary arterial hypertension.
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DOI:
10.1002/ehf2.13184
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发表时间:
2021-04
期刊:
影响因子:
3.8
通讯作者:
Rådegran G
Rådegran G
中科院分区:
医学3区
文献类型:
--
作者:
Arvidsson M;Ahmed A;Bouzina H;Rådegran G

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肺动脉高压(PAH)可引起右心功能不全。开发能够识别PAH的新诊断方法,并允许在血管重塑和明显的右心衰竭(HF)发展之前更早地开始治疗,可能会潜在地改善预后。蛋白多糖和炎症蛋白参与了血管重塑。我们的目标是研究它们作为区分呼吸困难人群中PAH的生物标志物的潜力。对152例PAH患者(n=48)、慢性血栓栓塞性肺动脉高压(n=20)、心力衰竭射血分数降低(n=36)或保留(n=33)、心力衰竭不伴肺动脉高压(n=315)和20例健康人(n=20)的血浆进行了近距离延伸分析。对右心导管术患者进行血流动力学检测。血浆前列腺素水平低于所有其他疾病组(P<0.001),但高于对照组(P=0.003)。合并人群中作为多环芳烃分化标记物的前列腺素的受试者工作特征曲线涵盖了所有其他研究的疾病组,其敏感性为74%,特异性为83.3%(曲线下面积=0.84,P<0.001)。心得安与平均右房压(r S=0.65,P<0.001)、N端脑利钠肽原(r S=0.64,P<0.01)相关。(0.001)、心脏指数(r S=0.31,P=0.0.029)、每搏输出量指数(r S=0.41,P=0.0.004)、右室每搏做功指数(r S=0.31,P=0.0.032)、6分钟步行距离(r S=0.41,P=0.0.005)、混合静脉血氧饱和度(r S=0.42,P=0.0.003)。血浆前列腺素水平可将PAH患者与对照组和包括心力衰竭在内的其他呼吸困难组区分开来。它在多环芳烃分化中的潜力可以通过包含在多标记物小组中而得到增强。需要更大的研究来评估它与其他呼吸困难病因的区别能力,以及它在PAH风险分层和病理生物学中的潜在作用。
Right ventricular dysfunction may arise because of pulmonary arterial hypertension (PAH). Development of new diagnostic methods able to identify PAH and allow for earlier treatment initiation, before the development of vascular remodelling and manifest right heart failure (HF), could potentially improve prognosis. Proteoglycans and inflammatory proteins are involved in vascular remodelling. We aimed to investigate their potential as biomarkers to differentiate PAH in a dyspnoeic population. Plasma from 152 patients with PAH (n = 48), chronic thrombo‐embolic pulmonary hypertension (n = 20), pulmonary hypertension due to HF with reduced (n = 36) or preserved (n = 33) ejection fraction, and HF without pulmonary hypertension (n = 15) and 20 healthy controls were analysed with proximity extension assays. Haemodynamics were assessed in the patients with right heart catheterization. Plasma prolargin levels in PAH were lower compared with all the other studied disease groups (P < 0.001) but higher than the controls' levels (P = 0.003). Receiver operating characteristic curve of prolargin as a PAH‐differentiating marker in a pooled population, encompassing all the other studied disease groups, had a sensitivity of 74% and a specificity of 83.3% (area under the curve = 0.84, P < 0.001). Prolargin correlated with the mean right atrial pressure (r s = 0.65, P < 0.001), N‐terminal pro‐brain natriuretic peptide (r s = 0.64, P < 0.001), cardiac index (r s = −0.31, P = 0.029), stroke volume index (r s = −0.41, P = 0.004), right ventricular stroke work index (r s = −0.31, P = 0.032), six‐minute walking distance (r s = −0.41, P = 0.005), and mixed venous blood oxygen saturation (r s = −0.42, P = 0.003). Plasma prolargin levels differentiate PAH patients from controls and the other investigated dyspnoea groups including HF. Its potential in PAH differentiation may be enhanced by inclusion in a multi‐marker panel. Larger studies are needed to evaluate its discriminative ability of PAH in relation to other dyspnoea aetiologies and its potential role in PAH risk stratification and pathobiology.
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