Department of Clinical Physiology, Karolinska University Hospital, Stockholm, Sweden.
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
Acta Anaesthesiol Scand. 2023 Feb;67(2):206-212. doi: 10.1111/aas.14168. Epub 2022 Nov 28.
Critically ill Covid-19 patients are likely to develop the sequence of acute pulmonary hypertension (aPH), right ventricular strain, and eventually right ventricular failure due to currently known pathophysiology (endothelial inflammation plus thrombo-embolism) that promotes increased pulmonary vascular resistance and pulmonary artery pressure. Furthermore, an in-hospital trans-thoracic echocardiography (TTE) diagnosis of aPH is associated with a substantially increased risk of early mortality. The aim of this retrospective observational follow-up study was to explore the mortality during the 1-24-month period following the TTE diagnosis of aPH in the intensive care unit (ICU).
A previously reported cohort of 67 ICU-treated Covid-19 patients underwent an electronic medical chart-based follow-up 24 months after the ICU TTE. Apart from the influence of aPH versus non-aPH on mortality, several TTE parameters were analyzed by the Kaplan-Meier survival plot technique (K-M). The influence of biomarkers for heart failure (NTproBNP) and myocardial injury (Troponin-T), taken at the time of the ICU TTE investigation, was analyzed using receiver-operator characteristics curve (ROC) analysis.
The overall mortality at the 24-month follow-up was 61.5% and 12.8% in group aPH and group non-aPH, respectively. An increased relative mortality risk continued to be present in aPH patients (14.3%) compared to non-aPH patients (5.6%) during the 1-24-month period. The easily determined parameter of a tricuspid valve regurgitation, allowing a measurement of a systolic pulmonary artery pressure (regardless of magnitude), was associated with a similar K-M outcome as the generally accepted diagnostic criteria for aPH (systolic pulmonary artery pressure >35 mmHg). The biomarker values of NTproBNP and Troponin-T at the time of the TTE did not result in any clinically useful ROC analysis data.
The mortality risk was increased up to 24 months after the initial examination in ICU-treated Covid-19 patients with a TTE diagnosis of aPH, compared to non-aPH patients. Certain individual TTE parameters were able to discriminate 24-month risk of morality.
危重症 COVID-19 患者可能会因目前已知的病理生理学(内皮炎症加血栓栓塞)而发生急性肺动脉高压(aPH)、右心室应变,最终发展为右心衰竭,从而导致肺血管阻力和肺动脉压增加。此外,院内经胸超声心动图(TTE)诊断 aPH 与早期死亡率显著增加相关。本回顾性观察性随访研究旨在探讨 TTE 诊断 ICU 中 aPH 后 1-24 个月的死亡率。
对先前报告的 67 例 ICU 治疗的 COVID-19 患者进行了基于电子病历的随访,随访时间为 ICU TTE 后 24 个月。除了 aPH 与非 aPH 对死亡率的影响外,还通过 Kaplan-Meier 生存图技术(K-M)分析了几个 TTE 参数。使用接收器工作特征曲线(ROC)分析 ICU TTE 检查时心力衰竭(NTproBNP)和心肌损伤(Troponin-T)的生物标志物的影响。
24 个月随访时的总死亡率分别为 aPH 组 61.5%和非 aPH 组 12.8%。在 1-24 个月期间,aPH 患者的相对死亡风险持续增加(14.3%),而非 aPH 患者(5.6%)。三尖瓣反流等易于确定的参数可测量收缩期肺动脉压(无论大小),与普遍接受的 aPH 诊断标准(收缩期肺动脉压>35mmHg)具有相似的 K-M 结果。TTE 时 NTproBNP 和 Troponin-T 的生物标志物值没有产生任何有临床意义的 ROC 分析数据。
与非 aPH 患者相比,在 ICU 治疗的 COVID-19 患者中,TTE 诊断为 aPH 的患者在初始检查后 24 个月的死亡风险增加。某些特定的 TTE 参数能够区分 24 个月的死亡率风险。