Department of Clinical Physiology, Department of Molecular Medicine and Surgery, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
Section of Thoracic Anaesthesia and Intensive Care, Perioperative Medicine and Intensive Care, Karolinska University Hospital, Stockholm, Sweden.
Acta Anaesthesiol Scand. 2021 Jul;65(6):761-769. doi: 10.1111/aas.13819. Epub 2021 Mar 27.
Critically ill Covid-19 pneumonia patients are likely to develop the sequence of acute pulmonary hypertension, right ventricular (RV) strain, and eventually RV failure due to known pathophysiology (endothelial inflammation plus thrombo-embolism) that promotes increased pulmonary vascular resistance and pulmonary artery pressure. This study aimed to investigate the occurrence of acute pulmonary hypertension (aPH) as per established trans-thoracic echocardiography (TTE) criteria in Covid-19 patients receiving intensive care and to explore whether short-term outcomes are affected by the presence of aPH.
Medical records were reviewed for patients treated in the intensive care units at a tertiary university hospital over a month. The presence of aPH on the TTE was noted, and plasma NTproBNP and troponin were measured as markers of cardiac failure and myocardial injury, respectively. Follow-up data were collected 21 d after the performance of TTE.
In total, 26 of 67 patients (39%) had an assessed systolic pulmonary artery pressure of > 35 mmHg (group aPH), meeting the TTE definition of aPH. NTproBNP levels (median [range]: 1430 [102-30 300] vs. 470 [45-29 600] ng L ; P = .0007), troponin T levels (63 [22-352] vs. 15 [5-407] ng L ; P = .0002), and the 21-d mortality rate (46% vs. 7%; P < .001) were substantially higher in patients with aPH compared to patients not meeting aPH criteria.
TTE-defined acute pulmonary hypertension was frequently observed in severely ill Covid-19 patients. Furthermore, aPH was linked to biomarker-defined myocardial injury and cardiac failure, as well as an almost sevenfold increase in 21-d mortality.
由于已知的病理生理学（内皮炎症加血栓栓塞）导致肺血管阻力和肺动脉压增加，危重症新冠肺炎肺炎患者可能会出现急性肺动脉高压、右心室（RV）应变，最终 RV 衰竭的序列。本研究旨在调查在接受重症监护的新冠肺炎患者中，按照既定的经胸超声心动图（TTE）标准发生急性肺动脉高压（aPH）的情况，并探讨 aPH 的存在是否会影响短期结局。
回顾性分析了一家三级大学医院重症监护病房一个月内治疗的患者的病历。注意到 TTE 上存在 aPH，并测量血浆 NTproBNP 和肌钙蛋白作为心力衰竭和心肌损伤的标志物。在 TTE 后 21 天收集随访数据。
共有 67 例患者中的 26 例（39%）的收缩期肺动脉压评估值>35mmHg（组 aPH），符合 TTE 定义的 aPH。NTproBNP 水平（中位数[范围]：1430[102-30300] vs. 470[45-29600]ng L；P=.0007）、肌钙蛋白 T 水平（63[22-352] vs. 15[5-407]ng L；P=.0002）和 21 天死亡率（46% vs. 7%；P<.001）在 aPH 患者中明显高于不符合 aPH 标准的患者。
在严重新冠肺炎患者中经常观察到 TTE 定义的急性肺动脉高压。此外，aPH 与生物标志物定义的心肌损伤和心力衰竭有关，21 天死亡率增加近 7 倍。
