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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.    Methods  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.    Results  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 −1 ;  P  = .0007), troponin T levels (63 [22‐352] vs. 15 [5‐407] ng L −1 ;  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.    Conclusion  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.

Acute pulmonary hypertension and short‐term outcomes in severe Covid‐19 patients needing intensive care