4.5 Article

Continuous long-term wireless measurement of right ventricular pressures and estimated diastolic pulmonary artery pressure in patients with severe COVID-19 acute respiratory distress syndrome

期刊

ESC HEART FAILURE
卷 8, 期 6, 页码 5213-5221

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WILEY PERIODICALS, INC
DOI: 10.1002/ehf2.13600

关键词

COVID-19; ARDS; Pulmonary hypertension; ePAD; Sildenafil

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In this study, continuous monitoring of right ventricular pressures and ePAD in mechanically ventilated patients with severe COVID-19 ARDS revealed significantly lower RVSP in survivors compared to non-survivors, suggesting successful lowering by pulmonary vasodilators. The ePAD was significantly higher in non-survivors compared to surviving patients, indicating a potential indicator of left heart failure. Treatment with pulmonary vasodilators may help improve patient survival.
Aims We continuously monitored right ventricular pressures and the estimated diastolic pulmonary artery pressure (ePAD) for up to 30 days in mechanically ventilated patients with severe COVID-19 acute respiratory distress syndrome in order to detect and treat right ventricular and pulmonary artery hypertension. Methods and Results We retrospectively evaluated right ventricular pressures and the ePAD measured in 30 invasively ventilated COVID-19 acute respiratory distress syndrome patients between 1 October 2020 and 31 March 2021. We divided the patients into two groups, survivors and non-survivors based on their 60 day mortality. Primary outcome variables were the values of right ventricular pressures and the ePAD over time after insertion of the right ventricular probe. Right ventricular systolic pressure [RVSP, (IQR; 25th to 75th percentile)] was significantly lower on the first and the last measurement day in the survivors compared with the non-survivors [Day 1: 38 (27-45) vs. 46 (44-49), P = 0.036; last day: 36 (27-44) vs. 51 (40-57) mmHg, P = 0.006]. 16/22 survivors and 7/8 non-survivors received sildenafil orally, one survivor received additionally inhaled nitric oxide and one survivor and one non-survivor each inhaled iloprost. On the last measurement day, both right ventricular pressure amplitude [31 (26-37) vs. 38 (35-47) mmHg, P = 0.027] and ePAD [22 (16-26) vs. 31 (23-34) mmHg, P = 0.043] were significantly lower in the survivors compared with the non-survivors. Four patients in the survivor group developed excessive high RVSP in the course of their disease (peak: 57/61/78/105 mmHg). After sildenafil 20 mg every 8 h, additional inhaled nitric oxide (20 ppm) in one and additional inhaled iloprost 20 mu g every 4 h in another patient RVSP consecutively decreased substantially in all four patients until the end of the measurement period (47/23/42/47 mmHg). Conclusions The RVSP and right ventricular pressure amplitude both were significantly lower in the survivors compared with those in the non-survivors with a significant decrease in RVSP over time in the survivors suggesting successful lowering by pulmonary vasodilators. The ePAD as an indicator of left heart failure was significantly higher in non-survivors compared to the surviving patients.

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