In the present study LUS was positively correlated with pulmonary arterial pressure, and the correlation was stronger with increased disease severity. There are many reasons for increased pulmonary arterial pressure[12–14]. Patients with a history of underlying cardiopulmonary disease were excluded from the present study, and the observed changes in pulmonary arterial pressure were believed to be related to lung disease. During lung inflammation, inflammatory infiltration and alveolar exudate reduce the alveolar surface area available for diffusion, and diffusion time is prolonged. Hypoxic acidosis can cause swelling of pulmonary endothelial cells and pulmonary vasospasm, leading to pulmonary hypertension[12, 15].
The COVID-19 pneumonia outbreak and the 2003 severe acute respiratory syndrome outbreak were both caused by members of the coronavirus family. Angiotensin-converting enzyme-2 is a component of the renin-angiotensin system that protects blood vessels, and it is thought to be a functional receptor for coronaviruses on epithelial cells[16–18]. Another component of the renin-angiotensin system is angiotensin II, which causes alveolar epithelium inflammation and damage. The lung injury associated with coronavirus disease 2019 may be due to upregulation of angiotensin II and reduced angiotensin-converting enzyme-2 levels resulting in increased pulmonary vasoconstriction. The results of the present study suggest that these factors are associated with higher LUS and higher pulmonary arterial pressure.
Many studies[12–14] have investigated pulmonary arterial hypertension caused by pneumonia, but there are no reports of the use of pulmonary arterial pressure to predict LUS. In the present study LUS were dynamically evaluated, and echocardiography was performed simultaneously. LUS increased with worsening condition, and decreased with improving condition. Echocardiography indicated that the amount of tricuspid regurgitation increased with worsening condition, and pulmonary arterial pressure and the inner diameters of the pulmonary artery, right ventricle, and right atrium also increased. All of these parameters exhibited statistically significant changes, and all of them decreased with improving condition (Tables 2 and 3). These results suggest that changes in LUS and pulmonary arterial pressure can reflect lung lesions.
Hemodynamic characteristics indicate that increased pulmonary arterial pressure leads to increased right ventricular ejection resistance, which results in increased inner diameter of the right atrium, right ventricle, and pulmonary artery. Dynamic echocardiography can be used to monitor changes in pulmonary arterial pressure and the size of each chamber of the heart in real time, such that disease development can be assessed in a timely manner. The positive correlation between pulmonary arterial pressure and LUS in the current study also indicates a tendency in LUS. There were no significant changes in left heart size during the entire course of disease, indicating a low probability of left heart involvement, which is consistent with previous studies.
In the present study the rate of positivity for increased pulmonary arterial pressure in the 42 patients on day 8 was 92.9%. 3(3/42) patient was stable, which may be related to compensation by pulmonary blood vessels[12, 15]. The rate of positivity for LUS on day 8 was 90.5%, and the scores of 4 patients did not increase with worsening condition. In conjunction with CT findings this suggests that the region of lesion exacerbation did not involve the edge of the lung, which is outside the detection range of ultrasound and is consistent with the principles of lung ultrasound. The positivity rate for the combination of the two was 97.6%, which constitutes an improvement in the accuracy of disease progression evaluation. To date there have been no comparable previous reports.
The current study had some limitations. Some patients could not undergo oxygen therapy due to dyspnea. Compared with patients who did not undergo oxygen therapy, the estimation of pulmonary arterial pressure may be biased. Because the frequency of CT examination was not as high as that of ultrasound, not all patients have corresponding CT data at the three study timepoints utilized, and there is a lack of a basis for comparison. Fortunately, corresponding CT data were available for 7 negative patients, which provided a strong basis for diagnosis.