The assessment of pulmonary artery pressure is not singular. Right heart catheterization is an advanced method for the evaluation of pulmonary arterial pressure, but it is only used for certain patients because it is an invasive operation[15, 17]. Abbas et al. developed an algorithm to calculate PVR of patients with pre occipital PH, but this method may lead to false-positive results[18]. The most commonly used method in clinical practice is to calculate the maximum systolic pressure[16, 19, 20] using the tricuspid regurgitation velocity[21]. This method has been widely used and is based on the clear guidelines of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS); therefore, we opted to follow this method to evaluate pulmonary artery pressure in our study. However, this method requires good image quality and sufficient Doppler signal which may be disadvantageous in some settings, but the images of the 42 patients we selected all met the requirements.
In the present study, LUS was positively correlated with pulmonary arterial pressure, with the correlation becoming stronger with increasing disease severity. There are many reasons for increased pulmonary arterial pressure[14, 22, 23]. Patients with a history of underlying cardiopulmonary disease were excluded from the present study, and the observed changes in the 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, prolonging the diffusion time. Hypoxic acidosis can cause swelling of pulmonary endothelial cells and pulmonary vasospasm, leading to pulmonary hypertension[14, 24].
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 is thought to be a functional receptor for coronaviruses on epithelial cells[25–27]. Another component of the renin-angiotensin system is angiotensin II, which causes inflammation and damage of alveolar epithelium. The lung injury associated with COVID-19 may be due to the 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[14–16, 22, 23] have investigated pulmonary arterial hypertension caused by pneumonia; however, there are no reports on the use of pulmonary arterial pressure to predict LUS. In the present study, LUS was dynamically evaluated and echocardiography was performed simultaneously. LUS increased with worsening disease and decreased with improving disease condition. Echocardiography indicated that the amount of tricuspid regurgitation increased with worsening disease condition, and the pulmonary arterial pressure and the inner diameters, volumes of the pulmonary artery, right ventricle, and right atrium also increased. All 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 an efficient 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 the 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%. Three (3/42) patients were stable, which may be related to the compensation by pulmonary blood vessels[12, 24]. The rate of positivity for LUS on day 8 was 90.5%, and the scores of four patients did not increase with worsening disease conditions. 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 needed to undergo oxygen therapy for dyspnea. Compared with patients who did not undergo oxygen therapy, the estimation of pulmonary arterial pressure may be biased. Since the frequency of CT examination was not as high as that of ultrasound, thus not all patients have corresponding CT data at the three study timepoints, causing a lack of basis for comparison. Fortunately, corresponding CT data were available for seven negative patients, which provided a strong basis for diagnosis. At present, many studies[8, 9] describe the application of LUS and echocardiography in patients with COVID-19 pneumonia. The application of LUS in the literature is mainly denoted by the ultrasonic characteristics of different degrees of lung lesions; for example, B-line, white lung. Cardiac reports[9] also focus on intensive care unit (ICU) patients. Most of the patients we evaluated were non-ICU patients. Our comprehensive evaluation of patients' lungs (bilateral lung score) may better reflect the degree of illness. The change in pulmonary hemodynamics in patients with COVID-19 pneumonia is clear; we also found the change in pulmonary arterial pressure to be a sensitive indicator at the early stage of the disease. When it is inconvenient to perform double lung scoring in patients on ventilator support, pulmonary arterial pressure can be measured to reflect the severity of lung disease. This knowledge may help to guide the management of patients with severe disease.