In the present study of 32 consecutive patients with confirmed pulmonary embolism and COVID-19 infection, patients with a larger right ventricular diameter required oxygen support more often, which was correlated with the PESI score as an indicator of PE severity. It is notable that COVID-19 patients presenting primarily with PE usually belonged to the low-risk group according to the calculated PESI score and rarely progressed to right ventricular dysfunction and hemodynamic instability. Already-hospitalized patients with severe COVID-19 pneumonia who developed PE during their hospitalization had worse outcomes, probably due to several pathophysiological mechanisms involved in the pathogenesis of PE.
In the first months of the pandemic, it became clear that fast decision-making would determine the course of the disease, so diagnostic methods and guidelines were rapidly put in place to enhance efficiency. Diagnostics had to be precise but also involve a minimum duration of contact between the physician and patient to reduce the possibility of disease transmission. Point-of-care ultrasound is recommended for evaluating critically ill patients with respiratory failure, multisystem organ failure, or shock. Its advantages compared with traditional imaging modalities are rapid assessment of a patient’s change in status, easy bedside access with no need to transport already-critical patients on multi-organ support machines, and decreased potential for the transmission of SARS-CoV-2 to staff and others during transport [
14]. In our scans, the ultrasound was performed in the usual echocardiographic views—short and long parasternal axes, apical four-, two-, and three-chamber views, and the subcostal view. The parameters that were obtained (listed in
Supplementary Table S3) varied depending on the clinical aspect and the severity of the patient’s condition. As recommended, the goal was to assess the size and function of both the left and right ventricles, the presence of pericardial effusion, and indirectly measured right-chamber and pulmonary pressures to determine the cause of the deterioration of the patient’s condition [
15]. Taking into account that a significant percentage of critically ill patients have comorbidities, such as COPD or congestive heart failure, it is of undeniable importance to determine the cause of respiratory failure to apply a treatment plan [
16]. Congestive heart failure exacerbation, COPD exacerbation, COVID-19 acute respiratory distress syndrome (ARDS), and PE are common considerations in this patient population [
17]. Keeping in mind that more than half of the patients in our cohort had low-risk PE, without affecting the large pulmonary artery branches, the values of the functional parameters of the right ventricle were mostly in the physiological range. Nevertheless, a larger right ventricular diameter, as an indirect indicator of elevated pulmonary vascular pressure, was positively correlated with the need for oxygen support. This information might be crucial, as it isolates patients with a higher risk of deterioration, who can then be more closely monitored and in whom complications might be prevented. Lower (pathological) levels of PVAT were found in patients with PE who were already on anticoagulation therapy. These patients were mostly those who were already hospitalized with pneumonia and severe COVID-19 with higher PESI scores. Bearing in mind that these patients already had increased pulmonary pressures due to interstitial lung consolidations and, not rarely, were on mechanical ventilatory support, PVAT might point to an acute rise in pulmonary artery pressure as a sign of acute PE. Another study considering echocardiographic abnormalities and the connection to worse outcomes in COVID-19 patients is described in a paper by Vincenza Polito et al. [
18]. They concluded that RV systolic dysfunction, high pulmonary pressures, and poor RV–arterial coupling independently predict the risk of mortality and PE in hospitalized patients with COVID-19, both in the ICU and the ward. While the advantage of this study in comparison to ours was a larger cohort of patients (227 compared to 32), our study is novel in including only patients hospitalized with COVID-19 and confirmed PE by MSCT pulmonary angiography, as opposed to all hospitalized COVID-19 patients. Nevertheless, the mentioned study also showed significance in the early echocardiographic evaluation of patients and risk stratification.
Aside from POCUS, as an important method to quickly estimate a patient’s condition, the close monitoring of possible PE causes is of great importance, with deep vein thrombosis as one of the most significant. Deep vein thrombosis was identified as a source of emboli based on clinical findings or color Doppler ultrasound in only 12.5% of all of our patients, which is in accordance with several other reports, such as Mirsadraee et al. [
6], where only 23% of patients with a CTPA diagnosis of PE also had radiological evidence of peripheral deep vein thrombosis. Keeping this in mind, thrombotic complications of COVID-19 are more likely explained by a cluster of pathophysiological mechanisms and not only as a consequence of thromboembolism. Hemostatic changes occur in SARS-CoV-2 infection, which might be a specific effect of SARS-CoV-2 or a consequence of a cytokine storm, as observed in other viral diseases. Systemic inflammation can then be followed by disseminated intravascular coagulation, which may predispose COVID-19 patients to micro- and macrovascular pulmonary thrombosis. The local endothelial injury of pulmonary blood vessels by the virus itself or inflammatory cytokines forms predilection sites for in situ thrombosis [
19]. The potential interaction of novel antiviral and biological therapies (monoclonal antibodies), as well as other pharmacological agents being used in the treatment of COVID-19 patients, could disrupt the effect of anticoagulation therapy, which would explain the high prevalence of thrombotic complications in patients already on anticoagulation therapy [
20]. Lastly, patients with the most severe form of the disease on mechanical ventilatory support are bedridden and immobilized. A total of 10 (32.2%) patients from our cohort were diagnosed with PE during hospitalization, and all of them were already on anticoagulation therapy, although these were also the patients with the most severe forms of the disease. This points out the potential significance of multiple pathophysiological mechanisms being involved in thromboembolic complications and strongly affecting the coagulation status, which usually leads to a more severe hemodynamic deterioration and poor clinical outcomes. It is also important to note that pneumonia was present in two-thirds of the patients, which means that 32% of patients with CTPA-verified PE did not have any signs of viral pneumonia on CT. This implies that patients can have severe, life-threatening complications of the disease without respiratory tract involvement, especially in a younger population. This is why a quick and proper diagnostic algorithm can save time and prevent possible severe complications.
The main limitation of this study is the relatively small cohort of patients recruited from a single center. Echocardiography was focused solely on patients with confirmed or suspected complications of the disease, such as PE, in order to minimize unnecessary contact and prevent the disease from spreading. Disregarding the small sample size, this is the first study concerning only COVID-19 patients hospitalized in the ICU with verified PE. Future studies are required to determine whether similar results can be obtained in different clinical settings with a larger sample size. The lack of complete echocardiographic studies for all observed PE patients prevents the generalization of the obtained correlations with the major complications of the disease and poor clinical outcomes.