The role of Chest CT imaging in the COVID-19 infection is apparent as to determine the prevalence and severity of the disease, early screening, and making different diagnoses. In a study by Fang et al., the sensitivity of chest CT with COVID-19 was 98% (12). The typical CT findings are the multifocal bilateral distribution of ground-glass opacities, consolidations, air bronchogram, crazy-paving pattern, pulmonary vascular enlargement, linear opacification, and airway and pleural changes COVID-19 (7–8).
Our retrospective study showed a well-established cut-off value of MPAD ≥ 29 mm was an independent predictor of the severity of the COVID-19 infection. Enlargement of PA was an independent predictor of mortality and in-hospital duration. It was found to negatively correlate with the oxygen saturation at the time of the admission. Enlargement of PA, which can be detected by CT imaging, is a parameter that helps to predict adverse outcomes (13). Although PA enlargement is associated with poor prognosis in acute pulmonary edema, embolism, and heart failure, insufficient data on its prognostic significance and optimal cut-off PA diameter in COVID-19 infection. A normally mean PA diameter calculated in a healthy population was 26.1 ± 2.4 mm in men and 22.9 ± 1.9 mm in women (14). This value was 25.74 ± 3.48 mm in the entire study group. A study conducted by Esposito et al., which included 1461 patients, determined that an MPAD ≥ 31 mm in COVID-19 patients was an independent predictor of mortality (15). The study by Zhu et al. points to MPAD ≥ 29 mm as a significant predictor of subsequent death (10). Truong et al. demonstrated that the predictive value of MPAD is 31 mm or greater in diagnosis PH and associated with 2–3 fold increased mortality risk compared to normal (11). In parallel, we found similar findings in our study cohort with an MPAD ≥ 29 mm, and these patients have more inflammation, heart injuries, and co-morbid disease. MPAD, both as a continuous and categorical variable, predicted in-hospital mortality in various regression models adjusted with age, comorbidities, clinical status, and inflammatory parameters.
Besides being a primary lung disease, COVID-19 is an infectious pathology that disrupts the endothelial system by activating numerous inflammatory and prothrombotic cascades. Erdoğan et al. have suggested that disrupts the endothelial system, increased inflammatory process, myocarditis, and active coagulopathy are associated with the severity of COVID-19 and ultimately predict adverse outcomes (16). Increased inflammatory status is accompanied by the severity of the disease and increased mortality rates (13, 16). It may result in a decrease in lung capacity and increased PA pressure. In addition, many patients had elevated inflammatory parameters, liver enzymes, CPK, and prothrombin time (13). Furthermore, Cai et al. demonstrated the increase in liver enzymes from severe pneumonia might be related to increased pulmonary pressure (17). In our cohort, similar to these results, AST and inflammatory levels, hs-CRP, ferritin, troponin, BUN, WBC, D-Dimer, and creatinine levels were significantly associated with PA diameter. Although thrombocytopenia is a common finding in COVID-19 patients in previous studies, no correlation was found between platelet count and PA diameter in our study (18–19).
PH's etiology is considered multifactorial; pulmonary small vessel thrombosis, vasculopathy, hypoxemia, and vasoconstriction were reported as the leading cause of PH in COVID-19 disease. PH can rapidly worsen right heart function and impair oxygenation. Thus the length of hospital stay is prolonged, and the risk of the patient's multi-organ failure, bacterial infections, sepsis, hypercoagulation, and thrombosis. We found that severe CT findings of pneumonia and relation with hypoxemia were correlated with higher MPAD. It is the most severe reason for poorer outcomes.
COVID-19 has maybe affected the cardiovascular system. The underlying mechanism of cardiac damage is not clearly understood. Increased cardiac stress secondary to acute respiratory failure and progressive hypoxemia, direct myocardial infection of the virus, increased inflammatory status, or combination. Also, SARS-CoV-2 infects host cells by angiotensin-converting enzyme 2 (ACE2) receptors, leading to myocardial injury. It has been shown that cardiovascular complications and heart failure may be responsible for 40% of deaths in COVID-19 patients (20).
There is a need for criteria to predict the severity and prognosis of the disease in COVID-19 patients. Thus, increased MPAD may guide rapid and early diagnosis and treatment of high-risk patients.
In our study, pulmonary disease, CAD, CHF, and HT at the time of admission adversely affected the prognosis in COVID-19 patients. On the contrary, the presence of DM did not affect the prognosis in our patient population.
Limitation Of The Study
Although our study emphasized the association of PA diameter with mortality, there are several limitations. We did not know about the clinical condition and PA diameters of the patients before the COVID-19. There was also no follow-up data. Dynamic measurement of PA trunk diameter will reveal more information. Furthermore, our cohort included only hospitalized patients because these results cannot be generalized to all COVID-19 patients. The frequency of pulmonary embolism that could lead to PA enlargement was unknown. And lack of data on electrocardiography and echocardiography imaging.