The highly contagious 2019 novel coronavirus that causes coronavirus disease 2019 increased the scientific community's interest in diagnosing and monitoring COVID-19. Due to the findings about the association between COVID-19 infection and pulmonary disturbances, the need for the use of complementary tests that can be carried out, preserving the health of patients, has grown. In this context, single-photon emission computed tomography (SPECT) was performed during the COVID-19 pandemic to assess and try to diagnose lung lesions. The aim of this current review was to investigate the types of SPECT images most commonly used and the main pulmonary parenchymal lesions and different lung perfusion abnormalities observed in these images in individuals with COVID-19 in different countries in the world.

Electronic searches in the MEDLINE/PubMed, Embase, Scopus, Web of Science, and CINAHL databases were conducted in December 2022. Studies that used SPECT/CT scans to evaluate pulmonary involvements due to COVID-19, with no language restriction, were included. Two reviewers, who independently examined titles and abstracts, identified records through the database search and reference screening, and irrelevant studies were excluded based on the eligibility criteria. Relevant complete texts were analyzed for eligibility, and all relevant studies were included in a systematic review.

Eight studies with regular methodological quality were included. The types of SPECT examinations used in the included articles were SPECT/CT, Q SPECT/CT, and V/Q SPECT. The possible pulmonary complication most observed was pulmonary embolism.

This systematic review demonstrated that SPECT/CT scans, mainly with perfusion methods, allow the maximum extraction of benefits from pulmonary images, in safety, suggesting efficiency in the differential diagnosis, including of respiratory diseases of different etiology, and with diagnostics and additional analyses, can possibly aid the development of suitable therapeutic strategies for each patient. Randomized clinical trials and studies of good methodological quality are necessary to confirm the findings of this review and help better understand the types of SPECT images most commonly used and the main pulmonary parenchymal lesions observed in the images in individuals with COVID-19.

Coronavirus disease 2019 (COVID-19) is associated with an increase in venous thrombotic and cardiovascular (CV) events has been reported during hospitalization. No systematic ultrasound follow-up to evaluate sequelae was ever that took place carried out prospectively associated with the evaluation of CV morbidity-mortality at 3 months post-discharge. Consecutive patients hospitalized for COVID-19 in the Amiens-Picardie University Hospital between 1st February and 31st August 2020 were included. The primary objective was the thrombosis incidence at 3 months after hospital discharge. Thrombosis was defined as either venous thromboembolism (VTE) or a CV event (CVE: myocardial infarction (MI), stroke or peripheral arterial disease). A secondary objective was to determine the risk factors for thrombotic events. We included 498 patients (279 men; 56%) of median age 66 (55-76) years. The primary composite outcome occurred in 27 patients (5.4%); 19 patients (3.8%) presented a CVE (stroke, n = 5; MI, n = 9; and peripheral arterial disease, n = 5). Two patients (0.8%) presented VTE. Six patients (1.2%) died. In multivariate analysis, a previous CVE was associated with thrombosis (OR 3.11; 95% CI 1.17-8.24). COVID-19 was significantly associated with thrombotic events post hospital discharge. Special attention should be given to CVE in the follow-up of patients with a previous thrombotic event.

While our understanding of coronavirus disease 2019 (COVID-19) has evolved, uncertainty remains regarding utility of previously established pulmonary embolism (PE) screening guidelines in patients with COVID-19. Many studies have investigated the efficacy of D-dimer (DD) screenings for patients with COVID-19 admitted to inpatient services, but few have evaluated patients in the emergency department (ED). The purpose of this study was to investigate utility of DD threshold for PE screening in patients with COVID-19 presenting to the ED.

This was a retrospective, multicenter cohort including patients presenting to three EDs between March 1, 2020 and February 1, 2021 who tested positive for COVID-19 during ED visit or in 60 days prior to presentation and had DD ordered in ED. Patients were grouped by those who underwent computed tomography pulmonary angiogram (CTPA) to evaluate for PE and those who did not, and descriptive statistics were performed. Those who underwent CTPA were further divided into PE-positive and PE-negative groups. The discriminative ability of DD in predicting PE in patients with COVID-19 was analyzed using the receiver operating characteristic (ROC) curve.

A total of 570 patients with COVID-19 were included in the study, of which 107 underwent CTPA to evaluate for PE. History of diabetes, elevated glucose, elevated lactate dehydrogenase, elevated white blood cell count, elevated platelets, elevated respiratory rate, and lower temperature were associated with increased risk for PE. Compared to those without PE, patients with PE were significantly more likely to be hospitalized (100% vs. 82%, p = 0.020) and admitted to the ICU (64% vs. 24%, p = 0.002). Those with PE had a significantly higher median DD value (21,177 ng/mL) compared to PE-negative group (952 ng/mL, p < 0.001). The ROC curve for DD in predicting PE had an area under the curve of 0.91 (95% confidence interval [0.84, 0.98]). In our study population, the optimal DD threshold for predicting PE was 1815 ng/mL (sensitivity 93% and specificity 80%). A conservative threshold of 1089 ng/mL could be used with sensitivity 100% and specificity 58%.

DD is often elevated in patients with COVID-19, regardless of PE. While the classically used DD cutoff is 500 ng/mL, our study demonstrated a threshold of 1089 ng/mL safely predicted PE in patients with COVID-19 .

The global outbreak of coronavirus disease 2019 (COVID-19) presents numerous obstacles for healthcare professionals. The present study aimed to evaluate and compare the role of serum biomarkers like- C-reactive protein (CRP), interleukin-6 (IL-6), and D-dimers in the severity of COVID-19 infection.

A cross-sectional, observational retrospective pilot study was conducted in Udaipur, Rajasthan, wherein data was collected from 250 subjects, out of which, data of 100 subjects were included as per the inclusion criteria. The data was recorded retrospectively among the health professionals via Google Forms in Udaipur, Rajasthan.

There were 1 (1%), 3 (3%), 31 (31%) and 65 (65%) participants with minor elevation (0.3-1.0), moderate elevation (1-10), marked elevation (10-50) and severe elevation (>50) of CRP respectively. The difference between the groups was statistically highly significant with a significantly higher number of study participants with a severe elevation of CRP levels (χ2 = 107.84, P < 0.001). The results showed that there was a significant difference between the groups with IL6 in 0-7 range while 96 (96%) study participants had >7 IL6, and the difference was statistically highly significant (2 = 84.640, P 0.001).

In conclusion, the existing body of research indicates a discernible correlation between COVID-19 infection and the fluctuation of biomarker levels. This supplement has the potential to be utilised in clinical practice as a means of informing treatment decisions and determining the necessity of admission to the intensive care unit (ICU).

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the resulting coronavirus disease 2019 (COVID-19) represented a global public health crisis and the most significant pandemic in modern times. Transmission characteristics, and the lack of effective antiviral treatment protocol and protective vaccines, pushed healthcare systems, particularly intensive care units (ICUs), to their limits and led to extreme quarantine measures to control the pandemic. It was evident from an early stage that patient stratification approaches needed to be developed to better predict disease progression. In the present study, the predictive value of clinical and blood biomarkers for the outcomes of patients with COVID-19 hospitalized in the ICU were investigated, taking age and sex into consideration. The present study analyzed blood samples from 3,050 patients with COVID-19 hospitalized in the ICU. The analysis revealed that the levels of procalcitonin, N-terminal pro-B-type natriuretic peptide, D-dimer, ferritin, liver enzymes, C-reactive protein and lactate dehydrogenase were increased and were associated with disease progression, resulting in a prolonged hospitalization period and severe COVID-19 related complications. Additionally, significant age and sex disparities among these biomarkers were documented and discussed in specific cases. On the whole, the results of the present study suggest a potential association of the demographic characteristics and blood biomarkers with prolonged hospitalization in the ICU and the mortality of patients with COVID-19.

The coronavirus disease 2019 (COVID-19) pandemic that began in early 2020 resulted in significant mortality from respiratory tract infections. Existing imaging modalities such as chest X-ray (CXR) lacks sensitivity in its diagnosis while computed tomography (CT) scan carries risks of radiation and contamination. Point-of-care ultrasound (POCUS) has the advantage of bedside testing with higher diagnostic accuracy. We aim to describe the various applications of POCUS for patients with suspected severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection in the emergency department (ED) and intensive care unit (ICU).

We performed literature search on the use of POCUS in the diagnosis and management of COVID-19 in MEDLINE, Embase and Scopus databases using the following search terms: "ultrasonography", "ultrasound", "COVID-19", "SARS-CoV-2", "SARS-CoV-2 variants", "emergency services", "emergency department" and "intensive care units". Search was performed independently by two reviewers with any discrepancy adjudicated by a third member.

Lung POCUS in patients with COVID-19 shows different ultrasonographic features from pulmonary oedema, bacterial pneumonia, and other viral pneumonia, thus useful in differentiating between these conditions. It is more sensitive than CXR, and more accessible and widely available than CT scan. POCUS can be used to diagnose COVID-19 pneumonia, screen for COVID-19-related pulmonary and extrapulmonary complications, and guide management of ICU patients, such as timing of ventilator weaning based on lung POCUS findings.

POCUS is a useful and rapid point-of-care modality that can be used to aid in diagnosis, management, and risk stratification of COVID-19 patients in different healthcare settings.

Lung tissue has a certain regenerative ability and triggers repair procedures after injury. Under controllable conditions, lung tissue can restore normal structure and function. Disruptions in this process can lead to respiratory system failure and even death, causing substantial medical burden. The main types of respiratory diseases are chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), and acute respiratory distress syndrome (ARDS). Multiple cells, such as lung epithelial cells, endothelial cells, fibroblasts, and immune cells, are involved in regulating the repair process after lung injury. Although the mechanism that regulates the process of lung repair has not been fully elucidated, clinical trials targeting different cells and signaling pathways have achieved some therapeutic effects in different respiratory diseases. In this review, we provide an overview of the cell type involved in the process of lung regeneration and repair, research models, and summarize molecular mechanisms involved in the regulation of lung regeneration and fibrosis. Moreover, we discuss the current clinical trials of stem cell therapy and pharmacological strategies for COPD, IPF, and ARDS treatment. This review provides a reference for further research on the molecular and cellular mechanisms of lung regeneration, drug development, and clinical trials.

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection. Acute respiratory distress syndrome (ARDS) is a common sepsis-associated injury that can increase postoperative mortality but the mechanism is still unclear.

The role of neutrophils in the pathophysiology of sepsis was deeply challenged after the discovery of NETosis, a process resulting in neutrophil extracellular traps (NETs) release. NETs can support thrombin generation and the concept of immunothrombosis has emerged as a new innate response to infection. Immunothrombosis leads to thrombosis in microvessels and supports immune cells together with specific thrombus-related molecules. ARDS is a common sepsis-associated organ injury. Immunothrombosis participates in thrombosis in pulmonary capillaries. Intervention regarding immunothrombosis in ARDS is a key scientific problem. PAD4 is the key enzyme regulating the NET skeleton protein histone H3 to citrulline histone to form NETs in immune thrombosis. This review summarizes NETosis and immunohaemostasis, ARDS and therapeutic opportunities targeting PAD4 via PAD4 inhibitors and lncRNAs potentially, providing future therapies.

We identified and summarized the fundamental definition of ARDS and the concept of immune thrombosis and its composition. NETs activation has become particularly relevant in the formation of immune thrombosis. The taskforce highlighted the intervention targets of PAD4, including noncoding RNAs, potentially providing future therapeutic targets to confront the high postoperative mortality of ARDS.

Worldwide medical and scientific communities are focusing on further understanding coronavirus disease 2019 (COVID-19) complications and its long-term impact on survivors. Pneumatocele cases are being reported more as a consequence of this virus and a cause of pneumothorax in certain patients. In this case vignette, we present a previously healthy male with COVID-19 symptoms who required hospitalization for hypoxia and who required readmission for bilateral pneumothorax from the delayed rupture of pneumatoceles. We describe this rare pathology and provide hypotheses for possible etiologies.

Immediate thrombolysis in submassive pulmonary embolism on the basis of bedside echocardiography can be a lifesaving decision in areas where computed tomography (CT) pulmonary angiogram is not readily available.

Bedside echocardiography can be a rapid diagnostic and decision-making tool for immediate thrombolysis in submassive pulmonary embolism with evidence of progressively failing ventricles. We report a case of submassive pulmonary embolism in a 26-year-old male under testosterone replacement therapy, who was successfully thrombolyzed based on bedside echocardiography findings.

To (1) identify discriminatory demographic, laboratory and initial CXR findings; (2) explore correlation between D-dimer and radiographic severity scores; and (3) assess accuracy of published D-dimer thresholds to identify pulmonary thromboembolism (PTE) in COVID-19 patients.

Retrospective study including all COVID-19 patients admitted from 1st to 30th April 2020 meeting inclusion criteria from 25 (blinded) hospitals. Demographics, blood results, CXR and CTPA findings were compared between positive and negative PTE cohorts using uni- and multivariable logistic regression. Published D-dimer cut-offs were applied.

389 patients were included [median age 63; 237 males], of which 26.2% had a PTE. Significant univariable discriminators for PTE were peak D-dimer, sex, neutrophil count at the time of the D-dimer and at admission, abnormal CXR, and CXR zonal severity score. Only neutrophil count at peak D-dimer remained significant for predicting PTE on multivariable analysis (p = 0.008). When compared with the published literature, sensitivity for PTE were lower than those published at all cut-off values, however specificity at different cut-offs was variable.

In this multicentre COVID-19 cohort, univariable admission factors that could indicate pulmonary thromboembolism were male sex, high neutrophil count and abnormal CXR with a greater CXR zonal severity score. The accuracy levels of published D-dimer thresholds were not reproducible in our population.

This is a large multicentre study looking at the discriminatory value of simple variables to determine if a patient with COVID-19 has PTE or not, in addition to comparing D-dimer cut off values against published values.

Chest CT is the reference test for assessing pulmonary injury in suspected or diagnosed COVID-19 with signs of clinical severity. This study aimed to evaluate the association of a lung ultrasonography score and unfavorable clinical evolution at 28 days.

The eChoVid is a multicentric study based on routinely collected data that was conducted in 8 emergency units in France; patients were included between March 19, 2020 and April 28, 2020 and underwent lung ultrasonography, a short clinical assessment by 2 emergency physicians blinded to each other's assessment, and chest CT. Lung ultrasonography consisted of scoring lesions from 0 to 3 in 8 chest zones, thus defining a global score (GS) of severity from 0 to 24. The primary outcome was the association of lung damage severity as assessed by the GS at day 0 and patient status at 28 days. Secondary outcomes were comparing the performance between GS and CT scan and the performance between a new trainee physician and an ultrasonography expert in scores.

For the 328 patients analyzed, the GS showed good performance in predicting clinical worsening at 28 days (area under the receiver operating characteristic curve [AUC] 0.83, sensitivity 84.2%, specificity 76.4%). The GS showed good performance in predicting the CT severity assessment (AUC 0.84, sensitivity 77.2%, specificity 83.7%).

A lung ultrasonography GS is a simple tool that can be used in the emergency department to predict unfavorable assessment at 28 days in patients with COVID-19.

Pulmonary thromboembolism (PTE) is a common complication in coronavirus disease 2019 (COVID-19) patients. Elevated D-dimer levels are observed even in the absence of PTE, reducing its discriminative ability as a screening test. It is unknown whether conventional D-dimer cut-off values, as used in the YEARS algorithm, apply to COVID-19 patients. This study aimed to determine the optimal D-dimer cut-off value to predict PTE in COVID-19 patients. All confirmed COVID-19 patients with a computed tomography pulmonary angiography (CTPA) performed ≤5 days after admission due to suspicion of PTE between March 2020 and February 2021, at Medisch Spectrum Twente, The Netherlands, were retrospectively analyzed. The association between PTE and D-dimer levels prior to CTPA, and other potential predictors, was analyzed using logistic regression analyses. The optimal cut-off value was identified using receiver operating characteristic (ROC) curve analyses. In 142 patients, PTE prevalence was 20.4%. The optimal cut-off value was 750 ng/mL (sensitivity 100%; specificity 19.5%; negative predictive value 100%; positive predictive value 24.2%). In total, 15 of 113 (13%) patients without PTE had a D-dimer level ≥500 and <750 ng/mL. In our population of patients hospitalized with COVID-19, a D-dimer level <750 ng/mL safely excluded PTE. Compared to the YEARS 500 ng/mL cut-off value, 13% fewer patients are in need of a CTPA, with similar sensitivity. Future research is required for external validation.

A limited number of studies have described thrombotic complications in pregnant women with COVID-19. Here we report on fatal pulmonary embolism in a pregnant woman with laboratory confirmed SARS-CoV-2 infection.

A 28-year-old Kazakh woman was hospitalized with muscle pain, dry cough and a temperature of 37.5 °C at the 29th week of gestation. Upon admission, a blood test demonstrated elevated neutrophil-to-lymphocyte ratio, decreased levels of erythrocytes and hemoglobin, as well as prolonged prothrombin and activated partial thromboplastin time. Within 14 days of admission, she experienced respiratory distress and underwent transfer to the intensive care unit, intubation and a cesarean section. The patient received intravenous antibiotics, antiviral medications, systemic corticosteroids and dual anticoagulation with aspirin and enoxaparin. Death outcome was reported on day 18 of illness despite aggressive supportive care. Histological analysis demonstrated that obstruction of the main pulmonary arthery and disseminated intravascular coagulation were the causes of death.

This case demonstrates that in the management of pregnancy and childbirth in patients with suspected or confirmed COVID-19 infection, special attention should be paid to coagulation system parameters and timely appropriate prophylaxis of thromboembolic complications, which has yet to be determined.

Although vaccinations and antiviral drugs are widely used in the clinical treatment worldwide, there is little investigation on the clinical outcomes and effectiveness of oral Azvudine tablets (FNC) treatment in COVID-19 hospitalized patients. The previous data showed Azvudine treatment was closely related to reduced virus shedding time, but the potential role of Azvudine on inflammatory response is scarce. Thus, this study is to investigate inflammatory predictors and effectiveness of oral Azvudine tablets treatment in COVID-19 hospitalized patients.

A total of 600 out of hospitalized patients were retrospectively collected over a 2-month period, of whom 60 out of hospitalized patients infected SARS-CoV-2. 32 of hospitalized patients who received Azvudine tablets were collected and the rest did not. Oral Azvudine tablets treatment: 5 mg/day for 7-14 days. We analyzed the routine blood tests, blood coagulation test, NT-proBNP, Troponin (cTNl), Creatine kinase MB (CK-MB) after oral Azvudine tablets treatment compared with that in before oral Azvudine tablets treatment. Also, we compared the CT chest and length of Stay after Azvudine treatment.

We found that the number and percentage of eosinophil increased significantly, but the levels of C-reactive protein (C-RP) and IL-6 reduced remarkably after Azvudine treatment. In blood coagulation tests, the results showed that activated partial thromboplastin time (APTT) (mean ± SEM: 2.950 ± 2.268s) and fibrinogen (mean ± SEM: 0.8910 ± 0.5134g/L) downregulated slightly, while there was similar in the level of D-Dimer (mean ± SEM: 0.1660 ± 0.3108 μg/mL) before and after Azvudine treatment. The expression of NT-proBNP reduced in Azvudine treatment (mean ± SEM: 897.1 ± 557.1pg/mL). Chest computed tomography (CT) scan reports also demonstrated that Azvudine treatment improved lung symptoms in COVID-19 hospitalized patients. Moreover, there is no difference in the average of length of stay in Azvudine treatment (the average of LOS days: 9.0) and no treatment (the average of LOS days: 9.0).

Oral Azvudine tablets treatment was associated with decreased inflammatory response and improved blood coagulation function, which should be substantial clinical benefits in COVID-19 hospitalized patients.

A good understanding of the possible risk factors for coronavirus disease 19 (COVID-19) severity could help clinicians in identifying patients who need prioritized treatment to prevent disease progression and adverse outcomes. COVID-19-linked coagulopathy is one of the life-threatening severe acute respiratory syndrome coronavirus 2 infections. Growing evidence indicates a correlation between abnormal coagulation and increased risk of venous thromboembolism; in COVID-19-infected patients, yet a clear understanding of the role of coagulopathy in the severity of COVID-19 illness is still unresolved. This retrospective cohort study was thus undertaken to investigate the role of coagulation dysfunction with COVID-19 mortality/severity. Blood samples from 1000 hospitalized patients with COVID-19 pneumonia were collected. The study participants were both male and female in equal ratios with a mean age of 48.94. Patients were followed-up until discharge either for recovery or death. All biochemical investigations-complete blood count and coagulation profile including D-dimers, prothrombin time, partial prothrombin time, and international normalized ratio was performed in COVID-19 survivors and in non-survivors admitted in intensive care unit. In the survivor group, all coagulation parameters were within normal limits, and 8.7% had a low red blood count. The most common risk factors associated with COVID-19 patients were diabetes mellitus (2.8%), hypertension (10.8%), and heart disease (3%). In the non-survivor group, the coagulation parameters were above the normal range (prothrombin in 31.5%, PTT in 10.5%, international normalized ratio in 26.3%, D-dimer in 36.8%) with thrombocytopenia in 21.04% of patients. Other complications were pulmonary embolism in 21.05% and venous thromboembolism in 15.7% of non-survivors. A significant association was found between increased markers of coagulopathy and the severity of SARS-CoV2 infection. Furthermore, the severity of infection was observed to increase with risk factors such as age, heart disease, hypertension, and DM eventually affecting COVID-19 prognosis and mortality.

COVID-19 patients can exhibit a wide range of clinical manifestations affecting various organs and systems. Neurological symptoms have been reported in COVID-19 patients, both during the acute phase of the illness and in cases of long-term COVID. Moderate symptoms include ageusia, anosmia, altered mental status, and cognitive impairment, and in more severe cases can manifest as ischemic cerebrovascular disease and encephalitis. In this narrative review, we delve into the reported neurological symptoms associated with COVID-19, as well as the underlying mechanisms contributing to them. These mechanisms include direct damage to neurons, inflammation, oxidative stress, and protein misfolding. We further investigate the potential of small molecules from natural products to offer neuroprotection in models of neurodegenerative diseases. Through our analysis, we discovered that flavonoids, alkaloids, terpenoids, and other natural compounds exhibit neuroprotective effects by modulating signaling pathways known to be impacted by COVID-19. Some of these compounds also directly target SARS-CoV-2 viral replication. Therefore, molecules of natural origin show promise as potential agents to prevent or mitigate nervous system damage in COVID-19 patients. Further research and the evaluation of different stages of the disease are warranted to explore their potential benefits.

Venous thromboembolism (VTE), clinically manifested as deep vein thrombosis (DVT) or acute pulmonary embolism (PE), is the third most common acute cardiovascular syndrome following myocardial infarction and stroke. The annual incidence of PE is between 39 and 115 per 100,000 inhabitants. The incidence of VTE is almost eight times higher in people aged 80 and older than in the fifth decade of life. We performed a retrospective study of 226 COVID-19 patients and selected group of patients who experienced a pulmonary thrombotic event. The incidence of PE in hospitalized COVID-19 patients was approximately 1.9-8.9%. The retrospective nature of the analyzed cohorts and relatively short observation periods could have led to underestimation of the actual incidence of PE. This study underlines the role of novel inflammatory biomarkers such as neutrophil to lymphocyte ratio and platelet to lymphocyte ratio in patients with a pulmonary thrombotic event in COVID-19. We suggest that these biomarkers may have high assessment value and complement routinely used biomarkers.

Since the report of the first case of COVID-19 in Wuhan, China, on December 31, 2019, several associated thrombotic complications have been reported, mainly venous thromboembolic events, and myocardial infarctions, in addition to peripheral arterial thrombosis and cerebral vascular events, which have been attributed to a hypercoagulable state. We aimed to know the prevalence and prognostic biomarkers in patients with pulmonary thromboembolism (PE) and SARS Cov-2 pneumonia. Hospitalized patients with SARS Cov-2 pneumonia who have had clinical, biomarker, and imaging data (chest angiography) of pulmonary thromboembolism were included. Descriptive statistics and prevalence rates were calculated. For the analysis between the groups, the paired Student's t and the Wilcoxon test were performed. CT angiography was performed on 26 patients at our institution, with a diagnosis of severe pneumonia secondary to SARS-CoV2. 9 of the patients (34.6%) had a venous thromboembolic disease. Type 2 DM was the most frequent comorbidity up to 55.5% of the total; it was followed by obesity and overweight in 55.5%, and in third place, by systemic arterial hypertension in 33.3% of the cases, 1 (11.1%) patient had chronic kidney disease and 1 (11.1%) patient with a history of cancer, only 1 patient met criteria and was treated with thrombolysis. 6 (66.6%) of the patients had segmental PE, 3 (33.3%) patients had subsegmental PE, and 4 (44.4%) patients presented pulmonary infarction.

Persistent dyspnea is frequent in post-COVID patients, even in the absence of pulmonary embolism (PE). In this scenario, the role of lung perfusion scintigraphy is unclear. The present study correlated scintigraphy-based semiquantitative perfusion parameters with chest high-resolution computed tomography (hrCT) volumetric indexes and clinical data in post-COVID patients with persistent dyspnea.

Sixty patients (30 post-COVID and 30 not previously affected by COVID-19) with persistent dyspnea submitted to lung perfusion scintigraphy and hrCT were retrospectively recruited. Perfusion rates of the pulmonary fields and hrCT-based normalized inflated, emphysematous, infiltrated, collapsed, and vascular lung volumes were calculated. Inflammatory and coagulation biomarkers were collected. PE at imaging was an exclusion criterion.

Compared to controls, reduced perfusion rates of the lower pulmonary fields and higher perfusion rates of the middle ones were observed in post-COVID patients, while hrCT findings were superimposable between the two groups. Perfusion rates of lower pulmonary fields were significantly associated only with abnormal lung volumes at hrCT.

In post-COVID dyspnea without PE, lung perfusion scintigraphy may reveal a pulmonary involvement not detectable by hrCT. Post-COVID patients may show decreased perfusion rates of lower pulmonary fields in the presence of normal vascular density and markers of inflammation/coagulation.

During 2019, the SARS-CoV-2 emerged from China, and during months, COVID-19 spread in many countries around the world. The expanding data about pathogenesis of this virus could elucidate the exact mechanism by which COVID-19 caused death in humans. One of the pathogenic mechanisms of this disease is coagulation. Coagulation disorders that affect both venous and arterial systems occur in patients with COVID-19. The possible mechanism involved in the coagulation could be excessive inflammation induced by SARS-CoV-2. However, it is not yet clear well how SARS-CoV-2 promotes coagulopathy. However, some factors, such as pulmonary endothelial cell damage and some anticoagulant system disorders, are assumed to have an important role. In this study, we assessed conducted studies about COVID-19-induced coagulopathy to obtain clearer vision of the wide range of manifestations and possible pathogenesis mechanisms.

The novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) causes major challenges to the healthcare system. SARS-CoV-2 infection leads to millions of deaths worldwide and the mortality rate is found to be greatly associated with pre-existing clinical conditions. The existing dataset strongly suggests that cardiometabolic diseases including hypertension, coronary artery disease, diabetes and obesity serve as strong comorbidities in coronavirus disease (COVID-19). Studies have also shown the poor outcome of COVID-19 in patients associated with angiotensin-converting enzyme-2 polymorphism, cancer chemotherapy, chronic kidney disease, thyroid disorder, or coagulation dysfunction. A severe complication of COVID-19 is mostly seen in people with compromised medical history. SARS-CoV-2 appears to attack the respiratory system causing pneumonia, acute respiratory distress syndrome, which lead to induction of severe systemic inflammation, multi-organ dysfunction, and death mostly in the patients who are associated with pre-existing comorbidity factors. In this article, we highlighted the key comorbidities and a variety of clinical complications associated with COVID-19 for a better understanding of the etiopathogenesis of COVID-19.

Since the first description of COVID-19 infection, among clinical manifestations of the disease, including fever, dyspnea, cough, and fatigue, it was observed a high incidence of thromboembolic events potentially evolving towards acute respiratory distress syndrome (ARDS) and COVID-19-associated-coagulopathy (CAC). The hypercoagulation state is based on an interaction between thrombosis and inflammation. The so-called CAC represents a key aspect in the genesis of organ damage from SARS-CoV-2. The prothrombotic status of COVID-19 can be explained by the increase in coagulation levels of D-dimer, lymphocytes, fibrinogen, interleukin 6 (IL-6), and prothrombin time. Several mechanisms have been hypothesized to explain this hypercoagulable process such as inflammatory cytokine storm, platelet activation, endothelial dysfunction, and stasis for a long time. The purpose of this narrative review is to provide an overview of the current knowledge on the pathogenic mechanisms of coagulopathy that may characterize COVID-19 infection and inform on new areas of research. New vascular therapeutic strategies are also reviewed.

Background and objective COVID-19 may predispose to both venous and arterial thromboembolism (VTE and ATE) due to excessive inflammation, immobilization, and hypoxia. The purpose of this study is to evaluate clinical and laboratory risk factors, as well as related medications such as anticoagulants, to predict the risk of thromboembolic disease and/or death in COVID-19 patients. Methods Over a period of 14 months (from August 2020 to September 2021), a total of 145 consecutive patients with signs and symptoms suspicious of pulmonary embolism (PE) were referred for perfusion single-photon emission computed tomography/computed tomography (Q SPECT/CT). All patients had a history of SARS‑CoV‑2 infection, diagnosed with a positive real-time polymerase chain reaction (RT-PCR) test. Results Among the 145 patients included in the study, the risk of PE was found to be greater in elderly patients (odds ratio [OR] [95% CI]: 1.05 [1.02‑1.07]; p<0.001) and in patients with higher maximum d-dimer levels (OR [95% CI]: 1.14 [1.01‑1.3]; p=0.04). We also analyzed the utility of the maximum d-dimer level for predicting acute PE with receiver operating characteristic (ROC) curve analysis. For d‑dimer = 0.5 mg/dL, cut-off sensitivity is 91%, specificity is 23%, and for d-dimer = 1 mg/dL, cut-off sensitivity is 79%, specificity is 43% Conclusion D-dimer titers were higher in the PE group in our study. Another significant finding was that, possibly due to thromboinflammation, anticoagulants did not prevent the development of PE in COVID-19 patients.

To analyze the diagnostic performance of pulmonary CT angiography and to compare different D-dimer cutoffs for the diagnosis of acute pulmonary embolism in patients with and without SARS-CoV-2 infections.

We retrospectively analysed all consecutive pulmonary CT angiography studies done for suspected pulmonary embolism in a tertiary hospital during two time periods: the first December 2020 through February 2021 and the second December 2017 through February 2018. D-dimer levels were obtained less than 24 h before the pulmonary CT angiography studies. We analysed the sensitivity, specificity, positive and negative predictive values, area under the receiver operating curve (AUC), and pattern of pulmonary embolism for six different values of D-dimer and the extent of the embolism. During the pandemic period, we also analysed whether the patients had COVID-19.

After excluding 29 poor-quality studies, 492 studies were analysed; 352 of these were done during the pandemic, 180 in patients with COVID-19 and 172 in patients without COVID-19. The absolute frequency of pulmonary embolism diagnosed was higher during the pandemic period (34 cases during the prior period and 85 during the pandemic; 47 of these patients had COVID-19). No significant differences were found in comparing the AUCs for the D-dimer values. The optimum values calculated for the receiver operating characteristic curves differed between patients with COVID-19 (2200 mcg/l), without COVID-19 (4800 mcg/l), and diagnosed in the prepandemic period (3200 mcg/l). Peripheral distribution of the emboli was more common in patients with COVID-19 (72%) than in those without COVID-19 and than in those diagnosed before the pandemic [OR 6.6, 95% CI: 1.5-24.6, p < 0.05 when compared to central distribution].

The number of CT angiography studies and the number of pulmonary embolisms diagnosed during the pandemic increased due to SARS-CoV-2 infection. The optimal d-dimer cutoffs and the distribution of the pulmonary embolisms differed between the groups of patients with and without COVID-19.

To establish the impact of COVID-19 on the pre-test probability for VTE in patients with suspected VTE. This was a retrospective, observational, cross-sectional study of patients 18 years and older undergoing diagnostic tests for VTE in an integrated healthcare system covering a population of 465,000 during the calendar year of 2020. We adjusted for risk factors such as age, sex, previous VTE, ongoing anticoagulant treatment, malignancy, Charlson score, ward care, ICU care and wave of COVID-19. In total, 303 of 5041 patients had a positive diagnosis of COVID-19 around the time of investigation. The prevalence of VTE in COVID-positive patients was 10.2% (36/354), 14.7% (473/3219) in COVID-19 negative patients, and 15.6% (399/2589) in patients without a COVID-19 test. A COVID-positive status was not associated with an increased risk for VTE (crude odds ratio 0.64, 95% CI 0.45-0.91, adjusted odds ratio 0.46, 95%CI 0.19-1.16). We found no increased VTE risk in COVID-positive patients. This indicates that COVID-19 status should not influence VTE workup.The study was pre-registered on May 26, 2020 at ClinicalTrials.gov with identifier NCT04400877.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection has frequent acute cardiovascular manifestations, but long-term sequelae are yet to be described. Our main objective is to describe the echocardiographic findings of patients with a previous SARS-CoV-2 infection.

A single-center prospective study was conducted. Patients who tested positive for SARS-CoV-2 were selected and submitted to a transthoracic echocardiogram six months after infection. A complete echocardiographic assessment was performed, including tissue Doppler, E/E' ratio, and ventricular longitudinal strain. Patients were divided into two subgroups according to their need for admission to the ICU.

A total of 88 patients were enrolled. The mean values and respective standard deviations of the echocardiographic parameters were as follows: left ventricular ejection fraction 60.8 ± 5.9%; left ventricular longitudinal strain 17.9 ± 3.6%; tricuspid annular plane systolic excursion 22.1 ± 3.6 mm; a longitudinal strain of the free wall of the right ventricle 19.0 ± 6.0%. We found no statistically significant differences between subgroups.

At the six-month follow-up, we found no significant impact of past SARS-CoV-2 infection on the heart using echocardiography parameters.

Given the high risk of thrombosis and anticoagulation-related bleeding in patients with hypoxemic COVID-19 pneumonia, identifying the lowest effective dose of anticoagulation therapy for these patients is imperative.

To determine whether therapeutic anticoagulation (TA) or high-dose prophylactic anticoagulation (HD-PA) decreases mortality and/or disease duration compared with standard-dose prophylactic anticoagulation (SD-PA), and whether TA outperforms HD-PA; and to compare the net clinical outcomes among the 3 strategies.

The ANTICOVID randomized clinical open-label trial included patients with hypoxemic COVID-19 pneumonia requiring supplemental oxygen and having no initial thrombosis on chest computer tomography with pulmonary angiogram at 23 health centers in France from April 14 to December 13, 2021. Of 339 patients randomized, 334 were included in the primary analysis-114 patients in the SD-PA group, 110 in the HD-PA, and 110 in the TA. At randomization, 90% of the patients were in the intensive care unit. Data analyses were performed from April 13, 2022, to January 3, 2023.

Patients were randomly assigned (1:1:1) to receive either SD-PA, HD-PA, or TA with low-molecular-weight or unfractionated heparin for 14 days.

A hierarchical criterion of all-cause mortality followed by time to clinical improvement at day 28. Main secondary outcome was net clinical outcome at day 28 (composite of thrombosis, major bleeding, and all-cause death).

Among the study population of 334 individuals (mean [SD] age, 58.3 [13.0] years; 226 [67.7%] men and 108 [32.3%] women), use of HD-PA and SD-PA had similar probabilities of favorable outcome (47.3% [95% CI, 39.9% to 54.8%] vs 52.7% [95% CI, 45.2% to 60.1%]; P = .48), as did TA compared with SD-PA (50.9% [95% CI, 43.4% to 58.3%] vs 49.1% [95% CI, 41.7% to 56.6%]; P = .82) and TA compared with HD-PA (53.5% [95% CI 45.8% to 60.9%] vs 46.5% [95% CI, 39.1% to 54.2%]; P = .37). Net clinical outcome was met in 29.8% of patients receiving SD-PA (20.2% thrombosis, 2.6% bleeding, 14.0% death), 16.4% receiving HD-PA (5.5% thrombosis, 3.6% bleeding, 11.8% death), and 20.0% receiving TA (5.5% thrombosis, 3.6% bleeding, 12.7% death). Moreover, HD-PA and TA use significantly reduced thrombosis compared with SD-PA (absolute difference, -14.7 [95% CI -6.2 to -23.2] and -14.7 [95% CI -6.2 to -23.2], respectively). Use of HD-PA significantly reduced net clinical outcome compared with SD-PA (absolute difference, -13.5; 95% CI -2.6 to -24.3).

This randomized clinical trial found that compared with SD-PA, neither HD-PA nor TA use improved the primary hierarchical outcome of all-cause mortality or time to clinical improvement in patients with hypoxemic COVID-19 pneumonia; however, HD-PA resulted in significantly better net clinical outcome by decreasing the risk of de novo thrombosis.

ClinicalTrials.gov Identifier: NCT04808882.

Dual-energy computed tomography (DECT) has been used for detecting pulmonary embolism, but the role of lung perfusion DECT as a predictor of prognosis of coronavirus disease 2019 (COVID-19) has not been defined yet. The aim of our study was to explore whether the enhancement pattern in COVID-19+ patients relates to the disease outcome. A secondary aim was to compare the lung volumes in two subgroups of patients. In this observational study, we considered all consecutive COVID-19+ patients who presented to the emergency room between January 2021 and December 2021 with respiratory symptoms (with mild to absent lung consolidation) and were studied by chest contrast-enhanced DECT to be eligible. Two experienced radiologists post-processed the images using the "lung-analysis" software (SyngoVia). Absolute and relative enhancement lung volumes were assessed. Patients were stratified in two subgroups depending on clinical outcome at 30 days: (i) good outcome (i.e., discharge, absence of clinical or imaging signs of disease); (ii) bad outcome (i.e., hospitalization, death). Patient sub-groups were compared using chi-square test or Fisher test for qualitative parameters, chi-square test or Spearman's Rho test for quantitative parameters, Students' t-test for parametric variables and Wilcoxon test for non-parametric variables. We enrolled 78 patients (45M), of whom, 16.7% had good outcomes. We did not observe any significant differences between the two groups, both in terms of the total enhancement evaluation (p = 0.679) and of the relative enhancement (p = 0.918). In contrast, the average lung volume of good outcome patients (mean value of 4262 mL) was significantly larger than that of bad outcome patients (mean value of 3577.8 mL), p = 0.0116. All COVID-19+ patients, with either good or bad outcomes, presented similar enhancement parameters and relative enhancements, underlining no differences in lung perfusion. Conversely, a significant drop in lung volume was identified in the bad outcome subgroup eligible compared to the good outcome subgroup.

A few days after being infected with SARS-CoV-2, a fraction of people remain asymptomatic but suffer from a decrease in arterial oxygen saturation in the absence of apparent dyspnea. In light of our clinical investigation on the modulation of molecules belonging to the renin angiotensin system (RAS) in COVID-19 patients, we propose a model that explains 'silent hypoxia'. The RAS imbalance caused by SARS-CoV-2 results in an accumulation of angiotensin 2 (Ang II), which activates the angiotensin 2 type 1 receptor (AT1R) and triggers a harmful cascade of intracellular signals leading to the nuclear translocation of the hypoxia-inducible factor (HIF)-1α. HIF-1α transactivates many genes including the angiotensin-converting enzyme 1 (ACE1), while at the same time, ACE2 is downregulated. A growing number of cells is maintained in a hypoxic condition that is self-sustained by the presence of the virus and the ACE1/ACE2 ratio imbalance. This is associated with a progressive worsening of the patient's biological parameters including decreased oxygen saturation, without further clinical manifestations. When too many cells activate the Ang II-AT1R-HIF-1α axis, there is a 'hypoxic spillover', which marks the tipping point between 'silent' and symptomatic hypoxia in the patient. Immediate ventilation is required to prevent the 'hypoxic spillover'.

COVID-19 is a respiratory disease caused by infection with severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2). Thrombotic complications appear to be of particular importance in patients with COVID-19. This study aimed to investigate Changes in the level of Antiphospholipid antibodies (Anticardiolipin and Anti-β2-glycoprotein-I) and thromboembolic indices in COVID-19 patients during 3 weeks.

This cross-sectional study was performed on adults with Covid-19 hospitalized at Al-Zahra Hospital in Isfahan. The case group includes the patients admitted to the internal ward or ICU who despite receiving prophylactic or anticoagulant doses suffer from thrombotic complications and the control group includes COVID-19 patients without thromboembolic events. The sample size of 120 people was considered. Anticardiolipin and anti-β2-glycoprotein-I antibodies, coagulation profiles including Fibrinogen, PTT, PT Troponin, ESR, CRP, and D-dimer were examined. After collection, the data were entered into spss24 software and analyzed.

The results showed that there was no statistically significant difference in the changes of anticardiolipin and anti-beta-2 glycoprotein in IgM and IgG as well as in the changes of ESR, CRP, PTT, PT, and fibrinogen in the two groups (P > 0.05).

Our study showed that there was no statistically significant relationship between anti-phospholipid antibodies (anticardiolipin and anti-beta-2 glycoprotein) and thromboembolic events. Therefore anticardiolipin and anti-beta-2 glycoprotein is probably the puzzles causing thrombosis in COVID-19 patients, and other inflammatory responses should be examined among the cases.

Thrombosis is a known complication of SARS-CoV-2 infection, particularly within a severely symptomatic subset of patients with COVID-19 disease, in whom an aggressive host immune response leads to cytokine storm syndrome (CSS). The incidence of thrombotic events coinciding with CSS may contribute to the severe morbidity and mortality observed in association with COVID-19. This review provides an overview of pharmacologic approaches based upon an emerging understanding of the mechanisms responsible for thrombosis across a spectrum of COVID-19 disease involving an interplay between immunologic and pro-thrombotic events, including endothelial injury, platelet activation, altered coagulation pathways, and impaired fibrinolysis.

To investigate whether COVID-19 patients with pulmonary embolism had higher mortality and assess the utility of D-dimer in predicting acute pulmonary embolism.

Using the National Collaborative COVID-19 retrospective cohort, a cohort of hospitalized COVID-19 patients was studied to compare 90-day mortality and intubation outcomes in patients with and without pulmonary embolism in a multivariable cox regression analysis. The secondary measured outcomes in 1:4 propensity score-matched analysis included length of stay, chest pain incidence, heart rate, history of pulmonary embolism or DVT, and admission laboratory parameters.

Among 31,500 hospitalized COVID-19 patients, 1117 (3.5%) patients were diagnosed with acute pulmonary embolism. Patients with acute pulmonary embolism were noted to have higher mortality (23.6% vs.12.8%; adjusted Hazard Ratio (aHR) = 1.36, 95% CI [1.20-1.55]), and intubation rates (17.6% vs. 9.3%, aHR = 1.38[1.18-1.61]). Pulmonary embolism patients had higher admission D-dimer FEU (Odds Ratio(OR) = 1.13; 95%CI [1.1-1.15]). As the D-dimer value increased, the specificity, positive predictive value, and accuracy of the test increased; however, sensitivity decreased (AUC 0.70). At cut-off D-dimer FEU 1.8 mcg/ml, the test had clinical utility (accuracy 70%) in predicting pulmonary embolism. Patients with acute pulmonary embolism had a higher incidence of chest pain and history of pulmonary embolism or deep vein thrombosis.

Acute pulmonary embolism is associated with worse mortality and morbidity outcomes in COVID-19. We present D-dimer as a predictive risk tool in the form of a clinical calculator for the diagnosis of acute pulmonary embolism in COVID-19.

Symptoms of long COVID-19 syndrome (long COVID-19) are reported by 80% of convalescents up to several months after contracting the coronavirus-19 disease (COVID-19). The study aimed to assess the frequency and correlations of long COVID symptoms with sex, disease severity, time since the onset of the disease, and exercise capacity in a population of Polish convalescents hospitalized as a part of a rehabilitation program after COVID-19. The retrospective analysis was carried out based on medical records concerning reported symptoms, comorbidities, exercise capacity, fatigue and dyspnea on Borg's scale, arterial oxygen saturation (SpO₂), spirometric parameters, chest X-rays/computed tomography scans, systolic pulmonary artery pressure, and left ventricular ejection fraction. The study involved 471 patients aged 63.83 ± 9.93 years who had been hospitalized 191.32 ± 75.69 days from the onset of COVID-19, of which 269 (57.1%) were women. The most common symptoms were fatigue (99.57%), dyspnea (99.36%), and myalgia (97.03%). Women reported more symptoms than men (p < 0.001) and rated their fatigue as more severe (p = 0.021). Patients with depressed moods reported more physical symptoms than others (p < 0.001). Most long COVID symptoms, including dyspnea, fatigue, and depressive symptoms, were found with the same frequency in patients 12-24 weeks and >24 weeks after recovery (p = 0.874, p = 0.400, and p = 0.320, respectively), regardless of acute COVID-19 severity (p = 0.240, p = 0.826, and p = 0.108, respectively). Dyspnea severity correlated with forced vital capacity (FVC) (r = -0.153, p = 0.005), and forced expiratory volume in one second (FEV1) (r = -0.142, p = 0.008). Fatigue severity correlated with impaired FVC and FEV1 (both r = -0.162, p = 0.003). Fatigue and dyspnea inversely correlated with the distance in a six-minute walk test (r = -0.497, p < 0.001, and r = -0.327, p < 0.001). In conclusion, in our cohort, long COVID symptoms are more common in women. Dyspnea/fatigue and depressive symptoms do not tend to subside after an average six-month recovery period. The intensity of perceived fatigue may be exaggerated by the coexistence of neuropsychiatric disorders. Increased fatigue and dyspnea correlate with impaired spirometric parameters and significantly affects convalescents' exercise capacity.

To study the role of combined CTPA and indirect CT venogram to diagnose venous thromboembolism (VTE) in patients with COVID-19 pneumonia and to compare the clinical characteristics, laboratory parameters, CT findings and clinical outcomes between the VTE positive and negative groups.

In this retrospective study, 131 patients with COVID-19 pneumonia who underwent CTPA and venogram between August 2020 and January 2021 were included. Relevant demographical, clinical and laboratory data and CT images were collected. Two thoracic radiologists independently reviewed the CTPA and venogram images.

VTE was identified in 29 patients (22% of the study population). CT venogram identified DVT in 9 patients. No statistical difference was observed between the two groups with respect to age, gender, BMI and presence of comorbidities. There was a significant difference in the hospital stay duration, which is increased in the VTE positive group. The number of patients who were dependent on oxygen and mortality were also high in the positive group. There was statistically significant difference in the mean D-dimer value and the mean Neutrophil/lymphocyte ratio, which were higher in the VTE positive group.

Combined CTPA and venogram can be used as a one-stop investigation for diagnosing PE and DVT of lower limbs in patients with COVID-19 pneumonia. CTPA with venogram should be performed in patients with D-dimer value in the range of 1000 - 1200 μg/L and above to rule out VTE as the hospital stay duration and final outcomes vary between the positive and negative groups.

The pandemic of COVID-19 in worldwide causes recent millions of morbidity and mortality in all countries and is the most important challenge in the world in recent years. Coronavirus is a single-stranded RNA virus and infection with COVID-19 leads to acute respiratory distress syndrome, lung inflammation, cytokine storm, and death. The other complications include endothelial dysfunction, activation of coagulation, thromboembolic events, and vascular disease. Cardiovascular complications such as myocardial and stroke ischemia, pulmonary thromboembolism, systemic arterial, and deep vein thrombosis were reported. In this review, we presented immuno-pathological mechanisms and the effects of COVID-19 on the cardiovascular system, heart, vessels, coagulation system, and molecular glance of immuno-inflammation to the COVID-19's pathology on the cardiovascular system.

Corona virus disease (COVID-19) has been associated with ophthalmic manifestations which can occur during or following the infection.

To explore the systemic status in ophthalmic patients who had a recent history of COVID-19 or those with positive COVID-19 antibody status.

Retrospective case series.

30 patients with history of COVID-19 infection and positive COVID-19 antibodies were included in the study. The median age was 49 years (mean 48.7 ± 13.7 years), 20 were males (66.7%) and 10 (33.3%) were females. Patients with VA>/= 6/60 were included in group 1 and those with VA<6/60 were included in group 2. D-dimer/serum Ferritin levels were raised in group 2 compared to group 1with (p=0.013)/(p=0.018) respectively.

Serum D-dimer and ferritin levels were statistically significant and were higher in patients with sight threatening ocular manifestations. ESR and CRP were raised even after recovery from COVID-19 although they were not statistically significant.

Although the findings of acute new coronavirus disease (COVID-19) infection on dual-energy computed tomography (DECT) have recently been defined, the long-term changes in lung perfusion associated with COVID-19 pneumonia have not yet been clarified. We aimed to examine the longterm course of lung perfusion in COVID-19 pneumonia cases using DECT and to compare changes in lung perfusion to clinical and laboratory findings.

On initial and follow-up DECT scans, the presence and extent of perfusion deficit (PD) and parenchymal changes were assessed. The associations between PD presence and laboratory parameters, initial DECT severity score, and symptoms were evaluated.

The study population included 18 females and 26 males with an average age of 61.32 ± 11.3 years. Follow-up DECT examinations were performed after the mean of 83.12 ± 7.1 (80-94 days) days. PDs were detected on the follow-up DECT scans of 16 (36.3%) patients. These 16 patients also had ground-glass parenchymal lesions on the follow-up DECT scans. Patients with persistent lung PDs had significantly higher mean initial D-dimer, fibrinogen, and C-reactive protein values than patients without PDs. Patients with persistent PDs also had significantly higher rates of persistent symptoms.

Ground-glass opacities and lung PDs associated with COVID-19 pneumonia can persist for up to 80-90 days. Dual-energy computed tomography can be used to reveal long-term parenchymal and perfusion changes. Persistent PDs are commonly seen together with persistent COVID-19 symptoms.

This study aimed to describe the baseline characteristics of coronavirus disease 2019 (COVID-19) patients with pulmonary embolism, and to examine the Geneva score, pulmonary embolism severity index (PESI), radiological and biochemical findings.

From March 2020 to June 2021, the files of 41 COVID-19 patients with pulmonary embolism were accessed.

Mean D-dimer value was 6.04 mg/dl and 61% of the patients received at least one dose of anticoagulant treatment. In patients receiving deep venous thrombosis prophlaxis, an optimal D-dimer cut-off point was calculated as 5.69 mg/dl. The area under the curve was 0.753 (p = 0.007; sensivity 64%; specificity 62.5%). The mean Geneva score was 4.31, mean PESI was 72.48 and mean Qanadli score was 11.29.

According to this study, traditional clinical predictive scores had little discriminatory power in these patients, and a higher D-dimer cut-off value should be considered to better diagnose patients for pulmonary embolism.

This study aimed to determine the maximum diameters of the pulmonary artery and ascending aorta and their ratio to each other to enable early diagnosis and treatment of possible pulmonary hypertension and to prevent possible complications in patients infected with severe acute respiratory syndrome coronavirus 2.

A total of 120 patients aged 40 years and older, 60 patients (30 females and 30 males) with severe acute respiratory syndrome coronavirus 2 infection and 60 individuals (30 females and 30 males), were included in this retrospective study. Maximum pulmonary artery and maximum ascending aorta diameters were measured at the level of bifurcatio trunci pulmonalis in the transverse axial plane by computed tomography, and their ratios to each other were determined.

Our study revealed a statistically significant increase in maximum pulmonary artery and maximum ascending aorta diameters in both genders in patients with coronavirus disease 2019 compared to the control group and a statistically significant increase was found in the maximum pulmonary artery-maximum ascending aorta ratio in women with coronavirus disease 2019 compared to the control group (P < .05).

Knowing the diameters of maximum pulmonary artery and maximum ascending aorta and the maximum pulmonary artery-maximum ascending aorta ratio in hospitalized severe acute respiratory syndrome coronavirus 2-infected patients is a valuable predictive marker of pulmonary hypertension and a guide in determining the appropriate treatment. These data, which are easy to calculate from thorax computed tomography, may be beneficial in the prognosis of the disease.