Deep vein thrombosis (DVT) and pulmonary embolism (PE) are key complications of coronavirus disease 2019 (COVID-19). The study's primary outcome was assessing the utility of Wells DVT, Wells PE scores, and D-dimers in diagnosing DVT and PE. Secondary outcomes were the risk factors for the development of PE and DVT in COVID-19 patients. We compared COVID-19 patients with a positive and negative lower extremity (LE) duplex. A similar approach was made for patients who underwent imaging for PE. The prevalence of PE was 23.8% (26 out of 109 patients), and the prevalence of DVT was 33% (35 out of 106). A D-dimer of 500 ng/mL had a sensitivity of 95.6% and 93.7% for the diagnosis of PE and DVT, respectively. A Wells DVT score of 3 points had a specificity of 92.9% and sensitivity of 8.8% for DVT diagnosis in COVID-19. A Wells PE score of 4 had a specificity of 100% and a sensitivity of 20% for the diagnosis of PE. The combined approach of using a Wells DVT score of 3 in suspected DVT and a Wells PE score of 4 in suspected PE and D-dimers of 500 ng/ml has a sensitivity of 94.2% and 96.1%, respectively. In the suspected DVT group, male gender (OR 3.88, 95% CI 1.55-9.7, P=0.004), lower body mass index (BMI) (OR 0.92, 95% CI 0.86-0.99, P=0.037), antiplatelet use (OR 0.19, 95% CI 0.04-0.88, P=0.035), systolic blood pressure ≤100 mmhg (OR 4.96, 95% CI 1.37-17.86, P=0.014), absolute lymphocytes ≤1 (OR 2.57, 95% CI 1.07-6.12, P=0.033), D-dimer ≥500 ng/ml (OR 6.42, 95% CI 1.40-29.38, P=0.016), blood urea nitrogen (BUN) ≥20 mg/dl (OR 2.33, 95% CI 1.00-5.41, P=0.048), and intubation (OR 3.32, 95% CI 1.26-8.78, P=0.015) were found to be statistically significant for DVT. In the suspected PE group, history of cancer (OR 10.69, 95% CI 1.06-107.74, P=0.044), total WBC count (OR 1.07, 95% CI 0.95-1.21, P=0.032), platelets ≥ 400,000 (OR 5.13, 95% CI 1.79-14.68, P=0.002), D-dimer levels ≥ 500 ng/ml (OR 25.47, 95% CI 3.27-197.97, P=0.002), Wells PE score (OR 2.46, 95% CI 1.50-4.06, P<0.001), pulmonary embolism rule-out criteria (PERC) score (OR 1.79, 95% CI 1.05-3.05, P=0.054), and Sequential Organ Failure Assessment (SOFA) score (OR 1.91, 95% CI 1.16-3.12, P=0.002) were statistically significant. The combined approach of using a Wells DVT score of 3 in suspected DVT and Wells PE score of 4 in suspected PE and D-dimers of 500 ng/ml may be used to diagnose PE and DVT in COVID-19. Venous thromboembolism (VTE) occurrence in COVID-19 is associated with non-traditional risk factors such as intubation and higher severity of systemic inflammation, and these patients may benefit from more aggressive testing for VTE.

Background-Previous studies on coronavirus disease 2019 (COVID-19) were limited to specific geographical locations and small sample sizes. Therefore, we used the National Inpatient Sample (NIS) 2020 database to determine the risk factors for severe outcomes and mortality in COVID-19. Methods-We included adult patients with COVID-19. Univariate and multivariate logistic regression was performed to determine the predictors of severe outcomes and mortality in COVID-19. Results-1,608,980 (95% CI 1,570,803–1,647,156) hospitalizations with COVID-19 were included. Severe complications occurred in 78.3% of COVID-19 acute respiratory distress syndrome (ARDS) and 25% of COVID-19 pneumonia patients. The mortality rate for COVID-19 ARDS was 54% and for COVID-19 pneumonia was 16.6%. On multivariate analysis, age > 65 years, male sex, government insurance or no insurance, residence in low-income areas, non-white races, stroke, chronic kidney disease, heart failure, malnutrition, primary immunodeficiency, long-term steroid/immunomodulatory use, complicated diabetes mellitus, and liver disease were associated with COVID-19 related complications and mortality. Cardiac arrest, septic shock, and intubation had the highest odds of mortality. Conclusions-Socioeconomic disparities and medical comorbidities were significant determinants of mortality in the US in the pre-vaccine era. Therefore, aggressive vaccination of high-risk patients and healthcare policies to address socioeconomic disparities are necessary to reduce death rates in future pandemics.

This study examines in-hospital mortality and complicated COVID-19 infection among adult congenital heart disease (ACHD) patients admitted with COVID-19, using the National Inpatient Sample (NIS). A total of 4219 COVID-19 patients with ACHD were included. We demonstrated that COVID-19 patients with ACHD were more likely to experience in-hospital mortality (OR 1.04, 95% CI 1.04-1.04, P < 0.01) and complicated COVID-19 infection (OR: 1.30, 95% CI: 1.11-1.53, P < 0.01). In our sub-group analy-sis, COVID-19 patients with tetralogy of Fallot (TOF) had higher mortality and COVID-19 patients with atrial septal defects (ASD) had a higher incidence of complicated infection when compared to COVID-19 patients with all other ACHDs. Risk factors for mor-tality among COVID-19 patients with ACHD include advanced age, lower income, unrepaired ACHD, mal-nutrition, and chronic liver disease. Accordingly, we recommend aggressive preventive care with vaccina-tion and non-pharmacologic measures in order to improve survival for ACHD patients. (Curr Probl Cardiol 2023;48:101644.)

Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), primarily a respiratory virus causing coronavirus disease 2019 (COVID-19) pneumonia, induces a hypercoagulable state. Previous studies comparing the prevalence of venous thromboembolism (VTE) in patients with COVID-19 pneumonia and those with influenza pneumonia revealed a higher risk of pulmonary embolism (PE) and deep vein thrombosis (DVT) associated with COVID-19 pneumonia. However, these studies have not adequately accounted for the severity and acuity of the presenting viral pneumonia. Methods: In this retrospective study, we rigorously adjusted for critical illness using a nationally representative dataset to investigate whether COVID-19 pneumonia is independently linked to a higher risk of PE and DVT. Results: After comprehensive multivariate adjustment, our findings demonstrated that patients with COVID-19 pneumonia maintained significantly higher odds of developing acute inpatient PE [adjusted odds ratio (aOR): 2.48; 95% confidence interval (CI): 2.16–2.86; P<0.01] and DVT (aOR: 1.66; 95% CI: 1.41–1.96; P<0.01) during the early pandemic compared to patients with influenza pneumonia. Furthermore, we identified congenital heart disease and malnutrition as novel risk factors for acute PE in COVID-19 patients. Conclusions: Our study suggests that the higher prevalence of acute inpatient PE over DVT in patients with COVID-19 pneumonia may support a “thrombus in situ” mechanism of SARS-CoV-2-mediated pulmonary thrombosis. Consequently, clinicians should maintain a high index of suspicion for PE, even in the absence of DVT, among patients with COVID-19 pneumonia and should follow evidence-based guidelines for diagnosis and management.

Multifocal pneumonia amidst this global pandemic is often attributed to COVID-19, resulting in missed diagnosis of other potentially fatal illnesses such as eosinophilic pneumonia. Eosinophilic pneumonia is often associated with antibiotics and non-steroidal anti-inflammatory drugs. A 65-year-old male presented to the emergency department for a four-day history of fatigue, cough, and worsening dyspnea; CT thorax showed extensive multifocal pneumonia, and COVID-19 was suspected. COVID-19 testing using reverse transcription polymerase chain reaction was negative, and complete blood count revealed peripheral eosinophilia, which is not expected in COVID-19. The patient was being treated concomitantly with daptomycin and ceftaroline for septic arthritis and methicillin-resistant Staphylococcus aureus bacteremia. We reconsidered our initial diagnosis and held daptomycin, after which the patient started to improve. Due to hypoxia, steroids were added, which resulted in a dramatic improvement of the patient's symptoms. Daptomycin can have toxic effects, resulting in the accumulation of eosinophils in the lung parenchyma. Symptoms usually arise by the third week and include dyspnea, peripheral eosinophilia, and infiltrates involving the outer one-third of the lung fields. FDA drug safety guidance helped to establish this diagnosis. The treatment options include the removal of offending agents and steroids in severe cases.

Coronavirus disease 2019 (COVID-19) infection is associated with troponin elevation, which is associated with increased mortality. However, it is not clear if troponin elevation is independently linked to increased mortality in COVID-19 patients. Although there is considerable literature on risk factors for mortality in COVID-19-associated myocardial injury, the Global Registry of Acute Coronary Events (GRACE), Thrombolysis in Myocardial Infarction (TIMI), and Sequential Organ Failure Assessment (SOFA) scores have not been studied in COVID-19-related myocardial injury. This data is important in risk-stratifying COVID-19 myocardial injury patients. Of the 1,500 COVID-19 patients admitted to our hospitals, 217 patients who had troponin levels measured were included. Key variables were collected manually, and univariate and multivariate cox regression analysis was done to determine the predictors of mortality in COVID-19-associated myocardial injury. The differences in clinical profiles and outcomes of COVID-19 patients with and without troponin elevation were compared. Mortality was 26.5% in the normal troponin group and 54.6% in the elevated troponin group. Patients with elevated troponins had increased frequency of hypotension (p = 0.01), oxygen support (p < 0.01), low absolute lymphocyte (p < 0.01), elevated blood urea nitrogen (p < 0.01), higher C-reactive protein (p < 0.01), higher D-dimer (p < 0.01), higher lactic acid (p < 0.01), and higher Quick SOFA (qSOFA), SOFA, TIMI, and GRACE (all scores p < 0.01). On univariate cox regression, troponin elevation (hazard ratio (HR) = 1.85, 95% confidence interval (CI) = 1.18-2.88, p < 0.01), TIMI score >3 (HRv = 1.79, 95% CI = 1.11-2.75, p = 0.01), and GRACE score >140 (HR = 2.27, 95% CI = 1.45-3.55, p < 0.01) were highly associated with mortality, whereas cardiovascular disease (HR = 1.40, 95% CI = 0.89-2.21, p = 0.129) and cardiovascular risk factors (HR = 1.15, 95% CI = 0.73-1.81, p = 0.52) were not. After adjusting for age, use of a non-rebreather or high-flow nasal cannula, hemoglobin <8.5 g/dL, suspected or confirmed source of infection, and qSOFA and SOFA scores (HR = 1.18, 95% CI = 1.07-1.29, p < 0.01) were independently associated with mortality, whereas troponin (HR = 1.08, 95% CI = 0.63-1.85, p = 0.76), TIMI score (HR = 1.02, 95% CI = 0.99-1.06, p = 0.12) and GRACE scores (HR = 1.01, 95% CI = 0.99-1.02, p = 0.10) were not associated with mortality. Our study shows that troponin, GRACE score, and TIMI score are not independent predictors of mortality in COVID-19 myocardial injury. This may be because troponin elevation in COVID-19 patients may be related to demand ischemia rather than acute coronary syndrome-related. This was shown by the association of troponin with a higher degree of systemic inflammation and end-organ dysfunction. Therefore, we recommend SOFA scores in risk-stratifying COVID-19 patients with myocardial injury.