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Background 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. Methodology 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. Results 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. Conclusions 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.
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INTRODUCTION: This is a case of new-onset systemic lupus erythematosus (SLE) manifesting as acute pneumonitis during pregnancy. No prior reports have documented pneumonitis as the presenting manifestation of SLE in pregnant women. Case Presentation. A 23-year-old pregnant female presented with high-grade fever, cough, arthralgias, and respiratory failure. Infectious workup was negative. She was positive for ANA, anti-dsDNA, anti-SSA, hypocomplementemia, and pulmonary infiltrates, supporting the diagnosis of SLE and pneumonitis. The patient received methylprednisolone achieving adequate clinical and serological response. CONCLUSION: When SLE patients present with fever, cough, and respiratory failure, pulmonary infiltrates should raise the suspicion of pneumonitis in the absence of infection and hemorrhage. Even though acute lupus pneumonitis (ALP) is rare and seen only in 2% of SLE patients, a high index of suspicion aids in prompt diagnosis of this life-threatening condition. Also, positive anti-SSA antibodies may be associated with lupus pneumonitis.