Project description:During the clinical care of hospitalized patients with COVID-19, diminished QRS amplitude on the surface electrocardiogram (ECG) was observed to precede clinical decompensation, culminating in death. This prompted investigation into the prognostic utility and specificity of low QRS complex amplitude (LoQRS) in COVID-19. We retrospectively analyzed consecutive adults admitted to a telemetry service with SARS-CoV-2 (n = 140) or influenza (n = 281) infection with a final disposition-death or discharge. LoQRS was defined as a composite of QRS amplitude <5 mm or <10 mm in the limb or precordial leads, respectively, or a ≥50% decrease in QRS amplitude on follow-up ECG during hospitalization. LoQRS was more prevalent in patients with COVID-19 than influenza (24.3% vs 11.7%, p = 0.001), and in patients who died than survived with either COVID-19 (48.1% vs 10.2%, p <0.001) or influenza (38.9% vs 9.9%, p <0.001). LoQRS was independently associated with mortality in patients with COVID-19 when adjusted for baseline clinical variables (odds ratio [OR] 11.5, 95% confidence interval [CI] 3.9 to 33.8, p <0.001), presenting and peak troponin, D-dimer, C-reactive protein, albumin, intubation, and vasopressor requirement (OR 13.8, 95% CI 1.3 to 145.5, p = 0.029). The median time to death in COVID-19 from the first ECG with LoQRS was 52 hours (interquartile range 18 to 130). Dynamic QRS amplitude diminution is a strong independent predictor of death over not only the course of COVID-19 infection, but also influenza infection. In conclusion, this finding may serve as a pragmatic prognostication tool reflecting evolving clinical changes during hospitalization, over a potentially actionable time interval for clinical reassessment.
Project description:(1) Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) penetrates the respiratory epithelium through angiotensin-converting enzyme-2 (ACE2) binding. Myocardial and endothelial expression of ACE2 could account for the growing body of reported evidence of myocardial injury in severe forms of Human Coronavirus Disease 2019 (COVID-19). We aimed to provide insight into the impact of troponin (hsTnI) elevation on SARS-CoV-2 outcomes in patients hospitalized for COVID-19. (2) Methods: This was a retrospective analysis of hospitalized adult patients with the SARS-CoV-2 infection admitted to a university hospital in France. The observation period ended at hospital discharge. (3) Results: During the study period, 772 adult, symptomatic COVID-19 patients were hospitalized for more than 24 h in our institution, of whom 375 had a hsTnI measurement and were included in this analysis. The median age was 66 (55-74) years, and there were 67% of men. Overall, 205 (55%) patients were placed under mechanical ventilation and 90 (24%) died. A rise in hsTnI was noted in 34% of the cohort, whereas only three patients had acute coronary syndrome (ACS) and one case of myocarditis. Death occurred more frequently in patients with hsTnI elevation (HR 3.95, 95% CI 2.69-5.71). In the multivariate regression model, a rise in hsTnI was independently associated with mortality (OR 3.12, 95% CI 1.49-6.65) as well as age ≥ 65 years old (OR 3.17, 95% CI 1.45-7.18) and CRP ≥ 100 mg/L (OR 3.62, 95% CI 1.12-13.98). After performing a sensitivity analysis for the missing values of hsTnI, troponin elevation remained independently and significantly associated with death (OR 3.84, 95% CI 1.78-8.28). (4) Conclusion: Our study showed a four-fold increased risk of death in the case of a rise in hsTnI, underlining the prognostic value of troponin assessment in the COVID-19 context.
Project description:Cardiac involvement has been reported in patients with COVID-19, which may be reflected by electrocardiographic (ECG) changes. Two COVID-19 cases in our report exhibited different ECG manifestations as the disease caused deterioration. The first case presented temporary SIQIIITIII morphology followed by reversible nearly complete atrioventricular block, and the second demonstrated ST-segment elevation accompanied by multifocal ventricular tachycardia. The underlying mechanisms of these ECG abnormalities in the severe stage of COVID-19 may be attributed to hypoxia and inflammatory damage incurred by the virus.
Project description:BackgroundThe outbreak of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in China has been declared a public health emergency of international concern. The cardiac injury is a common condition among the hospitalized patients with COVID-19. However, whether N terminal pro B type natriuretic peptide (NT-proBNP) predicted outcome of severe COVID-19 patients was unknown.MethodsThe study initially enrolled 102 patients with severe COVID-19 from a continuous sample. After screening out the ineligible cases, 54 patients were analyzed in this study. The primary outcome was in-hospital death defined as the case fatality rate. Research information and following-up data were obtained from their medical records.ResultsThe best cut-off value of NT-proBNP for predicting in-hospital death was 88.64 pg/mL with the sensitivity for 100% and the specificity for 66.67%. Patients with high NT-proBNP values (> 88.64 pg/mL) had a significantly increased risk of death during the days of following-up compared with those with low values (≤88.64 pg/mL). After adjustment for potential risk factors, NT-proBNP was independently correlated with in-hospital death.ConclusionNT-proBNP might be an independent risk factor for in-hospital death in patients with severe COVID-19.Trial registrationClinicalTrials, NCT04292964. Registered 03 March 2020.
Project description:Background and aimsBeckman Coulter hematology analysers identify leukocytes by their volume (V), conductivity (C) and scatter (S) of a laser beam at different angles. Each leukocyte sub-population [neutrophils (NE), lymphocytes (LY), monocytes (MO)] is characterized by the mean (MN) and the standard deviation (SD) of 7 measurements called "cellular population data" (@CPD), corresponding to morphological analysis of the leukocytes. As severe forms of infections to SARS-CoV-2 are characterized by a functional activation of mononuclear cells, leading to a cytokine storm, we evaluated whether CPD variations are correlated to the inflammation state, oxygen requirement and lung damage and whether CPD analysis could be useful for a triage of patients with COVID-19 in the Emergency Department (ED) and could help to identify patients with a high risk of worsening.Materials and methodThe CPD of 825 consecutive patients with proven COVID-19 presenting to the ED were recorded and compared to classical biochemical parameters, the need for hospitalization in the ward or ICU, the need for oxygen, or lung injury on CT-scan.Results40 of the 42 CPD were significantly modified in COVID-19 patients in comparison to 245 controls. @MN-V-MO and @SD-V-MO were highly correlated with C-reactive protein, procalcitonin, ferritin and D-dimers. SD-UMALS-LY > 21.45 and > 23.92 identified, respectively, patients with critical lung injuries (>75%) and requiring tracheal intubation. @SD-V-MO > 25.03 and @SD-V-NE > 19.4 identified patients required immediate ICU admission, whereas a @MN-V-MO < 183 suggested that the patient could be immediately discharged. Using logistic regression, the combination of 8 CPD with platelet and basophil counts and the existence of diabetes or obesity could identify patients requiring ICU after a first stay in conventional wards (area under the curve = 0.843).ConclusionCPD analysis constitutes an easy and inexpensive tool for triage and prognosis of COVID-19 patients in the ED.
Project description:SARS-CoV-2 infection increases the risk of thrombosis by different mechanisms not fully characterized. Although still debated, an increase in D-dimer has been proposed as a first-line hemostasis test associated with thromboembolic risk and unfavorable prognosis. We aim to systematically and comprehensively evaluate the association between thrombin generation parameters and the inflammatory and hypercoagulable state, as well as their prognostic value in COVID-19 patients. A total of 127 hospitalized patients with confirmed COVID-19, 24 hospitalized patients with SARS-CoV-2-negative pneumonia and 12 healthy subjects were included. Clinical characteristics, thrombin generation triggered by tissue factor with and without soluble thrombomodulin, and also by silica, as well as other biochemical parameters were assessed. Despite the frequent use of heparin, COVID-19 patients had similar thrombin generation to healthy controls. In COVID-19 patients, the thrombin generation lag-time positively correlated with markers of cell lysis (LDH), inflammation (CRP, IL-6) and coagulation (D-dimer), while the endogenous thrombin potential (ETP) inversely correlated with D-dimer and LDH, and positively correlated with fibrinogen levels. Patients with more prolonged lag-time and decreased ETP had higher peak ISTH-DIC scores, and had more severe disease (vascular events and death). The ROC curve and Kaplan Meier estimate indicated that the D-dimer/ETP ratio was associated with in-hospital mortality (HR 2.5; p = 0.006), and with the occurrence of major adverse events (composite end-point of vascular events and death) (HR 2.38; p = 0.004). The thrombin generation ETP and lag-time variables correlate with thromboinflammatory markers, and the D-dimer/ETP ratio can predict major adverse events in COVID-19.
Project description:Background: The association of known cardiovascular risk factors with poor prognosis of coronavirus disease 2019 (COVID-19) has been recently emphasized. Coronary artery calcium (CAC) score is considered a risk modifier in the primary prevention of cardiovascular disease. We hypothesized that the absence of CAC might have an additional predictive value for an improved cardiovascular outcome of hospitalized COVID-19 patients. Materials and methods: We prospectively included 310 consecutive hospitalized patients with COVID-19. Thirty patients with history of coronary artery disease were excluded. Chest computed tomography (CT) was performed in all patients. Demographics, medical history, clinical characteristics, laboratory findings, imaging data, in-hospital treatment, and outcomes were retrospectively analyzed. A composite endpoint of major adverse cardiovascular events (MACE) was defined. Results: Two hundred eighty patients (63.2 ± 16.7 years old, 57.5% male) were included in the analysis. 46.7% patients had a CAC score of 0. MACE rate was 21.8% (61 patients). The absence of CAC was inversely associated with MACE (OR 0.209, 95% CI 0.052-0.833, p = 0.027), with a negative predictive value of 84.5%. Conclusion: The absence of CAC had a high negative predictive value for MACE in patients hospitalized with COVID-19, even in the presence of cardiac risk factors. A semi-qualitative assessment of CAC is a simple, reproducible, and non-invasive measure that may be useful to identify COVID-19 patients at a low risk for developing cardiovascular complications.
Project description:Background & aimsCoronavirus disease 2019 (COVID-19) has a wide clinical spectrum, ranging from asymptomatic infection to severe diseases with high mortality rate. Early identification of high-risk COVID-19 patients may be beneficial to reduce morbidity and in-hospital mortality. This study aimed to investigate whether baseline levels of inflammatory markers such as C-reactive protein (CRP) and immune-cell-based inflammatory indices, neutrophil to lymphocyte ratio (NLR), derived-NLR (d-NLR), and platelet to lymphocyte ratio (PLR) at hospital admission are associated with adverse disease outcomes in COVID-19 patients.MethodsClinical data from 391 hospitalized COVID-19 patients in three Siloam Hospitals in Indonesia were retrospectively collected and analysed from March 20 to October 30, 2020.ResultsFifty-four (13.8%) hospitalized patients had clinical deterioration and required ICU treatment, categorizing them as severe COVID-19 cases. Older age, presence of underlying diseases, and increased inflammatory markers values at admission were significantly associated with severe cases. After adjustment of sociodemographic and comorbidities factors, CRP, NLR, and d-NLR values, but not PLRs, were identified as independent risk factors for disease severity and death in COVID-19 patients. The area under curve (AUC) of CRP, NLR, and d-NLR were 0.854, 0.848, and 0.854, respectively. The optimal cut-off points for CRP, NLR, and d-NLR for identification of COVID-19 patients with potential worse disease outcomes were 47 mg/L, 6, and 4, respectively.ConclusionInitial assessment of CRP, NLR, and d-NLR values at hospital admission may be important predictors for adverse disease outcomes in COVID-19 patients.
Project description:IntroductionCOVID-19 pneumonia results in an impairment of the diaphragmatic musculature that influences the development of respiratory failure during the patient's hospitalization. Diaphragmatic ultrasound is a useful, non-invasive, and accessible tool for measuring the function of this muscle.ObjectiveAssessing the morphological and functional ultrasound status of the diaphragm in patients admitted within the first 24 h for COVID-related pneumonia and its association with hospital morbidity and mortality (NCT05805579).Material and methodsObservational, prospective cohort study that included 68 patients admitted for COVID-19 pneumonia with respiratory failure. Diaphragmatic ultrasound was performed within the first 24 h of admission to the pulmonology ward. Clinical, analytical, and ultrasound variables were collected: excursion, thickness, and diaphragmatic shortening fraction (DSF). DSF < 20% was used to define diaphragmatic dysfunction (DD). Patients who showed favorable progression and were managed on the ward (HCONV) were compared to those who required admission to the respiratory monitoring unit (RMU).ResultsA total of 68 patients were included, of which 22 (32.35%) were admitted to the RMU. Diaphragmatic excursion at maximum volume was higher in the HCONV group compared to the RMU group (58.41 ± 17.83 vs. 50.03 ± 16.23; p = 0.123). Diaphragmatic dysfunction (DD) was observed in 21 (30.88%) patients, with a higher prevalence in the RMU group than in the HCONV group (15 (68.18%) vs. 6 (13.04%); p = 0.0001). In the multivariate analysis, age and DSF at admission were the best predictors of failure to discharge.ConclusionsPerforming diaphragmatic ultrasound to assess mobility and DSF within the first 24 h of admission for COVID-19 pneumonia proves valuable in determining short-term progression and the need for admission to a respiratory monitoring unit.
Project description:BackgroundBedside lung ultrasound (LUS) has emerged as a useful and non-invasive tool to detect lung involvement and monitor changes in patients with coronavirus disease 2019 (COVID-19). However, the clinical significance of the LUS score in patients with COVID-19 remains unknown. We aimed to investigate the prognostic value of the LUS score in patients with COVID-19.MethodThe LUS protocol consisted of 12 scanning zones and was performed in 280 consecutive patients with COVID-19. The LUS score based on B-lines, lung consolidation and pleural line abnormalities was evaluated.ResultsThe median time from admission to LUS examinations was 7 days (interquartile range [IQR] 3-10). Patients in the highest LUS score group were more likely to have a lower lymphocyte percentage (LYM%); higher levels of D-dimer, C-reactive protein, hypersensitive troponin I and creatine kinase muscle-brain; more invasive mechanical ventilation therapy; higher incidence of ARDS; and higher mortality than patients in the lowest LUS score group. After a median follow-up of 14 days [IQR, 10-20 days], 37 patients developed ARDS, and 13 died. Patients with adverse outcomes presented a higher rate of bilateral involvement; more involved zones and B-lines, pleural line abnormalities and consolidation; and a higher LUS score than event-free survivors. The Cox models adding the LUS score as a continuous variable (hazard ratio [HR]: 1.05, 95% confidence intervals [CI] 1.02 ~ 1.08; P < 0.001; Akaike information criterion [AIC] = 272; C-index = 0.903) or as a categorical variable (HR 10.76, 95% CI 2.75 ~ 42.05; P = 0.001; AIC = 272; C-index = 0.902) were found to predict poor outcomes more accurately than the basic model (AIC = 286; C-index = 0.866). An LUS score cut-off > 12 predicted adverse outcomes with a specificity and sensitivity of 90.5% and 91.9%, respectively.ConclusionsThe LUS score devised by our group performs well at predicting adverse outcomes in patients with COVID-19 and is important for risk stratification in COVID-19 patients.