OBJECTIVE: The pathogenesis of myocardial injury upon corona virus disease 2019 (COVID-19) infection remain unknown,evidence of impact on outcome is insufficient, therefore, we aim to investigate the risk factors for death among COVID-19 patients combined with hypertension, coronary heart disease or diabetes in this study. METHODS: This was a single-centered, retrospective, observational study. Patients of Sino-French Eco-City section of Tongji Hospital, Wuhan, China attended by Peking University Supporting Medical Team and admitted from Jan. 29, 2020 to Mar. 20, 2020 were included. The positive nucleic acid of COVID-19 virus and combination with hypertension, coronary heart disease or diabetes were in the standard. We collected the clinical data and laboratory examination results of the eligible patients to evaluate the related factors of death. RESULTS: In the study, 94 COVID-19 patients enrolled were divided into the group of death (13 cases) and the group of survivors (81 cases), the average age was 66.7 years. Compared with the survival group, the death group had faster basal heart rate(103.2 beats/min vs. 88.4 beats /min, P=0.004), shortness of breath(29.0 beats /min vs. 20.0 beats /min, P<0.001), higher neutrophil count(9.2×10⁹/L vs. 3.8×10⁹/L, P<0.001), lower lymphocyte count(0.5×10⁹/L vs. 1.1×10⁹/L, P<0.001), creatine kinase MB(CK-MB, 3.2 μg/L vs. 0.8 μg/L, P<0.001), high sensitivity cardiac troponin Ⅰ(hs-cTnⅠ, 217.2 ng/L vs. 4.9 ng/L, P<0.001), N-terminal pro brain natriuretic peptide(NT-proBNP; 945.0 μg/L vs. 154.0 μg/L, P<0.001), inflammatory factor ferritin(770.2 μg/L vs. 622.8 μg/L , P=0.050), interleukin-2 recepter(IL-2R, 1 586.0 U/mL vs. 694.0 U/mL, P<0.001), interleukin-6(IL-6, 82.3 ng/L vs. 13.0 ng/L, P<0.001), interleukin-10(IL-10, 9.8 ng/L vs. 5.0 ng/L, P<0.001)were higher than those in the survival group. Univariate logistic regression analysis showed that the risk factors for death were old age, low non oxygen saturation, low lymphocyte count, myocardial injury, abnormal increase of IL 2R, IL-6, and IL-10. Multivariate regression showed that old age (OR=1.11, 95%CI=1.03-1.19, P=0.026), low non oxygen saturation(OR=0.85, 95%CI=0.72-0.99, P=0.041), and abnormal increase of IL-10(＞9.1 ng/L, OR=101.93, 95%CI=4.74-2190.71, P=0.003)were independent risk factors for COVID-19 patients combined with hypertension, coronary heart disease or diabetes. CONCLUSION In COVID-19 patients combined with hypertension, coronary heart disease or diabetes, the risk factors for death were old age, low non oxygen saturation, low lymphocyte count, myocardial injury, and abnormal increase of IL-2R, IL-6, and IL-10. Old age, low non oxygen saturation and abnormal increase of IL-10 were independent risk factors.
Aged ; Betacoronavirus ; COVID-19 ; China/epidemiology* ; Coronary Disease/complications* ; Coronavirus Infections/mortality* ; Diabetes Mellitus ; Humans ; Hypertension/complications* ; Pandemics ; Pneumonia, Viral/mortality* ; Retrospective Studies ; Risk Factors ; SARS-CoV-2

Objective: To explore the clinical characteristics and prognosis of the new coronavirus 2019-nCoV patients combined with cardiovascular disease （CVD). Methods: A retrospective analysis was performed on 112 COVID-19 patients with CVD admitted to the western district of Union Hospital in Wuhan, from January 20, 2020 to February 15, 2020. They were divided into critical group (ICU, n=16) and general group (n=96) according to the severity of the disease and patients were followed up to the clinical endpoint. The observation indicators included total blood count, C-reactive protein (CRP), arterial blood gas analysis, myocardial injury markers, coagulation function, liver and kidney function, electrolyte, procalcitonin (PCT), B-type natriuretic peptide (BNP), blood lipid, pulmonary CT and pathogen detection. Results: Compared with the general group, the lymphocyte count (0.74 (0.34, 0.94)×10⁹/L vs. 0.99 (0.71, 1.29)×10⁹/L, P=0.03) was extremely lower in the critical group, CRP (106.98 (81.57, 135.76) mg/L vs. 34.34 (9.55,76.54) mg/L, P<0.001) and PCT (0.20 (0.15,0.48) μg/L vs. 0.11 (0.06,0.20) μg/L, P<0.001) were significantly higher in the critical group. The BMI of the critical group was significantly higher than that of the general group (25.5 (23.0, 27.5) kg/m² vs. 22.0 (20.0, 24.0) kg/m²，P=0.003). Patients were further divided into non-survivor group (17, 15.18%) group and survivor group (95, 84.82%). Among the non-survivors, there were 88.24% (15/17) patients with BMI> 25.0 kg/m², which was significantly higher than that of survivors (18.95% (18/95), P<0.001). Compared with the survived patients, oxygenation index (130 (102, 415) vs. 434 (410, 444), P<0.001) was significantly lower and lactic acid (1.70 (1.30, 3.00) mmol/L vs. 1.20 (1.10, 1.60) mmol/L, P<0.001) was significantly higher in the non-survivors. There was no significant difference in the proportion of ACEI/ARB medication between the critical group and the general group or between non-survivors and survivors （all P>0.05). Conclusion: COVID-19 patients combined with CVD are associated with a higher risk of mortality. Critical patients are characterized with lower lymphocyte counts. Higher BMI are more often seen in critical patients and non-survivor. ACEI/ARB use does not affect the morbidity and mortality of COVID-19 combined with CVD. Aggravating causes of death include fulminant inflammation, lactic acid accumulation and thrombotic events.
Betacoronavirus ; COVID-19 ; Cardiovascular Diseases/therapy* ; Coronavirus Infections/complications* ; Humans ; Pandemics ; Pneumonia, Viral/complications* ; Prognosis ; Retrospective Studies ; SARS-CoV-2 ; Treatment Outcome

Objective: To analyze the clinical characteristics of the severe or critically ill patients with novel coronavirus pneumonia (COVID-19), and evaluate the impact of complicated myocardial injury on the prognosis of these patients. Methods: A retrospective study was conducted in 54 patients who admitted to Tongji hospital from February 3, 2020 to February 24, 2020 and met the criteria of severe or critical conditions of COVID-19. The clinical characteristics and hospital mortality rate were analyzed and compared between the patients with or without myocardial injury, which was defined with 3 times higher serum cardiac troponin value. Results: The age of the 54 patients was 68.0(59.8, 74.3) years. Among all the patients, 24 (44.4%) patients were complicated with hypertension, 13 (24.1%) with diabetes, 8 (14.8%) with coronary heart disease, and 3 (5.6%) with previous cerebral infarction. During hospitalization, 24 (44.4%) of the patients were complicated with myocardial injury and 26 (48.1%) patients died in hospital. In-hospital mortality was significantly higher in patients with myocardial injury than in patients without myocardial injury (14 (60.9%) vs. 8 (25.8%), P=0.013). Moreover, the levels of C-reactive protein (153.6 (80.3, 240.7) ng/L vs. 49.8 (15.9, 101.9) ng/L) and N-terminal pro-B-type natriuretic peptide (852.0 (400.0, 2 315.3) ng/L vs. 197.0 (115.3, 631.0) ng/L) were significantly higher than patients without myocardial injury (all P<0.01). Conclusions: Prevalence of myocardial injury is high among severe or critically ill COVID-19 patients. Severe or critically ill COVID-19 patients with myocardial injury face a significantly higher risk of in-hospital mortality. The study suggests that it is important to monitor and manage the myocardial injury during hospitalization for severe or critically ill COVID-19 patients.
Aged ; Betacoronavirus ; COVID-19 ; Coronavirus Infections/complications* ; Critical Illness ; Heart Injuries ; Humans ; Middle Aged ; Pandemics ; Pneumonia, Viral/complications* ; Retrospective Studies ; SARS-CoV-2

Objective: Present study investigated the mechanism of heart failure associated with coronavirus infection and predicted potential effective therapeutic drugs against heart failure associated with coronavirus infection. Methods: Coronavirus and heart failure were searched in the Gene Expression Omnibus (GEO) and omics data were selected to meet experimental requirements. Differentially expressed genes were analyzed using the Limma package in R language to screen for differentially expressed genes. The two sets of differential genes were introduced into the R language cluster Profiler package for gene ontology (GO) and Kyoto gene and genome encyclopedia (KEGG) pathway enrichment analysis. Two sets of intersections were taken. A protein interaction network was constructed for all differentially expressed genes using STRING database and core genes were screened. Finally, the apparently accurate treatment prediction platform (EpiMed) independently developed by the team was used to predict the therapeutic drug. Results: The GSE59185 coronavirus data set was searched and screened in the GEO database, and divided into wt group, ΔE group, Δ3 group, Δ5 group according to different subtypes, and compared with control group. After the difference analysis, 191 up-regulated genes and 18 down-regulated genes were defined. The GEO126062 heart failure data set was retrieved and screened from the GEO database. A total of 495 differentially expressed genes were screened, of which 165 were up-regulated and 330 were down-regulated. Correlation analysis of differentially expressed genes between coronavirus and heart failure was performed. After cross processing, there were 20 GO entries, which were mainly enriched in virus response, virus defense response, type Ⅰ interferon response, γ interferon regulation, innate immune response regulation, negative regulation of virus life cycle, replication regulation of viral genome, etc. There were 5 KEGG pathways, mainly interacting with tumor necrosis factor (TNF) signaling pathway, interleukin (IL)-17 signaling pathway, cytokine and receptor interaction, Toll-like receptor signaling pathway, human giant cells viral infection related. All differentially expressed genes were introduced into the STRING online analysis website for protein interaction network analysis, and core genes such as signal transducer and activator of transcription 3, IL-10, IL17, TNF, interferon regulatory factor 9, 2'-5'-oligoadenylate synthetase 1, mitogen-activated protein kinase 3, radical s-adenosyl methionine domain containing 2, c-x-c motif chemokine ligand 10, caspase 3 and other genes were screened. The drugs predicted by EpiMed's apparent precision treatment prediction platform for disease-drug association analysis were mainly TNF-α inhibitors, resveratrol, ritonavir, paeony, retinoic acid, forsythia, and houttuynia cordata. Conclusions: The abnormal activation of multiple inflammatory pathways may be the cause of heart failure in patients after coronavirus infection. Resveratrol, ritonavir, retinoic acid, amaranth, forsythia, houttuynia may have therapeutic effects. Future basic and clinical research is warranted to validate present results and hypothesis.
Betacoronavirus ; COVID-19 ; Computational Biology ; Coronavirus Infections/complications* ; Gene Expression Profiling ; Gene Ontology ; Heart Failure/virology* ; Humans ; Pandemics ; Pneumonia, Viral/complications* ; SARS-CoV-2

Betacoronavirus ; COVID-19 ; Cardiovascular Diseases/complications* ; Consensus ; Coronavirus Infections/epidemiology* ; Epidemics ; Humans ; Pandemics ; Pneumonia, Viral/epidemiology* ; SARS-CoV-2

Betacoronavirus ; COVID-19 ; Coronavirus Infections/complications* ; Heart ; Heart Injuries ; Humans ; Pandemics ; Pneumonia, Viral/complications* ; SARS-CoV-2

Objective: To analyze the prognostic value of myocardial injury in patients with COVID-19. Method: Confirmed cases of COVID-19 patients admitted from January 31st to February 5th at isolation ward of Renmin Hospital of Wuhan University were divided into non-survival group （33 cases）and survival group (169 cases)according to the clinical outcomes 5 weeks after admission. Data including demographics, comorbidities, vital signs, laboratory results were obtained. Cardiac injury was defined as serum concentration of high sensitivity cardiac troponin I (hs-cTnI) above 0.04 μg/L. Univariate and multivariate Cox regression were used to analyze the prognostic value of myocardial injury in patients with COVID-19. Kaplan-Meier analysis was used to plotted survival curve and analyze the impact of myocardial injury on the survival outcome of COVID-19 patients. Results: A total of 202 patients were included, the age was 63 (51, 70) years old, 88 (43.6%) of them were male, 85 (42.1%) of them had comorbidities, 125 (61.9%) of them were severely to critically ill. Till March 11, 33 patients died, all of them were critically ill patients. The age, proportion of males, comorbidities, respire rate, serum levels of hs-cTnI and incidence of heart failure in the non-survival group were significantly higher than those in the survival group (all P<0.05). The hospitalization time of non-survival group was significantly shorter than that of survival group (6(4, 9) vs. 32(23, 36), P<0.001). Myocardial injury was an important prognostic factor of COVID-19 (HR=5.382, 95%CI 2.404-12.050, P<0.001). Kaplan-Meier survival analysis showed that the presence of myocardial injury was significantly associated with the reduced survival rate among COVID-19 patients (P<0.001). Conclusion: Myocardial injury is an important prognostic factor of COVID-19, COVID-19 patients with myocardial injury face a significantly higher risk of death.
Aged ; Betacoronavirus ; COVID-19 ; Coronavirus Infections/complications* ; Female ; Heart Injuries ; Humans ; Male ; Middle Aged ; Pandemics ; Pneumonia, Viral/complications* ; Prognosis ; Retrospective Studies ; SARS-CoV-2

Arrhythmias, Cardiac/complications* ; Betacoronavirus ; COVID-19 ; Coronavirus Infections/complications* ; Humans ; Pandemics ; Pneumonia, Viral ; SARS-CoV-2

Betacoronavirus ; Blood Coagulation Disorders ; epidemiology ; etiology ; Coronavirus Infections ; complications ; Disseminated Intravascular Coagulation ; epidemiology ; etiology ; Fibrin Fibrinogen Degradation Products ; analysis ; Humans ; Pandemics ; Pneumonia, Viral ; complications ; Venous Thromboembolism ; epidemiology ; etiology

Analgesia ; methods ; Betacoronavirus ; Conscious Sedation ; methods ; Consensus ; Coronavirus Infections ; complications ; Humans ; Pandemics ; Pneumonia, Viral ; complications