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1.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-323623

ABSTRACT

Background: In current pandemic of COVID-19, approximately 15% to 30% of critically ill COVID-19 patients developed acute respiratory distress syndrome (ARDS) with a high mortality. Extracorporeal membrane of oxygenation (ECMO) provides direct support for both lung and heart in ARDS. However, the role of ECMO in COVID-19 related ARDS was still controversial. The aim of this study was to provide insights into the mortality, intensive care unit (ICU) management, risk factors for mortality, 180-day short term prognosis of the COVID-19 related severe ARDS patients receiving ECMO treatment. Methods: : From Feb 2 nd , 2020 to April 27 th , 2020, we included adult COVID-19 related ARDS patients admitted to intensive care unit in Tongji Hospital. Totally, 53 patients were retrospectively analyzed. They were divided into ECMO (mechanical ventilation with ECMO, n=16) and non-ECMO group (mechanical ventilation, n=37). The primary outcome was all-cause 60-day mortality. The secondary outcomes were complications on ECMO, successful weaning from ECMO, and all-cause 180-day mortality. Results: : The all-cause 60-day mortality was 37.5% (6/16) in ECMO group and 86.5% (32/37) in non-ECMO group (HR, 0.196;95% CI, 0.053-0.721;p=0.014). 10 (62.5%) patients were successfully weaned from ECMO. The all-cause 180-day mortality was 56.3% (9/16) in ECMO group and 33 (89.2%, 33/37) in non-ECMO group (HR, 0.298;95% CI, 0.130-0.680;p=0.004). All the patients in ECMO group suffered from at least one device-related complication with coagulopathy (81.3%) being most frequently seen. Up to 180-day follow up after disease onset, the ECMO-treated survivors maintained good quality of life without severe complications or disabilities. Hypercapnia, thrombopenia, myocardial injury and elevation of IL-8 and IL-10 during ECMO treatment were strongly associated with death. Conclusion: This study showed the COVID-19 patients significantly benefited from ECMO treatment during severe ARDS, which supported the application of ECMO as an indicated strategy in the management of COVID-19 related ARDS.

2.
Ann Transl Med ; 9(15): 1221, 2021 Aug.
Article in English | MEDLINE | ID: covidwho-1337888

ABSTRACT

BACKGROUND: Coronavirus disease 2019 (COVID-19) is an ongoing public health crisis that has led to many deaths due to multiple organ dysfunction syndromes (MODS). This article describes the clinical characteristics, management, and outcomes of critically ill COVID-19 patients who survived the disease through mechanical circulatory support (MCS). METHODS: We studied 25 critically ill COVID-19 patients who underwent MCS from January 20, 2020, to April 10, 2020, at the Tongji Hospital of Huazhong University of Science and Technology. RESULTS: Thirteen (52%) of the 25 patients survived with MCS support, while 12 (48%) died. At the time of their hospital admission, we identified significant differences in their peak cardiac troponin I (cTnI) and interleukin 6 (IL-6) levels, as well as in their lymphocyte count and C-reactive protein (CRP) levels. Cox proportional hazards regression model revealed that receipt of renal replacement therapy (RRT) was associated with an approximately 20-fold improvement in survival [hazard ratio (HR) =0.049, 95% confidence interval (CI) =0.008 to 0.305]. The number of days spent on extracorporeal membrane oxygenation (ECMO) support and the use of hydrogen (pH) at the time of MCS was also associated with an increase in survival. This contrasted with high-sensitivity C-reactive proteins (hs-CRP) and lactate, associated with a decrease in survival during MCS. Further analysis of the determinants relating to a COVID-19 patient's chance of survival on/after MCS was also indicated by levels of IL-6 (ß=0.009, P=0.006), IL-8 (ß=0.031, P=0.020), and TNF-α (ß=0.107, P=0.014), which saw a significant increase in the 12 patients who died. This contrasts with the non-significant decrease in IL-6, IL-8, and TNF-α levels in the 13 patients who survived. CONCLUSIONS: These results indicate that pH, lactate, hs-CRP, ECMO duration, and RRT are important clinical determinants for assessing how MCS can increase the chances of critically ill COVID-19 patients surviving the disease.

3.
Front Med (Lausanne) ; 8: 582764, 2021.
Article in English | MEDLINE | ID: covidwho-1154222

ABSTRACT

Background: The coronavirus disease 2019 (COVID-19) has swept through the world at a tremendous speed, and there is still limited data available on the treatment for COVID-19. The mortality of severely and critically ill COVID-19 patients in the Optical Valley Branch of Tongji Hospital was low. We aimed to analyze the available treatment strategies to reduce mortality. Methods: In this retrospective, single-center study, we included 1,106 COVID-19 patients admitted to the Optical Valley Branch of Tongji Hospital from February 9 to March 9, 2020. Cases were analyzed for demographic and clinical features, laboratory data, and treatment methods. Outcomes were followed up until March 29, 2020. Results: Inflammation-related indices (hs-CRP, ESR, serum ferritin, and procalcitonin) were significantly higher in severe and critically ill patients than those in moderate patients. The levels of cytokines, including IL-6, IL2R, IL-8, and TNF-α, were also higher in the critical patients. Incidence of acute respiratory distress syndrome (ARDS) in the severely and critically ill group was 23.0% (99/431). Sixty-one patients underwent invasive mechanical ventilation. The correlation between SpO2/FiO2 and PaO2/FiO2 was confirmed, and the cut-off value of SpO2/FiO2 related to survival was 134.43. The mortality of patients with low SpO2/FiO2 (<134.43) at intubation was higher than that of patients with high SpO2/FiO2 (>134.43) (72.7 vs. 33.3%). Among critical patients, the application rates of glucocorticoid therapy, continuous renal replacement therapy (CRRT), and anticoagulation treatment reached 55.2% (238/431), 7.2% (31/431), and 37.1% (160/431), respectively. Among the intubated patients, the application rates of glucocorticoid therapy, CRRT, and anticoagulation treatment were respectively 77.0% (47/61), 54.1% (33/61), and 98.4% (60/61). Conclusion: No vaccines or specific antiviral drugs for COVID-19 have been shown to be sufficiently safe and effective to date. Comprehensive treatment including ventilatory support, multiple organ function preservation, glucocorticoid use, renal replacement therapy, anticoagulation, and restrictive fluid management was the main treatment strategy. Early recognition and intervention, multidisciplinary collaboration, multi-organ function support, and personalized treatment might be the key for reducing mortality.

4.
J Am Heart Assoc ; 9(21): e017736, 2020 11 03.
Article in English | MEDLINE | ID: covidwho-901509

ABSTRACT

Background There has been significant controversy regarding the effects of pre-hospitalization use of renin-angiotensin system (RAS) inhibitors on the prognosis of hypertensive COVID-19 patients. Methods and Results We retrospectively assessed 2,297 hospitalized COVID-19 patients at Tongji Hospital in Wuhan, China, from January 10th to March 30th, 2020; and identified 1,182 patients with known hypertension on pre-hospitalization therapy. We compared the baseline characteristics and in-hospital mortality between hypertensive patients taking RAS inhibitors (N=355) versus non-RAS inhibitors (N=827). Of the 1,182 hypertensive patients (median age 68 years, 49.1% male), 12/355 (3.4%) patients died in the RAS inhibitors group vs. 95/827 (11.5%) patients in the non-RAS inhibitors group (p<0.0001). Adjusted hazard ratio for mortality was 0.28 (95% CI 0.15-0.52, p<0.0001) at 45 days in the RAS inhibitors group compared with non-RAS inhibitors group. Similar findings were observed when patients taking angiotensin receptor blockers (N=289) or angiotensin converting enzyme inhibitors (N=66) were separately compared with non-RAS inhibitors group. The RAS inhibitors group compared with non-RAS inhibitors group had lower levels of C-reactive protein (median 13.5 vs. 24.4 pg/mL; p=0.007) and interleukin-6 (median 6.0 vs. 8.5 pg/mL; p=0.026) on admission. The protective effect of RAS inhibitors on mortality was confirmed in a meta-analysis of published data when our data were added to previous studies (odd ratio 0.44, 95% CI 0.29-0.65, p<0.0001). Conclusions In a large single center retrospective analysis we observed a protective effect of pre-hospitalization use of RAS inhibitors on mortality in hypertensive COVID-19 patients; which might be associated with reduced inflammatory response.


Subject(s)
Angiotensin Receptor Antagonists/therapeutic use , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Antihypertensive Agents/therapeutic use , Coronavirus Infections/mortality , Hospital Mortality , Hypertension/drug therapy , Patient Admission , Pneumonia, Viral/mortality , Renin-Angiotensin System/drug effects , Adult , Aged , COVID-19 , China , Coronavirus Infections/diagnosis , Coronavirus Infections/therapy , Female , Humans , Hypertension/diagnosis , Hypertension/mortality , Male , Middle Aged , Pandemics , Pneumonia, Viral/diagnosis , Pneumonia, Viral/therapy , Prognosis , Protective Factors , Retrospective Studies , Risk Assessment , Risk Factors
5.
Int J Cardiol ; 324: 131-138, 2021 02 01.
Article in English | MEDLINE | ID: covidwho-893924

ABSTRACT

Fulminant myocarditis (FM) is a form of acute myocardial inflammation leading to rapid-onset hemodynamic instability due to cardiogenic shock or life-threatening arrhythmias. As highlighted by recent registries, FM is associated with high rates of death and heart transplantation, regardless of the underlying histology. Because of a paucity of evidence-based management strategies exists for this disease, an International workshop on FM was held in Wuhan, China, in October 2019, in order to share knowledge on the disease and identify areas of consensus. The present report highlights both agreements and controversies in FM management across the world, focusing the attention on areas of opportunity, FM definition, the use of endomyocardial biopsy and viral identification on heart specimens, treatment algorithms including immunosuppression and the timing of circulatory support escalation. This report incorporates the most recent recommendations from national and international professional societies. Main areas of interest and aims of future prospective observational registries and randomized controlled trials were finally identified and suggested.


Subject(s)
COVID-19/epidemiology , Disease Management , Education/methods , Internationality , Myocarditis/epidemiology , COVID-19/therapy , China/epidemiology , Education/trends , Heart Failure/epidemiology , Heart Failure/therapy , Humans , Myocarditis/therapy
6.
SSRN; 2020.
Preprint | SSRN | ID: ppcovidwho-1093

ABSTRACT

Background: Overall death cause of COVID-19 patients has been reported but attribution of myocardial injury remains undetermined. br br Methods: We extracted d

7.
SSRN; 2020.
Preprint | SSRN | ID: ppcovidwho-864

ABSTRACT

Coronavirus disease 2019 (COVID-19) has been pandemic and is leading to many deaths due to refractory respiratory failure. Here, we report our experience of tre

8.
J Mol Cell Cardiol ; 147: 74-87, 2020 10.
Article in English | MEDLINE | ID: covidwho-722814

ABSTRACT

BACKGROUND: Cardiac injury, as measured by troponin elevation, has been reported among hospitalized coronavirus disease 2019 (COVID-19) patients and portends a poor prognosis. However, how the dynamics of troponin elevation interplay with inflammation and coagulation biomarkers over time is unknown. We assessed longitudinal follow-up of cardiac injury, inflammation and coagulation markers in relation to disease severity and outcome. METHODS: We retrospectively assessed 2068 patients with laboratory-confirmed COVID-19 between January 29 and April 1, 2020 at Tongji Hospital in Wuhan, China. We defined cardiac injury as an increase in high sensitivity cardiac troponin-I (hs-cTnI) above the 99th of the upper reference limit. We explored the dynamics of elevation in hs-cTnI and the relationship with inflammation (interleukin [IL]-6, IL-8, IL-10, IL-2 receptor, tumor necrosis factor-α, C-reactive protein) and coagulation (d-dimer, fibrinogen, international normalized ratio) markers in non-critically ill versus critically ill patients longitudinally and further correlated these markers to survivors and non-survivors. RESULTS: Median age was 63 years (first to third quartile 51-70 years), 51.4% of whom were women. When compared to non-critically ill patients (N = 1592, 77.0%), critically ill (defined as requiring mechanical ventilation, in shock or multiorgan failure) patients (N = 476, 23.0%), had more frequent cardiac injury on admission (30.3% vs. 2.3%, p < 0.001), with increased mortality during hospitalization (38.4% vs. 0%, p < 0.001). Among critically ill patients, non-survivors (N = 183) had a continuous increase in hs-cTnI levels during hospitalization, while survivors (N = 293) showed a decrease in hs-cTnI level between day 4 and 7 after admission. Specifically, cardiac injury is an independent marker of mortality among critically ill patients at admission, day 4-7 and 8-14. Consistent positive correlations between hs-cTnI and interleukin (IL)-6 on admission (r = 0.59), day 4-7 (r = 0.66) and day 8-14 (r = 0.61; all p < 0.001) and d-dimer (at the same timepoints r = 0.54; 0.65; 0.61, all p < 0.001) were observed. A similar behavior was observed between hs-cTnI and most of other biomarkers of inflammation and coagulation. CONCLUSIONS: Cardiac injury commonly occurs in critically ill COVID-19 patients, with increased levels of hs-cTnI beyond day 3 since admission portending a poor prognosis. A consistent positive correlation of hs-cTnI with IL-6 and d-dimer at several timepoints along hospitalization could suggest nonspecific cytokine-mediated cardiotoxicity.


Subject(s)
Coronavirus Infections/pathology , Cytokines/blood , Heart Injuries/pathology , Pneumonia, Viral/pathology , Troponin I/blood , Aged , Betacoronavirus , Biomarkers/blood , Blood Coagulation/physiology , COVID-19 , Coronavirus Infections/blood , Critical Illness , Female , Heart Injuries/blood , Heart Injuries/diagnosis , Humans , Inflammation , Longitudinal Studies , Male , Middle Aged , Pandemics , Pneumonia, Viral/blood , Prognosis , Retrospective Studies , SARS-CoV-2
9.
Sci China Life Sci ; 63(11): 1678-1687, 2020 11.
Article in English | MEDLINE | ID: covidwho-610883

ABSTRACT

Coronavirus disease 2019 (COVID-19) is a global pandemic which has caused numerous deaths worldwide. The present study investigated the roles of hypoproteinemia in the clinical outcome and liver dysfunction of COVID-19 patients. In this retrospective study, we extracted data from 2,623 clinically confirmed adult COVID-19 patients (>18 years old) between January 29, 2020 and March 6, 2020 in Tongji Hospital, Wuhan, China. The patients were divided into three groups-non-critically ill, critically ill, and death groups-in accordance with the Chinese Clinical Guideline for COVID-19. Serum albumin, low-density lipoproteins cholesterol (LDL-C), and high-density lipoproteins cholesterol (HDL-C) concentrations and inflammatory cytokines levels were measured and compared among these three groups. The median age of these 2,623 patients was 64 years old (interquartile range (IQR), 52-71). Among the patients enrolled in the study, 2,008 (76.6%) were diagnosed as non-critically ill and 615 (23.4%) were critically ill patients, including 383 (14.6%) critically ill survivors and 232 (8.8%) critically ill deaths in the hospital. Marked hypoalbuminemia occurred in 38.2%, 71.2%, and 82.4% patients in non-critically ill, critically ill, and death groups, respectively, on admission and 45.9%, 77.7%, and 95.6% of these three groups, respectively, during hospitalization. We also discovered that serum low-density lipoprotein (LDL) and HDL levels were significantly lower in critically ill and death groups compared to non-critically ill group. Meanwhile, the patients displayed dramatically elevated levels of serum inflammatory factors, while a markedly prolonged activated partial thromboplastin time (APTT) in critically ill patients reflected coagulopathy. This study suggests that COVID-19-induced cytokine storm causes hepatotoxicity and subsequently critical hypoalbuminemia, which are associated with exacerbation of disease-associated inflammatory responses and progression of the disease and ultimately leads to death for some critically ill patients.


Subject(s)
COVID-19/blood , COVID-19/complications , Coronavirus Infections/blood , Coronavirus Infections/complications , Liver Diseases/etiology , Serum Albumin, Human/metabolism , Aged , COVID-19/mortality , China , Cholesterol, HDL/blood , Cholesterol, LDL/blood , Coronavirus Infections/mortality , Critical Illness , Cytokines/blood , Female , Humans , Liver Diseases/blood , Male , Middle Aged , Prognosis , Retrospective Studies , Risk Factors , SARS-CoV-2 , Thromboplastin/metabolism , Time Factors
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