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Elderly Male With Cardiovascular-Related Comorbidities Has a Higher Rate of Fatal Outcomes: A Retrospective Study in 602 Patients With Coronavirus Disease 2019.

ABSTRACT: Elderly with comorbidities have shown a higher rate of fatal outcomes when suffering coronavirus disease 2019 (COVID-19). However, a delineation of clinical significances of hematologic indices and underlying comorbidities in the progression and outcome of COVID-19 remains undefined. Six hundred two COVID-19 patients with established clinical outcomes (discharged or deceased) from Hankou Hospital of Wuhan, China between January 14, 2020 and February 29, 2020 were retrospectively analyzed. Of the 602 patients with COVID-19, 539 were discharged and 63 died in the hospital. The deceased group showed higher leukocyte and neutrophil counts but lower lymphocyte and platelet counts. Longer activated partial thromboplastin time (APTT) and prothrombin time (PT), as well as higher D-dimer and C-reactive protein levels, were found in non-survivors. Our observations suggest that these parameters could serve as potential predictors for the fatal outcome and in the discharged group. A higher neutrophil count and D-dimer level but lower lymphocyte were associated with a longer duration of hospitalization. A multivariable Cox regression analysis showed that higher neutrophil count, prolonged PT, and low lymphocyte count were risk factors for patients with COVID-19. Also, we found an association of lower lymphocyte count and higher C-reactive protein levels with the elderly group and those with cardiovascular-related comorbidities. The significantly different hematologic profiles between survivors and non-survivors support that distinct hematologic signatures in COVID-19 patients will dictate different outcomes as a prognostic marker for recovery or fatality. Lymphopenia and aggressive inflammatory response might be major causes for fatal outcomes in the elderly male and especially those with cardiovascular-related comorbidities.

SUBMITTER: Zhan XY

PROVIDER: S-EPMC8215131 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ObjectivesExisting findings regarding the relationship between comorbidities and the severity of coronavirus disease 2019 (COVID-19) are inconsistent and insufficient. The aim of this study was to evaluate the association between different comorbidities and the severity of COVID-19.MethodsThe PubMed, Embase, and Cochrane Library databases were searched to identify studies reporting the rates of comorbidities in COVID-19 patients with severe/fatal outcomes. Subgroup analyses were conducted according to disease severity and the country of residence. Odds ratios (OR) with 95% confidence intervals (CI) were pooled using random-effects models.ResultsA total of 34 eligible studies were identified. In patients with severe/fatal COVID-19, the most prevalent chronic comorbidities were obesity (42%, 95% CI 34-49%) and hypertension (40%, 95% CI 35-45%), followed by diabetes (17%, 95% CI 15-20%), cardiovascular disease (13%, 95% CI 11-15%), respiratory disease (8%, 95% CI 6-10%), cerebrovascular disease (6%, 95% CI 4-8%), malignancy (4%, 95% CI 3-6%), kidney disease (3%, 95% CI 2-4%), and liver disease (2%, 95% CI 1-3%). In order of the prediction, the pooled ORs of the comorbidities in patients with severe or fatal COVID-19 when compared to patients with non-severe/fatal COVID-19 were as follows: chronic respiratory disease, OR 3.56 (95% CI 2.87-4.41); hypertension, OR 3.17 (95% CI 2.46-4.08); cardiovascular disease, OR 3.13 (95% CI 2.65-3.70); kidney disease, OR 3.02 (95% CI 2.23-4.08); cerebrovascular disease, OR 2.74 (95% CI 1.59-4.74); malignancy, OR 2.73 (95% CI 1.73-4.21); diabetes, OR 2.63 (95% CI 2.08-3.33); and obesity, OR 1.72 (95% CI 1.04-2.85). No correlation was observed between liver disease and COVID-19 aggravation (OR 1.54, 95% CI 0.95-2.49).ConclusionsChronic comorbidities, including obesity, hypertension, diabetes, cardiovascular disease, cerebrovascular disease, respiratory disease, kidney disease, and malignancy are clinical risk factors for a severe or fatal outcome associated with COVID-19, with obesity being the most prevalent and respiratory disease being the most strongly predictive. Knowledge of these risk factors could help clinicians better identify and manage the high-risk populations.

Project description:AimsCardiovascular complications, including myocarditis, are observed in coronavirus disease 2019 (COVID-19). Major cardiac involvement is a potentially lethal feature in severe cases. We sought to describe the underlying pathophysiological mechanism in COVID-19 lethal cardiogenic shock.Methods and resultsWe report on a 48-year-old male COVID-19 patient with cardiogenic shock; despite extracorporeal life support, dialysis, and massive pharmacological support, this rescue therapy was not successful. Severe acute respiratory syndrome coronavirus 2 RNA was detected at autopsy in the lungs and myocardium. Histopathological examination revealed diffuse alveolar damage, proliferation of type II pneumocytes, lymphocytes in the lung interstitium, and pulmonary microemboli. Moreover, patchy muscular, sometimes perivascular, interstitial mononuclear inflammatory infiltrates, dominated by lymphocytes, were seen in the cardiac tissue. The lymphocytes 'interlocked' the myocytes, resulting in myocyte degeneration and necrosis. Predominantly, T-cell lymphocytes with a CD4:CD8 ratio of 1.7 infiltrated the interstitial myocardium, reflecting true myocarditis. The myocardial tissue was examined for markers of ferroptosis, an iron-catalysed form of regulated cell death that occurs through excessive peroxidation of polyunsaturated fatty acids. Immunohistochemical staining with E06, a monoclonal antibody binding to oxidized phosphatidylcholine (reflecting lipid peroxidation during ferroptosis), was positive in morphologically degenerating and necrotic cardiomyocytes adjacent to the infiltrate of lymphocytes, near arteries, in the epicardium and myocardium. A similar ferroptosis signature was present in the myocardium of a COVID-19 subject without myocarditis. In a case of sudden death due to viral myocarditis of unknown aetiology, however, immunohistochemical staining with E06 was negative. The renal proximal tubuli stained positively for E06 and also hydroxynonenal (4-HNE), a reactive breakdown product of the lipid peroxides that execute ferroptosis. In the case of myocarditis of other aetiology, the renal tissue displayed no positivity for E06 or 4-HNE.ConclusionsThe findings in this case are unique as this is the first report on accumulated oxidized phospholipids (or their breakdown products) in myocardial and renal tissue in COVID-19. This highlights ferroptosis, proposed to detrimentally contribute to some forms of ischaemia-reperfusion injury, as a detrimental factor in COVID-19 cardiac damage and multiple organ failure.

Project description:Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus. Although it is known that the COVID-19 acute respiratory distress syndrome (ARDS) is associated with higher incidence of pulmonary barotrauma, unique mechanisms causing the aforementioned complication are still to be investigated. The goal of this research was to investigate the incidence of barotrauma among COVID-19 patients treated in the intensive care unit (ICU) and to examine different clinical outcomes among those subjects. This retrospective observational cohort study included adult COVID-19 patients admitted to ICU from September 1, 2020, to February 28, 2022. All admitted subjects received invasive respiratory support. Subjects were divided into two groups based on occurrence of pulmonary barotrauma. Data were collected from available electronical medical records. In the study period, a total of 900 subjects met inclusion criteria. Pulmonary barotrauma occurred in 88 (9.8%) of them. Subcutaneous emphysema developed in 73 (83%), pneumomediastinum in 68 (77.3%) and pneumothorax in 54 (61.4%) subjects. A small group of subjects developed less common complications like pneumoperitoneum (8 subjects, 9.1%) and pneumopericardium (2 subjects, 2.3%). Survival rate was higher in control than in barotrauma group [396 (48.8%) vs. 22 (25.0%), P<0.05]. There was also a significant difference between two groups in PaO2/FiO2 ratio on admission, duration of non-invasive respiratory support before mechanical ventilation, duration of mechanical ventilation and duration of ICU and hospital stay, all in favour of control group. Development of barotrauma in patients with severe forms of COVID-19 disease and in need of respiratory support is associated with longer ICU and hospital stay as well as lower survival rates at hospital discharge. Further efforts are needed in understanding mechanism in developing barotrauma and finding new prevention and treatment options.

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Elderly Male With Cardiovascular-Related Comorbidities Has a Higher Rate of Fatal Outcomes: A Retrospective Study in 602 Patients With Coronavirus Disease 2019.

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