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J Thromb Haemost ; 20(1): 17-31, 2022 01.
Article in English | MEDLINE | ID: covidwho-1476312


The COVID-19 pandemic extended all around the world causing millions of deaths. In addition to acute respiratory distress syndrome, many patients with severe COVID-19 develop thromboembolic complications associated to multiorgan failure and death. Here, we review evidence for the contribution of neutrophils, platelets, and extracellular vesicles (EVs) to the thromboinflammatory process in COVID-19. We discuss how the immune system, influenced by pro-inflammatory molecules, EVs, and neutrophil extracellular traps (NETs), can be caught out in patients with severe outcomes. We highlight how the deficient regulation of the innate immune system favors platelet activation and induces a vicious cycle amplifying an immunothrombogenic environment associated with platelet/NET interactions. In light of these considerations, we discuss potential therapeutic strategies underlining the modulation of purinergic signaling as an interesting target.

COVID-19 , Extracellular Traps , Extracellular Vesicles , Thrombosis , Blood Platelets , Humans , Neutrophils , Pandemics , SARS-CoV-2
Front Cardiovasc Med ; 8: 654405, 2021.
Article in English | MEDLINE | ID: covidwho-1247849


Background: Accumulating evidence has revealed that coronavirus disease 2019 (COVID-19) patients may be complicated with myocardial injury during hospitalization. However, data regarding persistent cardiac involvement in patients who recovered from COVID-19 are limited. Our goal is to further explore the sustained impact of COVID-19 during follow-up, focusing on the cardiac involvement in the recovered patients. Methods: In this prospective observational follow-up study, we enrolled a total of 40 COVID-19 patients (20 with and 20 without cardiac injury during hospitalization) who were discharged from Zhongnan Hospital of Wuhan University for more than 6 months, and 27 patients (13 with and 14 without cardiac injury during hospitalization) were finally included in the analysis. Clinical information including self-reported symptoms, medications, laboratory findings, Short Form 36-item scores, 6-min walk test, clinical events, electrocardiogram assessment, echocardiography measurement, and cardiac magnetic resonance imaging was collected and analyzed. Results: Among 27 patients finally included, none of patients reported any obvious cardiopulmonary symptoms at the 6-month follow-up. There were no statistically significant differences in terms of the quality of life and exercise capacity between the patients with and without cardiac injury. No significant abnormalities were detected in electrocardiogram manifestations in both groups, except for nonspecific ST-T changes, premature beats, sinus tachycardia/bradycardia, PR interval prolongation, and bundle-branch block. All patients showed normal cardiac structure and function, without any statistical differences between patients with and without cardiac injury by echocardiography. Compared with patients without cardiac injury, patients with cardiac injury exhibited a significantly higher positive proportion in late gadolinium enhancement sequences [7/13 (53.8%) vs. 1/14 (7.1%), p = 0.013], accompanied by the elevation of circulating ST2 level [median (interquartile range) = 16.6 (12.1, 22.5) vs. 12.5 (9.5, 16.7); p = 0.044]. Patients with cardiac injury presented higher levels of aspartate aminotransferase, creatinine, high-sensitivity troponin I, lactate dehydrogenase, and N-terminal pro-B-type natriuretic peptide than those without cardiac injury, although these indexes were within the normal range for all recovered patients at the 6-month follow-up. Among patients with cardiac injury, patients with positive late gadolinium enhancement presented higher cardiac biomarker (high-sensitivity troponin I) and inflammatory factor (high-sensitivity C-reactive protein) on admission than the late gadolinium enhancement-negative subgroup. Conclusions: Our preliminary 6-month follow-up study with a limited number of patients revealed persistent cardiac involvement in 29.6% (8/27) of recovered patients from COVID-19 after discharge. Patients with cardiac injury during hospitalization were more prone to develop cardiac fibrosis during their recovery. Among patients with cardiac injury, those with relatively higher cardiac biomarkers and inflammatory factors on admission appeared more likely to have cardiac involvement in the convalescence phase.

Am J Hypertens ; 34(3): 282-290, 2021 04 02.
Article in English | MEDLINE | ID: covidwho-1003507


BACKGROUND: The risk that coronavirus disease 2019 (COVID-19) patients develop critical illness that can be fatal depends on their age and immune status and may also be affected by comorbidities like hypertension. The goal of this study was to develop models that predict outcome using parameters collected at admission to the hospital. METHODS AND RESULTS: This is a retrospective single-center cohort study of COVID-19 patients at the Seventh Hospital of Wuhan City, China. Forty-three demographic, clinical, and laboratory parameters collected at admission plus discharge/death status, days from COVID-19 symptoms onset, and days of hospitalization were analyzed. From 157 patients, 120 were discharged and 37 died. Pearson correlations showed that hypertension and systolic blood pressure (SBP) were associated with death and respiratory distress parameters. A penalized logistic regression model efficiently predicts the probability of death with 13 of 43 variables. A regularized Cox regression model predicts the probability of survival with 7 of above 13 variables. SBP but not hypertension was a covariate in both mortality and survival prediction models. SBP was elevated in deceased compared with discharged COVID-19 patients. CONCLUSIONS: Using an unbiased approach, we developed models predicting outcome of COVID-19 patients based on data available at hospital admission. This can contribute to evidence-based risk prediction and appropriate decision-making at hospital triage to provide the most appropriate care and ensure the best patient outcome. High SBP, a cause of end-organ damage and an important comorbid factor, was identified as a covariate in both mortality and survival prediction models.

Blood Pressure , COVID-19/diagnosis , Critical Illness/mortality , Diagnostic Tests, Routine , Hypertension , Risk Assessment/methods , Blood Pressure Determination/methods , Blood Pressure Determination/statistics & numerical data , COVID-19/epidemiology , COVID-19/physiopathology , COVID-19/therapy , China/epidemiology , Comorbidity , Diagnostic Tests, Routine/methods , Diagnostic Tests, Routine/statistics & numerical data , Female , Humans , Hypertension/diagnosis , Hypertension/epidemiology , Male , Middle Aged , Proportional Hazards Models , SARS-CoV-2/isolation & purification , Survival Analysis