Cardiovascular Complications of COVID-19

Brito, J; Silva, Beatriz Valente; Silva, Pedro Alves da; Cortez‐Dias, Nuno; Silva, Doroteia; Agostinho, João R.; Guimar, Tatiana; Brito, Dulce; Pinto, Fausto J.

doi:10.4103/hm.hm_28_20

Cited by 6 publications

(4 citation statements)

References 66 publications

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“…Because of the influence of COVID-19, accurate mortality might not have been observed at some degree. In a future study, we will take into account heart injury as a result of the new coronavirus (35)(36)(37). Secondly, the model does not consider some novel biomarker phenotypes associated with CHF.…”

Section: Study Strengths and Limitationsmentioning

confidence: 99%

Development and Validation of a Nomogram to Predict the 180-Day Readmission Risk for Chronic Heart Failure: A Multicenter Prospective Study

Gao

Yin

Xia

et al. 2021

Front. Cardiovasc. Med.

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Background: The existing prediction models lack the generalized applicability for chronic heart failure (CHF) readmission. We aimed to develop and validate a widely applicable nomogram for the prediction of 180-day readmission to the patients.Methods: We prospectively enrolled 2,980 consecutive patients with CHF from two hospitals. A nomogram was created to predict 180-day readmission based on the selected variables. The patients were divided into three datasets for development, internal validation, and external validation (mean age: 74.2 ± 14.1, 73.8 ± 14.2, and 71.0 ± 11.7 years, respectively; sex: 50.2, 48.8, and 55.2% male, respectively). At baseline, 102 variables were submitted to the least absolute shrinkage and selection operator (Lasso) regression algorithm for variable selection. The selected variables were processed by the multivariable Cox proportional hazards regression modeling combined with univariate analysis and stepwise regression. The model was evaluated by the concordance index (C-index) and calibration plot. Finally, the nomogram was provided to visualize the results. The improvement in the regression model was calculated by the net reclassification index (NRI) (with tenfold cross-validation and 200 bootstraps).Results: Among the selected 2,980 patients, 1,696 (56.9%) were readmitted within 180 days, and 1,502 (50.4%) were men. A nomogram was established by the results of Lasso regression, univariate analysis, stepwise regression and multivariate Cox regression, as well as variables with clinical significance. The values of the C-index were 0.75 [95% confidence interval (CI): 0.72–0.79], 0.75 [95% CI: 0.69–0.81], and 0.73 [95% CI: 0.64–0.83] for the development, internal validation, and external validation datasets, respectively. Calibration plots were provided for both the internal and external validation sets. Five variables including history of acute heart failure, emergency department visit, age, blood urea nitrogen level, and beta blocker usage were considered in the final prediction model. When adding variables involving hospital discharge way, alcohol taken and left bundle branch block, the calculated values of NRI demonstrated no significant improvements.Conclusions: A nomogram for the prediction of 180-day readmission of patients with CHF was developed and validated based on five variables. The proposed methodology can improve the accurate prediction of patient readmission and have the wide applications for CHF.

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Section: Study Strengths and Limitationsmentioning

confidence: 99%

Development and Validation of a Nomogram to Predict the 180-Day Readmission Risk for Chronic Heart Failure: A Multicenter Prospective Study

Gao

Yin

Xia

et al. 2021

Front. Cardiovasc. Med.

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“…In the early death cohort, cTnI levels (median [IQR], 591. 9 [199.3, 1750] 13.55 [7.075, 25.73] pg/mL, P = 0.8289) levels did not significantly differ between men and women.…”

Section: Biomarker Characteristics Of Study Patients At Admissionmentioning

confidence: 99%

“…Given the absence of an antiviral treatment that directly targets the cardiac injury associated with the disease, an urgent need exists to develop such alternative therapeutic strategies. SARS-CoV-2 is believed to induce the activation of immune and thrombotic pathways, which may contribute to organ injury [11][12][13]. A higher coagulation status or overactivation of immune pathways has been reported in patients with severe COVID-19 who died than survivors.…”

Section: Introductionmentioning

confidence: 99%

IL-6 and D-dimer Levels at Admission Predict Cardiac Injury and Early Mortality during SARS-CoV-2 Infection

Peng,

Du,

et al. 2024

CVIA

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Background: We previously described the mortality associated with cardiac injury in patients with coronavirus disease 2019 (COVID-19). The activation of immune and thrombotic biomarkers at admission, and their ability to predict cardiac injury and mortality patterns in COVID-19, remains unclear. Methods: This retrospective cohort study included 170 patients with COVID-19 with cardiac injury at the time of admission to Tongji Hospital in Wuhan between January 29, 2020, and March 8, 2020. The temporal evolution of inflammatory cytokines, coagulation markers, clinical treatment, and mortality were analyzed. Continuous variables are expressed as median (interquartile range). The Mann-Whitney test was used for two-group comparisons, whereas the Kruskal-Wallis test was used for comparisons among three groups. Categorical variables are expressed as proportions and percentages, and Fisher’s exact test was used to compare differences. A multivariate regression model was used to predict in-hospital death. A simple linear regression analysis was applied to examine the correlation between baseline biomarkers and peak cTnI levels. Results: Of the 170 patients, 60 (35.3%) died early (<21 d), and 61 (35.9%) died after a prolonged stay. The admission laboratory findings correlating with early death were elevated interleukin 6 (IL-6) (P < 0.0001), tumor necrosis factor-α (P = 0.0025), and C-reactive protein (P < 0.0001). We observed the trajectory of biomarker changes in patients after admission hospitalization, and determined that early mortality was associated with a rapidly increasing D-dimer level, and gradually decreasing platelet and lymphocyte counts. Multivariate and simple linear regression models indicated that the risk of death was associated with immune and thrombotic pathway activation. Elevated admission cTnI levels were associated with elevated IL-6 (P = 0.03) and D-dimer (P = 0.0021) levels. Conclusion: In patients with COVID-19 with cardiac injury, IL-6 and D-dimer levels at admission predicted subsequently elevated cTnI levels and early death, thus highlighting the need for early inflammatory cytokine-based risk stratification in patients with cardiac injury.

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“…The 2019 coronavirus disease (COVID-19) pandemic has drawn extensive global attention [1][2][3][4] and caused a large number of patient deaths [5]. Until now, there are 7,835 clinical studies related to COVID-19 according to the data from ClinicalTrials.gov, covering 708 drugs.…”

Section: Introductionmentioning

confidence: 99%

Hydroxychloroquine Attenuates hERG Channel by Promoting the Membrane Channel Degradation: Computational Simulation and Experimental Evidence for QT-Interval Prolongation with Hydroxychloroquine Treatment

Wang¹,

Feng²,

Liu³

et al. 2023

Cardiology

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Introduction: The coronavirus disease 2019 (COVID-19) pandemic has led to millions of confirmed cases and deaths worldwide and has no approved therapy. Currently, more than 700 drugs are tested in the COVID-19 clinical trials, and full evaluation of their cardiotoxicity risks is in high demand. Methods: We mainly focused on hydroxychloroquine (HCQ), one of the most concerned drugs for COVID-19 therapy, and investigated the effects and underlying mechanisms of HCQ on hERG channel via molecular docking simulations. We further applied the HEK293 cell line stably expressing hERG-wild-type channel (hERG-HEK) and HEK293 cells transiently expressing hERG-p.Y652A or hERG-p.F656A mutants to validate our predictions. Western blot analysis was used to determine the hERG channel, and the whole-cell patch clamp was utilized to record hERG current (IhERG). Results: HCQ reduced the mature hERG protein in a time- and concentration-dependent manner. Correspondingly, chronic and acute treatment of HCQ decreased the hERG current. Treatment with brefeldin A (BFA) and HCQ combination reduced hERG protein to a greater extent than BFA alone. Moreover, disruption of the typical hERG binding site (hERG-p.Y652A or hERG-p.F656A) rescued HCQ-mediated hERG protein and IhERG reduction. Conclusion: HCQ can reduce the mature hERG channel expression and IhERG via enhancing channel degradation. The QT prolongation effect of HCQ is mediated by typical hERG binding sites involving residues Tyr652 and Phe656.

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Cardiovascular Complications of COVID-19

Cited by 6 publications

References 66 publications

Development and Validation of a Nomogram to Predict the 180-Day Readmission Risk for Chronic Heart Failure: A Multicenter Prospective Study

Development and Validation of a Nomogram to Predict the 180-Day Readmission Risk for Chronic Heart Failure: A Multicenter Prospective Study

IL-6 and D-dimer Levels at Admission Predict Cardiac Injury and Early Mortality during SARS-CoV-2 Infection

Hydroxychloroquine Attenuates hERG Channel by Promoting the Membrane Channel Degradation: Computational Simulation and Experimental Evidence for QT-Interval Prolongation with Hydroxychloroquine Treatment

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