Frontiers in cardiovascular medicine
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Front Cardiovasc Med · Jan 2020
Cardiovascular Impairment in COVID-19: Learning From Current Options for Cardiovascular Anti-Inflammatory Therapy.
In December 2019, Coronavirus Disease 2019 (COVID-19) caused by SARS-CoV-2, occurred in China and has currently led to a global pandemic. In addition to respiratory involvement, COVID-19 was also associated with significant multiple organ dysfunction syndrome (MODS). Cardiovascular impairment has been observed and is now drawing growing attention. ⋯ We believe that targeting the central pathway (IL-1β, TNF-α, IL-6), balancing the Th1 and Th2 response, and administering long-term anti-inflammatory therapy might be promising prospects to reduce cardiovascular impairment and even MODS during the acute and recovery phases of COVID-19. The cardiovascular anti-inflammatory therapies might be of great application value to the management of COVID-19 patients and we further propose an algorithm for the selection of anti-inflammatory therapy for COVID-19 patients with or at high risk of cardiovascular impairment. We recommend to take the experiences in cardiovascular anti-inflammatory therapy as references in the management of COVID-19 and conduct related clinical trials, while the clinical translation of novel treatments from preclinical studies or in vitro drug screening should proceed with caution due to unguaranteed efficacy and safety profiles.
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Front Cardiovasc Med · Jan 2020
Cardiac Injury and Clinical Course of Patients With Coronavirus Disease 2019.
Background: Cardiac injury is recognized as one of the most common critical complications during exacerbation of coronavirus disease 2019 (COVID-19). This study aimed to investigate the effect of cardiac injury on the clinical course of COVID-19 and to examine its potential mechanism and treatments. Methods and Results: A total of 222 hospitalized patients with COVID-19 from Wuhan were selected for the study during February 10 to March 28, 2020. ⋯ The admission level of troponin was well-correlated with inflammatory factors and d-dimer levels and strongly predicted mortality. Cardiac injury is a manifestation secondary to hypoxia and systemic infection, but which nevertheless further complicates the disease course and increases the mortality rate. Troponin levels should be checked at admission and during hospitalization for triage, better monitoring, and managing those with COVID-19, especially in the most severe patients.
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Front Cardiovasc Med · Jan 2020
Myocardial Injury at Early Stage and Its Association With the Risk of Death in COVID-19 Patients: A Hospital-Based Retrospective Cohort Study.
Background: There are growing evidence demonstrating that coronavirus disease 2019 (COVID-19) is companied by acute myocardial injury. However, the associations of SARS-CoV-2-induced myocardial injury with the risk of death and prognosis after discharge in COVID-19 patients are unclear. Methods: This prospective cohort study analyzed 355 COVID-19 patients from two hospitals in different regions. ⋯ Conclusion: Myocardial injury at early stage elevates mortality of COVID-19 patients. Male elderly patients with hypertension are more vulnerable to myocardial injury. SARS-CoV-2-induced myocardial injury has not completely recovered in 14 days after discharge.
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Front Cardiovasc Med · Jan 2019
ReviewKarma of Cardiovascular Disease Risk Factors for Prevention and Management of Major Cardiovascular Events in the Context of Acute Exacerbations of Chronic Obstructive Pulmonary Disease.
There is compelling epidemiological evidence that airway exposure to cigarette smoke, air pollution particles, as well as bacterial and viral pathogens is strongly related to acute ischemic events. Over the years, there have been important animal and human studies that have provided experimental evidence to support a causal link. Studies show that patients with cardiovascular diseases (CVDs) or risk factors for CVD are more likely to have major adverse cardiovascular events (MACEs) after an acute exacerbation of chronic obstructive pulmonary disease (COPD), and patients with more severe COPD have higher cardiovascular mortality and morbidity than those with less severe COPD. ⋯ To date, there are no guidelines regarding the prevention, screening, and management of the modifiable risk factors for MACEs in the context of COPD or COPD exacerbations, and there is insufficient CVD risk control in those with COPD. A deeper insight of the modifiable risk factors shared by CVD, COPD, and acute exacerbations of COPD may improve the strategies for reduction of MACEs in patients with COPD through vaccination, tight control of traditional CV risk factors and modifying lifestyle. This review summarizes the most recent studies regarding the pathophysiology and epidemiology of modifiable risk factors shared by CVD, COPD, and COPD exacerbations that could influence overall morbidity and mortality due to MACEs in patients with acute exacerbations of COPD.
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Front Cardiovasc Med · Jan 2019
Differences in microRNA-29 and Pro-fibrotic Gene Expression in Mouse and Human Hypertrophic Cardiomyopathy.
Background: Hypertrophic cardiomyopathy (HCM) is characterized by myocyte hypertrophy and fibrosis. Studies in two mouse models (R92W-TnT/R403Q-MyHC) at early HCM stage revealed upregulation of endothelin (ET1) signaling in both mutants, but TGFβ signaling only in TnT mutants. Dysregulation of miR-29 expression has been implicated in cardiac fibrosis. ⋯ Pathway analysis predicted upregulation of the anti-hypertrophic/anti-fibrotic liver X receptor/retinoid X receptor (LXR/RXR) pathway only in human myectomy tissue. Conclusions: Our in vitro studies suggest that activation of ET1 signaling in cardiac myocytes increases reactive oxygen species and stimulates TGFβ secretion, which downregulates miR-29a and increases collagen in fibroblasts, thus contributing to fibrosis. Our gene expression studies in mouse and human HCM reveal allele-specific differences in miR-29 family/profibrotic gene expression in mouse HCM, and activation of anti-hypertrophic/anti-fibrotic genes and pathways in human HCM.