The double burden of disease of COVID-19 in cardiovascular patients: overlapping conditions could lead to overlapping treatments

González-Jaramillo, Nathalia; Low, Nicola; Franco, Oscar H.

doi:10.1007/s10654-020-00628-1

Cited by 17 publications

(15 citation statements)

References 16 publications

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“…As indicated earlier there is growing evidence that there exists a confluence of vascular and diffuse alveolar damage with SARS and possibly COVID‐19. Gonzalez‐Jaramillo et al, in a commentary on the double burden of COVID‐19, also implicate the RAS in chronic pulmonary diseases such as pulmonary fibrosis and pulmonary arterial hypertension 34 . Similarly, pulmonary arterial hypertension (PAH) is characterized by reduced ACE2 activity and the production of angiotensin‐1–7 by ACE2 activating MAS receptors improves experimental models of PAH 30 …”

Section: Exploration Of Treating the Host Concept Using Repurposed Agmentioning

confidence: 99%

“…Gonzalez-Jaramillo et al in a commentary on the double burden of COVID-19, also implicates the RAS in chronic pulmonary disease such as pulmonary This article is protected by copyright. All rights reserved.fibrosis and pulmonary arterial hypertension(31). Similarly, PAH is characterized by reduced ACE2 activity and the production of Angiotensin-(1-7) by ACE2 activating Mas receptors activation improves experimental models of PAH(27).As pointed out byCao and Li 2020 (25), SARS-CoV-2 can initially replicate in the upper respiratory track and later in the disease course replicate in the lower respiratory tract generating a secondary viremia with a subsequent attack on organ targets expressing ACE2.…”

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confidence: 99%

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A pharmacological framework for integrating treating the host, drug repurposing and the damage response framework in COVID‐19

Martin

Head

2020

Brit J Clinical Pharma

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With any new disease a framework for the development of preventative or treatment therapeutics is key; the absence of such in COVID‐19 has enabled ineffective and potentially unsafe treatments to be taken up by governments and clinicians desperate to have options for patients. As we still have few therapies and nil vaccines yet available, the void of a clear framework for research and practice is increasingly clear. We describe a framework that has been used to prioritise therapeutic research in previous pandemics which could be used to progress clinical pharmacology and therapeutics research in COVID‐19. This is particularly relevant as discussion has already moved on from antiviral therapeutics to delineating the treatment of the host from treatment and elimination of the infective agent. Focussing on the host brings together three concepts: host treatment, the damage response framework and therapeutic repurposing. The integration of these three areas plays to the traditional strength of pharmaceuticals in providing a period of stabilization to permit time for the development of novel antiviral drugs and vaccines. In integrating approaches to repurposing, host treatment and damage response we identified three key properties that a potentially effective repurposed drug must possess by way of a framework. There must be homology, i.e., the same or similar relation with the pathogenesis of the disease, ideally targeted to the conserved pathophysiological outcomes of the viral attack; there must be a defined locus within the spectrum to prevention to severe disease and the framework must draw upon the historical dose and safety experience of the repurposed drug. To illustrate, we have mapped therapeutics that impact upon a key dysregulated pathway in COVID‐19 – the renin angiotensin system – using this approach. Collectively this type of analysis reveals the importance of existing data (repurposed information and administrative observational data) and the importance of the details of the known pathophysiological response to viruses in approaches to treating the host.

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Section: Exploration Of Treating the Host Concept Using Repurposed Agmentioning

confidence: 99%

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confidence: 99%

A pharmacological framework for integrating treating the host, drug repurposing and the damage response framework in COVID‐19

Martin

Head

2020

Brit J Clinical Pharma

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“…It would be naïve to assume that health problems just disappear upon discharge from acute care or when viral RNA is no longer detectable, and equally naïve to take planned and systematic follow up of patients for granted [ 5 , 6 ]. Yet, the burden of disease resulting from physical and psychological sequelae of Covid-19 in patients surviving the disease as well as potential long-term adverse effects from treatments including steroids such as Dexamethasone are just beginning to catch attention [ 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

Prevalence and risk factors of disability and anxiety in a retrospective cohort of 432 survivors of Coronavirus Disease-2019 (Covid-19) from China

et al. 2020

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Objective To estimate the prevalence of disability and anxiety in Covid-19 survivors at discharge from hospital and analyze relative risk by exposures. Design Multi-center retrospective cohort study. Setting Twenty-eight hospitals located in eight provinces of China. Methods A total of 432 survivors with laboratory-confirmed SARS CoV-2 infection participated in this study. At discharge, we assessed instrumental activities of daily living (IADL) with Lawton’s IADL scale, dependence in activities of daily living (ADL) with the Barthel Index, and anxiety with Zung’s self-reported anxiety scale. Exposures included comorbidity, smoking, setting (Hubei vs. others), disease severity, symptoms, and length of hospital stay. Other risk factors considered were age, gender, and ethnicity (Han vs. Tibetan). Results Prevalence of at least one IADL problem was 36.81% (95% CI: 32.39–41.46). ADL dependence was present in 16.44% (95% CI: 13.23–20.23) and 28.70% (95% CI: 24.63–33.15) were screened positive for clinical anxiety. Adjusted risk ratio (RR) of IADL limitations (RR 2.48, 95% CI: 1.80–3.40), ADL dependence (RR 2.07, 95% CI 1.15–3.76), and probable clinical anxiety (RR 2.53, 95% CI 1.69–3.79) were consistently elevated in survivors with severe Covid-19. Age was an additional independent risk factor for IADL limitations and ADL dependence; and setting (Hubei) for IADL limitations and anxiety. Tibetan ethnicity was a protective factor for anxiety but a risk factor for IADL limitations. Conclusion A significant proportion of Covid-19 survivors had disability and anxiety at discharge from hospital. Health systems need to be prepared for an additional burden resulting from rehabilitation needs of Covid-19 survivors.

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“…23 Experimental animal studies have shown mixed findings with respect to the effects of ACE inhibitors and ARB on ACE2 levels or activity in tissue. [24][25][26][27][28][29][30] Some studies have shown that ARB may increase messenger RNA expression or protein levels of ACE2 in tissue 24,30 while others showed no effect. 27 These ostensibly inconsistent results demonstrate the complex RAAS responses and emphasize the notion that findings from experimental animal studies may not extrapolate to similar physiological responses in humans.…”

Section: Angiotensin-converting Enzymementioning

confidence: 99%

Potential Mechanisms of Cardiac Injury and Common Pathways of Inflammation in Patients With COVID-19

Centurión

Scavenius

García

et al. 2020

Critical Pathways in Cardiology: A Journal of Evidence-Based Medicine

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Due to the lack of prospective, randomized, controlled clinical studies on inflammation and cardiovascular involvement, the exact mechanism of cardiac injury among patients with Coronavirus Disease 2019 (COVID-19) still remains uncertain. It was demonstrated that there is a high and significantly positive linear correlation between troponin T and plasma high-sensitivity C-reactive protein levels, biomarkers of cardiac injury and systemic inflammation, respectively. Cardiac injury and inflammation is a relatively common association among patients hospitalized with COVID-19, and it is related to higher risk of in-hospital mortality. In our literature search, we identified several potential mechanisms of myocardial tissue damage, namely, coronavirus-associated acute myocarditis, angiotensin-converting enzyme 2 receptor binding affinity to the virus Spike protein, increased cytokine secretion, and hypoxia-induced cardiac myocyte apoptosis. Elucidation of the disease pathogenesis and prospective histopathological studies are crucial for future proper treatment in case of renewed outbreaks. Of interest is that with hundred of thousands of bodies available for autopsy studies, no prospective investigation has been reported so far. Strong efforts and continued research of the cardiovascular complications and identification of risk factors for poor prognosis in COVID-19 are steadily needed. The high morbidity and mortality of COVID-19, its monumental economic burden and social impact, the despair of a new pandemic outbreak, and the thread of potential utilization of novel severe acute respiratory syndrome coronavirus 2 as biologic weapons make it a preponderant necessity to better comprehend the therapeutic management of this lethal disease. Emerging as an acute infectious disease, COVID-19 may become a chronic epidemic because of genetic recombination. Therefore, we should be ready for the reemergence of COVID-19 or other coronaviruses.

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The double burden of disease of COVID-19 in cardiovascular patients: overlapping conditions could lead to overlapping treatments

Cited by 17 publications

References 16 publications

A pharmacological framework for integrating treating the host, drug repurposing and the damage response framework in COVID‐19

A pharmacological framework for integrating treating the host, drug repurposing and the damage response framework in COVID‐19

Prevalence and risk factors of disability and anxiety in a retrospective cohort of 432 survivors of Coronavirus Disease-2019 (Covid-19) from China

Potential Mechanisms of Cardiac Injury and Common Pathways of Inflammation in Patients With COVID-19

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