Evidence map›Paper›PMID 32871306›Full record

ReviewThrombosis research2020

COVID-19 and cardiovascular consequences: Is the endothelial dysfunction the hardest challenge?

Serena Del Turco, Annamaria Vianello, Rosetta Ragusa, Chiara Caselli, Giuseppina Basta

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Thrombosis research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07544186 (Effect of a Non-pharmacological Intervention), which is not on this map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.3field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT07544186 nacompletednot on this map

Effect of a Non-pharmacological Intervention (Nutritional Therapy and Pulmonary Rehabilitation) on Endothelial Function, Body Composition, and Physical Functionality in Recovered COVID-19 Patients.

TypeinterventionalSponsorInstituto Nacional de Enfermedades RespiratoriasRan2020 to 2023Enrolled43ConditionsSupplemental Nutrition Assistance Program Education, Post COVID Syndrome, Endothelial FunctionArmsL-citrulline supplementation
3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 103 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Serena Del TurcoInstitute of Clinical Physiology, CNR, San Cataldo Research Area, Via Moruzzi, 1, 56124 Pisa, Italy. Electronic address: serena@ifc.cnr.it.
Annamaria VianelloDepartment of Information Engineering, Telemedicine Section, University of Pisa, Italy.
Rosetta RagusaInstitute of Clinical Physiology, CNR, San Cataldo Research Area, Via Moruzzi, 1, 56124 Pisa, Italy.
Chiara CaselliInstitute of Clinical Physiology, CNR, San Cataldo Research Area, Via Moruzzi, 1, 56124 Pisa, Italy.
Giuseppina BastaInstitute of Clinical Physiology, CNR, San Cataldo Research Area, Via Moruzzi, 1, 56124 Pisa, Italy. Electronic address: lapina@ifc.cnr.it.
Istituto di Fisiologia Clinica · ITUniversity of Pisa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) has become a pandemic disease named Coronavirus Disease-19 (COVID-19) of epochal dimension. The clinical spectrum of COVID-19 is wide, ranging from asymptomatic forms to severe pneumonia, sepsis and multiple organ dysfunction syndromes resulting in poor outcomes. Among the various consequences of severe COVID-19, cardiovascular (CV) collapse appears the most serious and potentially lethal. On the other hand, pre-existent CV comorbidities are also associated with higher mortality. The most reliable hypothetical pathogenetic mechanism for CV complications and cardiac injury in severe COVID-19 patients appears to be a sustained endothelial dysfunction, caused by the interplay of inflammation and coagulation. In this review, we survey papers addressing issues related to severe COVID-19, characterized by enhanced lung microvascular loss, hypercytokinemia, hypoxemia and thrombosis. We discuss about how the virus-induced downregulation of the angiotensin converting enzyme-2 (ACE2) receptor, used to enter the host cell, could affect the renin-angiotensin system, attempting to clarify the doubts about the use of ACE inhibitors and Angiotensin-II receptor blockers in COVID-19 patients. Finally, we point out how the delicate and physiological homeostatic function of the endothelium, which turns into a disastrous battlefield of the complex interaction between "cytokine and coagulative storms", can be irreparably compromised and result in systemic inflammatory complications.

Indexed as

SARS-CoV-2Angiotensin-Converting Enzyme 2Angiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsCardiovascular DiseasesCOVID-19Endothelium, VascularHumansVirus InternalizationACE2 protein, humanAngiotensin-Converting Enzyme 2Angiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsCardiac injuryCOVID-19Endothelial dysfunctionInflammationThrombosis

Identifiers

PMID32871306
PMCPMC7451195
OpenAlexW3080607122

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.