This article is a Preprint
Preprints are preliminary research reports that have not been certified by peer review. They should not be relied on to guide clinical practice or health-related behavior and should not be reported in news media as established information.
Preprints posted online allow authors to receive rapid feedback and the entire scientific community can appraise the work for themselves and respond appropriately. Those comments are posted alongside the preprints for anyone to read them and serve as a post publication assessment.
SARS-CoV-2 infection leads to cardiac pericyte loss, fibrosis, cardiomyocyte hypertrophy, and diastolic dysfunction (preprint)
researchsquare; 2020.
Preprint
in English
| PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-105963.v1
ABSTRACT
Recovered COVID19 patients often display cardiac dysfunction, even after a relatively mild infection. Here, we present the first histological description of cardiac SARS-CoV-2 infection. Within the heart, the ACE2 receptor is mostly expressed by pericytes. Using a COVID19 hamster model, we demonstrate SARS-CoV-2 is replicating in pericytes, and reduced pericyte density is present after infection. In healthy animals, pericytes recover; however, when metabolic comorbidities are present, they fail to recover. These latter animals present with cardiac fibrosis, cardiomyocyte hypertrophy, and early signs of diastolic dysfunction, resembling HFpEF. Biopsies from recovered COVID19 patients showed similar results, with pericyte loss being present.
Full text:
Available
Collection:
Preprints
Database:
PREPRINT-RESEARCHSQUARE
Main subject:
Fibrosis
/
Severe Acute Respiratory Syndrome
/
Heart Failure, Diastolic
/
COVID-19
/
Heart Diseases
/
Hypertrophy
Language:
English
Year:
2020
Document Type:
Preprint
Similar
MEDLINE
...
LILACS
LIS