Patients with COVID-19 Present Impaired Endothelial Glycocalyx, Vascular Dysfunction, and Myocardial Deformation Resembling Those Observed in Patients with Hypertension 4 Months After Infection - European Medical Journal

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Patients with COVID-19 Present Impaired Endothelial Glycocalyx, Vascular Dysfunction, and Myocardial Deformation Resembling Those Observed in Patients with Hypertension 4 Months After Infection

1 Mins
Cardiology
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Authors:
Ignatios Ikonomidis,1 *Aikaterini Kountouri,2 Asimina Mitrakou,3 John Thymis,1 Konstantinos Katogiannis,1 Emmanouil Korakas,2 Charalampos Varlamos,1 Aristotelis Bamias,2 Konstantinos Thomas,4 Ioanna Andeadou,5 Maria Tsoumani,5 Dimitra Kavatha,4 Anastasia Antoniadou,4 Meletios A Dimopoulos,3 Vaia Lambadiari2

1. Laboratory of Preventive Cardiology, Second Cardiology Department Attikon University Hospital, Athens, Greece
2. 2nd Department of Internal Medicine, Attikon University Hospital, National and Kapodistrian University of Athens, Greece
3. Department of Clinical Therapeutics, Alexandra University Hospital, National and Kapodistrian University of Athens, Greece
4. 4th Department of Internal Medicine, Attikon University Hospital, National and Kapodistrian University of Athens, Greece
5. Laboratory of Pharmacology, Faculty of Pharmacy, National & Kapodistrian University of Athens Medical School, Greece
*Correspondence to [email protected]

Disclosure:

The authors have declared no conflicts of interest.

Citation:
EMJ Cardiol. ;9[1]:43-45. Abstract Review No. AR5.
Keywords:
Arterial stiffness, COVID-19, endothelial function, inflammation, oxidative stress, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2).

Each article is made available under the terms of the Creative Commons Attribution-Non Commercial 4.0 License.

BACKGROUND AND AIMS

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection has been associated with deregulations in vascular, endothelial, and myocardial function.1-7 Inflammation and oxidative stress have been suggested as possible pathophysiological mechanisms that lead to these impairments after COVID-19 infection.1-3 The aim of this study was to investigate premature alterations in arterial stiffness, in endothelial integrity, and in coronary and cardiac performance 4 months after COVID-19 infection.

MATERIALS AND METHODS

In this prospective observational case-control study, the authors consecutively recruited 70 patients 4 months after a confirmed infection by SARS-CoV-2, 70 age- and sex-matched patients with untreated hypertension (positive control), and 70 healthy individuals. The authors evaluated:

  • perfused boundary region (PBR) of the sublingual arterial microvessels (increased PBR indicates reduced endothelial glycocalyx thickness);
  • coronary flow reserve (CFR) by Doppler echocardiography;
  • flow-mediated dilation (FMD);
  • pulse wave velocity and central systolic blood pressure;
  • left ventricular global longitudinal strain; and
  • malondialdehyde (MDA), an oxidative stress marker.

RESULTS

Patients diagnosed with COVID-19 and patients with untreated hypertension displayed similar FMD and CFR, while both groups had lower FMD and CFR values than controls. Patients diagnosed with COVID-19 had similar PBR values with patients with untreated hypertension but both groups had greater PBR values compared to control group. Patients diagnosed with COVID-19 and patients with untreated hypertension had higher pulse wave velocity carotid-femoral and central aortic systolic blood pressure values compared with control group. Patients diagnosed with COVID-19 had similar left ventricular global longitudinal strain values with hypertensives but significantly different (less negative) from control group. Patients diagnosed with COVID-19 displayed much higher MDA levels than both patients with untreated hypertension and healthy individuals (Table 1).

Table 1: Markers of cardiac and vascular function.
CFR: coronary flow reserve; FMD: flow mediated dilatation; LVGLS: left ventricular global longitudinal strain; MDA: malondialdehyde; PBR5-25: perfused boundary region of the sublingual vessels with diameter 5-25 μm; PWVc-f: pulse wave velocity carotid to femoral; SBP-central: central (aortic) systolic blood pressure.

CONCLUSION

SARS-CoV-2 infection may cause endothelial and vascular dysfunction, which are linked to impaired longitudinal myocardial deformation 4 months after COVID-19 infection. The 10-fold increase of MDA in patients diagnosed with COVID-19 relative to patients with untreated hypertension and normal control indicate oxidative stress as a possible pathophysiological mechanism contributing to vascular, endothelial, and myocardial deregulations.

References
Okada H et al. Vascular endothelial injury exacerbates coronavirus disease 2019: the role of endothelial glycocalyx protection. Microcirculation. 2021;28(3):e12654. Goshua G et al. Endotheliopathy in COVID-19-associated coagulopathy: evidence from a single-centre, cross-sectional study. Lancet Haematol. 2020;7(8):e575-82. Varga Z et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet. 2020;395(10234):1417-8. Ratchford SM et al. Vascular alterations among young adults with SARS-CoV-2. Am J Physiol Heart Circ Physiol. 2021;320(1):H404-10. Sanjeev K et al. The COSEVAST study: unravelling the role of arterial stiffness in COVID-19 disease severity. medRxiv. 2020; DOI:10.1101/2020.12.18.20248317. Damiani E et al. Microvascular alterations in patients with SARS-COV-2 severe pneumonia. Ann Intensive Care. 2020;10(1):60 Rovas A et al. Microvascular dysfunction in COVID-19: the MYSTIC study. Angiogenesis. 2021;24(1):145-57.

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