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

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

2 Mins
Cardiology
EMJ Cardiology feature image
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
Disclosure:

The authors have declared no conflicts of interest.

Citation
EMJ Cardiol. ;9[1]:43-45. Abstract Review No. AR5.

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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