Vol 80, No 5 (2022)
Clinical vignette
Published online: 2022-03-02

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Sacubitril/valsartan improved microvascular endothelial function in a young patient with COVID-19-related mild left ventricular dysfunction

Marcin Hellmann1, Edyta Dąbrowska23, Marta Żarczyńska-Buchowiecka1, Marzena Romanowska-Kocejko1, Krzysztof Narkiewicz24, Marcin Gruchała3, Maria Dudziak1
Pubmed: 35235999
Kardiol Pol 2022;80(5):614-615.

Abstract

Not available

„ Clinical vignette

Sacubitril/valsartan improved microvascular endothelial function in a young patient with COVID-19-related mild left ventricular dysfunction

Marcin Hellmann1Edyta Dąbrowska23Marta Żarczyńska-Buchowiecka1Marzena Romanowska-Kocejko1Krzysztof Narkiewicz24Marcin Gruchała3Maria Dudziak1
1Department of Cardiac Diagnostics, Medical University of Gdansk, Gdańsk, Poland
2Translational Medicine Center, Medical University of Gdansk, Gdańsk, Poland
31stDepartment of Cardiology, Medical University of Gdansk, Gdańsk, Poland
4Department of Hypertension and Diabetology, Medical University, Gdańsk, Poland

Correspondence to:

Prof. Marcin Hellmann, MD, PhD,

Department of Cardiac Diagnostics,

Medical University of Gdańsk,

Smoluchowskiego 17, 80–214 Gdańsk, Poland,

phone: +48 58 349 33 80,

e-mail: marcin.hellmann@gumed.edu.pl

Copyright by the Author(s), 2022

DOI: 10.33963/KP.a2022.0063

Received: December 23, 2021

Accepted: February 10, 2022

Early publication date: March 2, 2022

COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), may induce serious cardiovascular disorders including heart failure, myocarditis, arrhythmias, and severe thromboembolic complications. Indeed, myocardial injury and cardiovascular complications might occur in more than half of patients after COVID-19 and portend a worse prognosis. Accumulating data suggest that SARS-CoV-2 affects endothelial function via inflammation of endothelium, causing microvascular disturbances and microthrombosis. Nowadays, COVID-19 is considered to be a systemic microvascular endothelial disorder with various clinical manifestations [1].

A 34-year-old-woman, with an unremarkable medical history, was referred to our cardiology outpatient clinic due to reduced exercise tolerance, dyspnea, tiredness, and palpitations for about 3 weeks after the diagnosis of SARS-CoV-2 infection. On admission, the levels of D-dimer, B-type natriuretic peptide, and cardiac troponin were within reference ranges. Two-dimensional echocardiography revealed mildly reduced left ventricular ejection fraction (LVEF, 49%) and enlargement of left ventricular (LV) volume. Global longitudinal strain (GLS) was also slightly reduced (–16.9%) (Figure 1A). Electrocardiography revealed ST-segment depression in leads V3-V6 and negative T wave in leads II, III, and aVF, whereas 24-hour electrocardiogram recording showed numerous premature ventricular complexes.

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Figure 1. A. Bull’s eye obtained by speckle tracking echocardiography before sacubitril/valsartan (S/V) therapy. B. Low microvascular perfusion on laser speckle contrast imaging with colors ranging from blue (low perfusion) to red (high perfusion) before S/V therapy. C. Flow-mediated skin fluorescence showing negative ischemic response and significantly reduced hyperemic response. D. Bull’s eye obtained by speckle tracking echocardiography after 3 months of S/V therapy. E. Important recovery of microvascular perfusion on laser speckle contrast imaging with colors ranging from blue (low perfusion) to red (high perfusion) after 3 months of S/V therapy. F. Flow-mediated skin fluorescence showing marked recovery of microvascular oscillations and endothelium-dependent hyperemic response after 3 months of S/V therapy

We subsequently performed microcirculation measurements on the forearm during and following a brachial artery occlusion using both laser speckle contrast imaging (LSCI, PeriCam PSI System, Perimed, Järfälla, Sweden) and flow-mediated skin fluorescence (FMSF, Angionica Ltd, Łódź, Poland) based on monitoring the intensity of a nicotinamide adenine dinucleotide (NADH) fluorescence [2]. LSCI revealed low microvascular perfusion and relatively weak post-occlusive reactive hyperemic response suggesting impairment of the endothelium-dependent vasodilatation potential (Figure 1B). Similarly, using FMSF, we observed very modest oscillations, negative ischemic response, and a significantly reduced hyperemic response also suggesting endothelial dysfunction (Figure 1C).

Based on the multifactorial beneficial role of sacubitril/valsartan (S/V) in the management of heart failure and improvement of endothelial function [3], therapy with this molecule (24 mg/26 mg, twice a day) and additionally bisoprolol (2.5 mg once a day) was started.

After three months of pharmacological therapy and absence of physical activity, a significant symptom reduction was noted. Echocardiography showed improved regional contractility with LVEF 55%, normalized LV volumes, and GLS (–20%) (Figure 1D). Likewise, microvascular parameters improved significantly. We observed better microvascular perfusion in LSCI (Figure 1E) and amelioration in all FMSF parameters (Figure 1F). Especially, the microvascular oscillations and endothelium-dependent hyperemic response showed marked recovery, suggesting a role of endothelial inflammation in the pathogenesis of COVID-19. Indeed, hyperinflammation and hypercoagulation are essential elements that drive the immunothrombotic vicious circle in COVID-19 [4].

Our diagnostic process has led us to the hypothesis of SARS-CoV-2-induced endotheliitis, which provides the rationale for therapies to stabilize and protect the endothelium. Indeed, the S/V molecule has been demonstrated to reduce proliferation and fibrosis, preserve endothelial function and integrity, and mitigate inflammation [5].

The presented case provides new insight into SARS-CoV2- induced cardiac and endothelial dysfunction and points out the possible role of sacubitril/valsartan. Its multifaceted protective influence on the cardiovascular system calls for considering this molecule an additional therapeutic option in COVID-19-related cardiovascular complications.

Article information

Conflict of interest: None declared.

Funding: None.

Open access: This article is available in open access under Creative Common Attribution-Non-Commercial-No Derivatives 4.0 International (CC BY-NC-ND 4.0) license, allowing to download articles and share them with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially. For commercial use, please contact the journal office at kardiologiapolska@ptkardio.pl.

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Polish Heart Journal (Kardiologia Polska)