Association of <scp>COVID</scp>‐19 with impaired endothelial glycocalyx, vascular function and myocardial deformation 4 months after infection

Lambadiari, Vaia; Mitrakou, Asimina; Kountouri, Aikaterini; Thymis, J; Katogiannis, K; Korakas, Emmanouil; Varlamos, Charalampos; Andreadou, Ioanna; Tsoumani, Maria; Triantafyllidi, Helen; Bamias, Aristotelis; Thomas, Konstantinos; Kazakou, Paraskevi; Grigoropoulou, Sotiria; Kavatha, Dimitra; Antoniadou, Anastasia; Dimopoulos, Meletios A.; Ikonomidis, Ignatios

doi:10.1002/ejhf.2326

Cited by 86 publications

(115 citation statements)

References 38 publications

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“…Particularly with respect to neuroinflammatory processes, a study that appeared recently on a preprint server, including 56 patients with persisting neurological deficits for more than 6 weeks after acute SARS-CoV-2 infection, showed a reduced effector molecule expression in memory T cells, which was significantly associated with the severity of cognitive impairment. 73 In addition, prolonged endothelial dysfunction and vascular inflammation have also been linked to ‘long-COVID’ syndrome, 74 , 75 albeit 18 F-FDG PET studies have not revealed areas of brain hypermetabolism, as would be expected in the case of unabating brain inflammation. 59 , 60 Crucially, ongoing blood–brain barrier dysfunction, as well as a prolonged hypercoagulable state that could precipitate cerebrovascular disease and hypoxic–ischemic neuronal injury, may also be implicated in neurological manifestations of ‘long-COVID’.…”

Section: Pathophysiological Mechanisms Underlying Neurological Manife...mentioning

confidence: 99%

“…Notably, a recent case-control prospective study reported an independent association between SARS-CoV-2 infection, oxidative stress, and endothelial/vascular dysfunction, which was associated with impaired cardiac performance and persistence of COVID-related symptoms 4 months after COVID-19 infection. 75 To date, however, there are no available data in ‘long-COVID’ patients with neurological symptoms in support of these hypotheses.…”

Section: Pathophysiological Mechanisms Underlying Neurological Manife...mentioning

confidence: 99%

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Neurological manifestations of long-COVID syndrome: a narrative review

Stefanou

Palaiodimou

Bakola

et al. 2022

Therapeutic Advances in Chronic Disease

140

128

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Accumulating evidence points toward a very high prevalence of prolonged neurological symptoms among coronavirus disease 2019 (COVID-19) survivors. To date, there are no solidified criteria for ‘long-COVID’ diagnosis. Nevertheless, ‘long-COVID’ is conceptualized as a multi-organ disorder with a wide spectrum of clinical manifestations that may be indicative of underlying pulmonary, cardiovascular, endocrine, hematologic, renal, gastrointestinal, dermatologic, immunological, psychiatric, or neurological disease. Involvement of the central or peripheral nervous system is noted in more than one-third of patients with antecedent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, while an approximately threefold higher incidence of neurological symptoms is recorded in observational studies including patient-reported data. The most frequent neurological manifestations of ‘long-COVID’ encompass fatigue; ‘brain fog’; headache; cognitive impairment; sleep, mood, smell, or taste disorders; myalgias; sensorimotor deficits; and dysautonomia. Although very limited evidence exists to date on the pathophysiological mechanisms implicated in the manifestation of ‘long-COVID’, neuroinflammatory and oxidative stress processes are thought to prevail in propagating neurological ‘long-COVID’ sequelae. In this narrative review, we sought to present a comprehensive overview of our current understanding of clinical features, risk factors, and pathophysiological processes of neurological ‘long-COVID’ sequelae. Moreover, we propose diagnostic and therapeutic algorithms that may aid in the prompt recognition and management of underlying causes of neurological symptoms that persist beyond the resolution of acute COVID-19. Furthermore, as causal treatments for ‘long-COVID’ are currently unavailable, we propose therapeutic approaches for symptom-oriented management of neurological ‘long-COVID’ symptoms. In addition, we emphasize that collaborative research initiatives are urgently needed to expedite the development of preventive and therapeutic strategies for neurological ‘long-COVID’ sequelae.

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Section: Pathophysiological Mechanisms Underlying Neurological Manife...mentioning

confidence: 99%

Section: Pathophysiological Mechanisms Underlying Neurological Manife...mentioning

confidence: 99%

Neurological manifestations of long-COVID syndrome: a narrative review

Stefanou

Palaiodimou

Bakola

et al. 2022

Therapeutic Advances in Chronic Disease

140

128

View full text Add to dashboard Cite

show abstract

“…Recent studies have reported endothelial dysfunction in patients with COVID-19 and convalescent survivors reflected by reduced brachial artery flow-mediated dilation (FMD) in response to hyperemia, which is a non-invasive method to assess systemic vascular endothelial function (11)(12)(13)(14)(15). However, these studies have been limited by their short interval between diagnosis and follow-up ranging from 23 to 120 days.…”

Section: Introductionmentioning

confidence: 99%

Persistent Endothelial Dysfunction in Coronavirus Disease-2019 Survivors Late After Recovery

et al. 2022

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BackgroundCoronavirus disease 2019 (COVID-19) can result in an endothelial dysfunction in acute phase. However, information on the late vascular consequences of COVID-19 is limited.MethodsBrachial artery flow-mediated dilation (FMD) examination were performed, and inflammatory biomarkers were assessed in 86 survivors of COVID-19 for 327 days (IQR 318–337 days) after recovery. Comparisons were made with 28 age-matched and sex-matched healthy controls and 30 risk factor-matched patients.ResultsBrachial artery FMD was significantly lower in the survivors of COVID-19 than in the healthy controls and risk factor-matched controls [median (IQR) 7.7 (5.1–10.7)% for healthy controls, 6.9 (5.5–9.4)% for risk factor-matched controls, and 3.5(2.2–4.6)% for COVID-19, respectively, p < 0.001]. The FMD was lower in 25 patients with elevated tumor necrosis factor (TNF)-α [2.7(1.2–3.9)] than in 61 patients without elevated TNF-α [3.8(2.6–5.3), p = 0.012]. Furthermore, FMD was inversely correlated with serum concentration of TNF-α (r = −0.237, p = 0.007).ConclusionSurvivors of COVID-19 have a reduced brachial artery FMD, which is inversely correlated with increased serum concentration of TNF-α. Prospective studies on the association of endothelial dysfunction with long-term cardiovascular outcomes, especially the early onset of atherosclerosis, are warranted in survivors of COVID-19.

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“…The mechanism for acute and persisting subclinical LV dysfunction is unknown, however MRI findings suggest adverse remodeling after myocarditis that may be detected by strain imaging. Another possible mechanism is endothelial and vascular dysfunction that causes subclinical LV function impairment that persists after acute COVID 19 [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

Subclinical Myocardial Dysfunction in Patients Recovered from COVID-19 Disease: Correlation with Exercise Capacity

Shimoni

Korenfeld

Goland

et al. 2021

Biology

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Aims: Myocardial abnormalities are common during COVID-19 infection and recovery. We examined left (LV) and right (RV) ventricular longitudinal strain in patients who had recovered from COVID-19 and assessed the correlation with exercise capacity. Methods and results: One hundred and eighty-four consecutive patients with history of COVID-19 disease who had been referred to rest or stress echocardiography because of symptoms, mainly dyspnea and chest pain, were included in the study. These patients were compared to 106 patients with similar age, symptoms, and risk factor profile with no history of COVID-19 disease. Clinical and echocardiographic parameters, including strain imaging, were assessed. The patient’s age was 48 ± 12 years. Twenty-two patients had undergone severe disease. There were no differences in the LV ejection fraction and diastolic function between the groups. However, LV and RV global and free wall strain were significantly lower (in absolute numbers) in patients who had recovered form COVID-19 infection (−20.41 ± 2.32 vs −19.39 ± 3.36, p = 0.001, −23.69 ± 3.44 vs −22.09 ± 4.20, p = 0.001 and −27.24 ± 4.7 vs −25.43 ± 4.93, p = 0.021, respectively). Global Longitudinal Strain (GLS) < −20% was present in only 37% of post COVID-19 patients. Sixty-four patients performed exercise echocardiography. Patients with GLS < −20% had higher exercise capacity with higher peak metabolic equivalent and exercise time compared to patients with GLS ≥ −20% (12.6 ± 2 vs 10 ± 2.5 METss and 8:00 ± 2:08 vs 6:24 ± 2:03 min, p < 0.001 and p = 0.003, respectively). Conclusion: In patients, who had recovered from COVID-19 infection, both LV and RV strain are significantly lower compared to control patients. The exercise capacity of these patients correlates with LV strain values. Rest and stress echocardiography in patients with symptoms after COVID-19 infection may identify patients that need further follow up to avoid long term complications of the disease. These preliminary results warrant further research, to test the natural history of these findings and the need and timing of treatment.

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Association of COVID‐19 with impaired endothelial glycocalyx, vascular function and myocardial deformation 4 months after infection

Abstract: SARS-CoV-2 infection may lead to endothelial and vascular dysfunction. We investigated alterations of arterial stiffness, endothelial coronary and myocardial function markers 4 months after COVID-19 infection.

Cited by 86 publications

References 38 publications

Neurological manifestations of long-COVID syndrome: a narrative review

Neurological manifestations of long-COVID syndrome: a narrative review

Persistent Endothelial Dysfunction in Coronavirus Disease-2019 Survivors Late After Recovery

Subclinical Myocardial Dysfunction in Patients Recovered from COVID-19 Disease: Correlation with Exercise Capacity

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