P6506Circulating microparticles preceding endothelial dysfunction and inflammatory process in patients with pseudoexfoliative glaucoma

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
E Oikonomou ◽  
E Bourouki ◽  
M Moschos ◽  
G Siasos ◽  
G Siasou ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Augmentation Index ◽  
Annexin V ◽  
Endothelial Damage ◽  
Pseudoexfoliative Glaucoma ◽  
Control Subjects ◽  
Inflammatory Status ◽  
And Control

Abstract Background Pseudoexfoliative glaucoma (PEX) is a type of glaucoma characterized by the secretion of a grey-white, fibrogranular material in several tissues. Microparticles are shed membrane vesicles released from a variety of cell types in response to cellular activation or apoptosis and correlate with the pathogenesis of cardiovascular diseases. Endothelial MPs may be used as biomarkers of endothelial function. Purpose To evaluated the role of endothelial dysfunction, arterial stiffness and systemic inflammation in patients with PEX compared to patients with Primary open angle glaucoma (POAG) and control subjects as well as the possible pathophysiologic role of a specific microparticle profile associated with endothelial damage. Methods We enrolled 29 subjects with PEX, 57 subjects with POAG and 44 control subjects. Endothelial function was evaluated by flow-mediated dilation (FMD). Pulse wave velocity (PWV) was measured as an index of aortic stiffness and augmentation index (AIx) as a measure of arterial wave reflections. Growth differentiation factor-15 (GDF-15) and intercellular adhesion molecule1 (ICAM1) were measured to evaluate systemic inflammatory status. Total circulating MPs and EMPs were isolated and analysed by flow cytometry, utilizing specific labels for EMPs (CD 144+) and Annexin V staining for phospatidylserine bearing-MPs (AnnexinV + MPs). Results There was a linear impairment in FMD (p=0.005), PWV (p=0.007) and Aix (p=0.02) and a stepwise increase in GDF-15 (p=0.001) and sICAM-1 levels (p=0.08) between the three study groups (control, POAG, PEX). Interestingly, the PEX subjects expressed greater levels of total circulating MPs (Annexin V+) [1698 (1199–5894) MPs/μL vs. 1641 (1470–2705) MPs/μL. vs 493 (417–1512) MPs/μL, p=0.004] and EMPs (CD144+)[1412 (645–1760) MPs/μL3 vs 1380 (498–2496) MPs/μL vs 34 (184–870) MPs/μL, p<0.001] compared to POAG and control subjects. Conclusion Pseudoexfoliative glaucoma is associated with impaired endothelial function, arterial wall properties and vascular inflammation with a parallel increase in EMPs. Our findings indicate the significant role of endothelial damage in the progress of glaucomatous disease especially in subjects with pseudoexfoliative glaucoma.

Abstract 14318: Long Noncoding RNA Differentiation Antagonizing Non-protein Coding RNA 201 Ameliorates Endothelial Dysfunction via Sponging MicroRNA-216a

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
rongxia li ◽  
Shujun Yang ◽  
Yu Chen ◽  
Weili Zhang
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Noncoding Rna ◽  
Protective Factor ◽  
Luciferase Assay ◽  
Protein Coding ◽  
Control Subjects ◽  
Vulnerable Plaques ◽  
And Control

Background: Endothelial dysfunction contributes to the initiation of atherosclerosis, which has been associated with the long noncoding RNAs (lncRNAs). However, the role of lncRNAs in endothelial function remains largely unknown. This study aimed to investigate whether the differentiation antagonizing non-protein coding RNA 201 (DANCR201) regulated the endothelial function. Methods and Results: The whole transcriptome sequencing was conducted to identify differentially expressed lncRNAs in the peripheral blood from patients with coronary artery diseases who had coronary calcified plaques (n=10), vulnerable plaques (n=5), and control subjects without coronary plaques (n=10). The characteristics of plaques were determined by the coronary computed tomography angiography. The results showed that DANCR201 was significantly downregulated in patients with vulnerable plaques compared to those with calcified plaques and control subjects. The RNA fluorescence in situ hybridization showed that DANCR201 was localized in both cytoplasm and nuclei. Next, we assessed the role of DANCR201 in endothelial function. In the replicative aging model of human umbilical vein endothelial cells (HUVECs), DANCR201 was found to decrease in senescent passage 20 cells compared with young passage 3 cells. Furthermore, DANCR201 overexpression in HUVECs significantly repressed monocytes adhesion to endothelium, inhibited the expression of pro-inflammatory cytokines interleukin 1β, intercellular cell adhesion molecule 1, tumor necrosis factor α, and promoted the abilities of endothelial proliferation and migration, indicating that DANCR201 was a protective factor for endothelial function. Bioinformatics analysis of miRNA-lncRNA interactions indicated that DANCR201 contained a candidate binding sequence of miR-216a which had been reported to promote the endothelial dysfunction through NF-κB pathway. The luciferase assay further showed that DANCR201 specifically combined with miR-216a. Conclusions: Our data indicated that DANCR201 can improve endothelial function via sponging miR-216a, ultimately maintaining vascular normalization. DANCR201 maybe a potential therapeutic target for atherosclerotic plaque progression and instability.

Abstract 12770: The Significant Role of Endothelium and Arterial Wall Properties in Patients With Pseudoexfoliative Glaucoma

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Georgia Siasou ◽  
Gerasimos Siasos ◽  
Marilita M Moschos ◽  
Nikolaos Gouliopoulos ◽  
Evangelos Oikonomou ◽  
...  
Keyword(s):  
Arterial Stiffness ◽  
Endothelial Function ◽  
Significant Role ◽  
Vascular Function ◽  
Arterial Wall ◽  
Augmentation Index ◽  
Open Angle Glaucoma ◽  
Anterior Segment ◽  
Pseudoexfoliative Glaucoma

Introduction: Primary open-angle glaucoma (POAG) is one of the most prevalent causes of irreversible blindness and is associated with endothelial dysfunction and arterial stiffness. Pseudoexfoliative glaucoma (PEG) is another type of glaucoma observed in pseudoexfoliation syndrome. It is characterized by the deposition of pseudoexfoliative material not only to the anterior segment of the eye, but also to the vessels, heart and other organs. Hypothesis: Endothelial function and arterial stiffness are impaired in patients with POAG and PEG supporting the significant role of vascular function impairment in the progression of the disease. Methods: Forty four POAG patients, 22 PEG and 38 healthy subjects (Cl) were included in this study. All subjects were free of cardiovascular or inflammatory diseases. Endothelial function was evaluated by flow-mediated dilatation (FMD). Carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness and augmentation index (AIx) as a measure of arterial wave reflections Results: Between the three study groups CL, POAG, PEG there was no difference in age (67±10years vs. 70±9years vs. 66±12yeras, p=0.12) or prevalence of male sex (70% vs. 57% vs. 50%, p=0.21). Importantly, there was a linear impairment of FMD (7.35±2.77% vs. 6.58±3.18% vs. 4.88±3.29%, p=0.006), PWV (7.98±1.56m/sec vs. 9.20±1.84m/sec vs. 9.22±2.16m/sec, p=0.004) and AIx (21.29±8.77% vs. 25.14±5.71% vs. 28.20±8.75%, p=0.002) from CL to POAG and PEG. Interestingly post hoc test after Scheffe correction revealed also that PEG subjects had not only significantly impaired FMD, compared to control subjects, but also compared to POAG subjects (4.88±3.29% vs. 6.58±3.18%, p=0.02). Conclusions: Endothelial function and arterial stiffness are significantly impaired in patients with pseudoexfoliative glaucoma. These findings shed some light in the pathophysiology of pseudoexfoliative glaucoma and support the theory that pseudoexfoliative fibrils may also accumulate and damage the arterial wall.

Temperature, Mitochondria, and Reye's Syndrome

PEDIATRICS ◽  
1983 ◽  
Vol 71 (6) ◽  
pp. 985-986
Author(s):  
R. DON BROWN ◽  
JOHN T. WILSON
Keyword(s):  
Mitochondrial Damage ◽  
Reye's Syndrome ◽  
Enhancing Effect ◽  
Control Subjects ◽  
Epidemiologic Data ◽  
Higher Temperature ◽  
And Control

In Reply.— El-Mallakh raises hypothetical questions about an enhancing effect of fever on mitochondrial damage associated with Reye's syndrome. Our article on aspirin and Reye's syndrome1 emphasized the role of prodromal illness in use of aspirin. Fever was only one of several [See table in the PDF] prodormal illness events that were different in patients as compared with control subjects. Results of our analysis of the epidemiologic data from the Ohio study reveal a statistically significant higher temperature in those children which Reye's syndrome as compared with unmatched control subjects (Table) as well as in patients and control subjects matched for record temperatures.1

Diabetes-induced endothelial dysfunction in streptozotocin-treated rats: role of prostaglandin endoperoxides and free radicals.

1993 ◽  
Vol 4 (6) ◽  
pp. 1327-1336
Author(s):  
F X Dai ◽  
A Diederich ◽  
J Skopec ◽  
D Diederich
Keyword(s):  
Free Radicals ◽  
Endothelial Dysfunction ◽  
Diabetic Rats ◽  
Renal Arteries ◽  
Radical Scavenger ◽  
Wistar Kyoto ◽  
And Control ◽  
A2 Receptors

The vasoactive responses of renal arteries from diabetic and control rats were compared in vitro in arteriograph assemblies. Diabetes was established by an iv injection of streptozotocin (55 mg/kg) in Wistar-Kyoto rats. Endothelium-dependent relaxations mediated by nitric oxide (EDNO) were impaired in arteries from the diabetic rats; the impairment in endothelial function increased with duration of the diabetic state. After 6 and 16 wk, the concentrations of acetylcholine required to produce 50% relaxation of norepinephrine preconstriction were 3.2 and 25 microM for arteries from diabetic rats and 0.4 microM in control arteries, representing 8- and 62-fold decreases in sensitivity to the endothelium-dependent vasodilator in the diabetic arteries. After 6 wk of diabetes, renal arteries also became 20-fold less sensitive to relaxation induced by histamine, another agonist that induces EDNO-mediated relaxations. The inhibition of EDNO production with L-NG-nitroarginine produced greater impairments in acetylcholine relaxations in arteries from diabetic rats than from control rats. Relaxations in response to acetylcholine were impaired in arteries from diabetic rats because of increased production of factors that opposed the vasorelaxant effects of EDNO, rather than from decreased production of EDNO. Pretreatment of the diabetic arteries with the hydroxyl radical scavenger dimethylthiourea normalized relaxations in response to acetylcholine. The blockade of prostaglandin H2-thromboxane A2 receptors with SQ 29548 also improved relaxations in response to acetylcholine in diabetic arteries. These data indicate that endothelial dysfunction in the renal arteries of diabetic rats may be mediated by the increased production of free radicals and of prostaglandin endoperoxides, which oppose the vasorelaxant effects of EDNO.

Abstract 4688: The Impact of Marfan Syndrome on Arterial Stiffness and Endothelial Function: The Role of Matrix Metalloproteinases

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Stella Brilli ◽  
Dimitris Tousoulis ◽  
Charalambos Antoniades ◽  
George Hatzis ◽  
Nikos Ioakeimidis ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Arterial Stiffness ◽  
Endothelial Function ◽  
Marfan Syndrome ◽  
Augmentation Index ◽  
Flow Mediated Dilation ◽  
Arterial Tree ◽  
Augmentation Pressure ◽  
The Impact

Background: Marfan syndrome is characterised by high risk of aortic dissections and increased cardiovascular risk. However, the impact of Marfan syndrome on endothelial function and arterial stiffness is unclear, while the role of matrix metalloproteinases is unknown. We examined the impact of Marfan syndrome on the elastic properties of the arterial tree, and vascular endothelial function, and we evaluated the potential role of matrix metalloproteinases in these effects. Methods: The study population consisted of 17 subjects with Marfan syndrome, aged 26.6±2.3 years old, with BMI 20.5±1.03Kg/m2 and 22 healthy individuals matched for gender, age (26.4±0.78 years old, p=NS) and BMI (22.4±0.86 Kg/m2). Arterial stiffness was evaluated by measuring carotid-femoral pulse wave velocity (PWV), while augmentation pressure and augmentation index (AIx) were also determined, as measures of arterial wave reflections. Endothelial function was evaluated by determining flow mediated dilation (FMD) in the brachial artery while matrix metalloproteinase 9 (MMP-9) levels were determined by ELISA. Results: Patients with Marfan syndrome had significantly lower pulse pressure in the radial artery (41.0±1.07mmHg) compared to controls (51.3±4.4mmHg). In addition, patients had higher AIx (17.6±2.4%) and augmentation pressure (5.44±0.65mmHg) compared to controls (7.72±3.43% and 2.41±1.14mmHg respectively, p<0.05 for both). However, the difference in PWV between patients and controls did not reach statistical significance (6.33±0.33 vs 5.96±0.23m/s respectively, p=NS). Patients with Marfan syndrome had lower FMD (2.05±1.13%) and higher plasma MMP-9 (827±70ng/ml) compared to controls (6.8±2.3% p<0.05 and 326±50ng/ml, p<0.01). Conclusions: Marfan syndrome is associated with increased MMP-9 levels, as well as with elevated augmentation index and augmentation pressure compared to healthy individuals, matched for age, gender and body mass index. Moreover, flow-mediated dilation is also impaired in these subjects. These findings suggest that Marfan syndrome directly affects the elastic properties and endothelial function of the arterial tree, with matrix metalloproteinases being important mediators in the pathophysiology of this syndrome.

The role of 5-HT7 receptors on isoproterenol-induced myocardial infarction in rats with high-fat diet exacerbated coronary endothelial dysfunction

2020 ◽  
Vol 39 (8) ◽  
pp. 1005-1018 ◽  
Author(s):  
I Cinar ◽  
Z Halici ◽  
B Dincer ◽  
B Sirin ◽  
E Cadirci
Keyword(s):  
Myocardial Infarction ◽  
Endothelial Dysfunction ◽  
High Fat Diet ◽  
Density Lipoprotein ◽  
Heart Tissue ◽  
High Fat ◽  
Inflammatory Status

The presence of 5-HT7r’s in both human and rat cardiovascular and immune tissues and their contribution to inflammatory conditions prompted us to hypothesize that these receptors contribute in acute myocardial infarction (MI) with underlying chronic endothelial dysfunction. We investigated the role of 5-HT7 receptors on heart tissue that damaged by isoproterenol (ISO)-induced MI in rats with high-fat diet (HFD). In vitro and in vivo effects of 5-HT7r agonist (LP44) and antagonist (SB269970) have been investigated on the H9C2 cell line and rats, respectively. For in vivo analyses, rats were fed with HFD for 8 weeks and after this period ISO-induced MI model has been applied to rat. To investigate the role of 5-HT7r’s, two different doses of LP44 and SB269970 were evaluated and compared with standard hypolipidemic agent, atorvastatin. In vitro studies showed that LP44 has protective and proliferative effects on rat cardiomyocytes. Also in in vivo studies stimulating 5-HT7r’s by LP44 improved blood lipid profile (decreased total cholesterol, low-density lipoprotein-C, and triglyceride, increased high-density lipoprotein), decreased cardiac damage markers (creatine kinase and troponin-I), and corrected inflammatory status (tumor necrosis factor-α, interleukin-6). Our results showed significant improvement in LP44 administered rats in terms of histopathologic analyses. In damaged tissues, 5-HT7 mRNA expression increased and agonist administration decreased this elevation significantly. We determined for the first time that 5-HT7r’s are overexpressed in ISO-induced MI of rats with underlying HFD-induced endothelial dysfunction. Restoration of this overexpression by LP44, a 5-HT7r agonist, ameliorated heart tissue in physiopathologic, enzymatic, and molecular level, showing the cardiac role of these receptors and suggesting them as future potential therapeutic targets.

DECREASED PROSTACYCLIN-LIKE ACTIVITY IN HENOCH-SCHONBEIN PURPURA

1987 ◽  
Author(s):  
J J F Belch ◽  
S Turi ◽  
M MacLaren ◽  
T J Beattie ◽  
C D Forbes
Keyword(s):  
Platelet Rich Plasma ◽  
Skin Lesions ◽  
Endothelial Damage ◽  
Common Type ◽  
Intestinal Involvement ◽  
Childhood Vasculitis ◽  
The Difference ◽  
Umbilical Arteries ◽  
And Control

Henoch-Schoniein purpura (HSP) is the most common type of childhood vasculitis. The skin lesions are the most obvious sign but visceral involvement carries a more serious prognosis. Increasing amounts of data are available regarding the possible role of prostacyclin (PGI2) in the pathogenesis of other vasculo-pathies, but no-one has previously investigated HSP. 17 HSP patients (mean age (SD) 5.7 (2.5) years) and 17 matched controls were studied. The ability of plasma (patient and control) to support PGI2 -like activity was tested. Human umbilical arteries were chopped into rings and incubated in buffer at 37° C. Aliquots of the supernatant were added to platelet rich plasma (PRP) and platelet aggregation measured (Malin's aggregometer). Repeated washings of the rings then depleted PGI. production. The rings were then incubated with test platelet poor plasma (PPP) at 37° C. PGI2 like activity was assessed as before and the results expressed as a percentage of the aggregation obtained by the same exhausted ring before addition of PPP. The results show that the ability of test PPP to support PGI2 like activity was reduced in 13/17 HSP patients. The difference between patients (21.3 (SD 20.5%) and controls (57.2 (SD 12.2%) was significant (p<0.001). Patients with renal and gastro-intestinal involvement (7.5 (SD 18.1%) were significantly different from those patients with only skin involvement (32.3 (SD 23.5%) (p<0.01). Plasma from six patients in which PGI^like activity was undetectable using the above method were further studied to detect PGI2 -inhibitory activity. Unexhausted umbilical rings were incubated at 37°C for 5mins. The baseline PGI2 like activity of the supernatant was compared with that produced after 5mins. incubation with test PPP (o patients, 6 controls). Less like activity was produced by the unexhausted rings when incubated with PPP from the HSP patients than with either control buffer or control PPP (both p<0.01). It seems likely that these abnormalities, having been demonstrated in yet another vasculitic syndrome, are secondary to endothelial damage. The disturbances, however, may well be of importance in extending the primary microvascular insult

The Role of Steroids in Endothelial Function in the Ageing Male

2010 ◽  
Vol 7 (2) ◽  
pp. 115
Author(s):  
Antonio Aversa ◽  
Roberto Bruzziches ◽  
Davide Francomano ◽  
Emanuela A Greco ◽  
Silvia Migliaccio ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Major Adverse Cardiovascular Events ◽  
Ageing Male ◽  
Vascular Beds ◽  
Endothelial Integrity ◽  
Considerable Body ◽  
Mineralocorticoid Activity ◽  
Male Ageing

Normal vascular endothelium is essential for the synthesis and release of substances affecting vascular tone, cell adhesion and the homoeostasis of clotting and fibrinolysis. The degeneration of endothelial integrity promotes adverse events leading to atherogenesis. Circulating levels of endogenous hormones decline during ageing and this may contribute to the occurrence of major adverse cardiovascular events, independently of gender differences. During the last decade more attention has been drawn to the importance of testosterone, oestradiol and adrenal androgens in the pathophysiology, prevention and treatment of male ageing-associated diseases. A considerable body of literature is available indicating that steroid hormones, particularly the sex steroids, are known to modulate endothelial function in all vascular beds and their deficiency may promote endothelial dysfunction. Testosterone decrease and increased mineralocorticoid activity in the ageing male are frequent and may yield endothelial dysfunction and increased cardiovascular burden; we recommend careful hormonal investigations in men who present comorbidities such as diabetes, hypertension and dyslipidaemia.

scholarly journals Lipoprotein(a) in the Nephrotic Syndrome

2000 ◽  
Vol 11 (3) ◽  
pp. 507-513
Author(s):  
CHANTAL DOUCET ◽  
VINCENT MOOSER ◽  
SOPHIE GONBERT ◽  
FRANÇOISE RAYMOND ◽  
JOHN CHAPMAN ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Plasma Concentrations ◽  
Lipoprotein A ◽  
Control Subjects ◽  
Large N ◽  
Catabolic Rate ◽  
Atherogenic Particle ◽  
Normal Urine ◽  
And Control

Abstract. Plasma levels of lipoprotein(a) (Lp(a)), an atherogenic particle, are elevated in kidney disease, which suggests a role of this organ in the metabolism of Lp(a). Additional evidence for a role of the kidney in the clearance of Lp(a) is provided by the fact that circulating N-terminal fragments of apolipoprotein(a) (apo(a)) are processed and eliminated by the renal route. To further understand the mechanism underlying such renal excretion, the levels of apo(a) fragments in plasma and urine relative to plasma Lp(a) levels were determined in patients with nephrotic syndrome (n = 15). In plasma, the absolute (24.7 ± 20.4 versus 2.16 ± 2.99 μg/ml, P < 0.0001) as well as the relative amounts of apo(a) fragments (4.6 ± 3.4% versus 2.1 ± 3.3% of total Lp(a), P < 0.0001) were significantly elevated in nephrotic patients compared with a control, normolipidemic population. In addition, urinary apo(a) excretion in patients with nephrotic syndrome was markedly elevated compared with that in control subjects (578 ± 622 versus 27.7 ± 44 ng/ml per mg creatinine, P < 0.001). However, the fractional catabolic rates of apo(a) fragments were similar in both groups (0.68 ± 0.67% and 0.62 ± 0.47% in nephrotic and control subjects, respectively), suggesting that increased plasma concentrations of apo(a) fragments in nephrotic subjects are more dependent on the rate of synthesis rather than on the catabolic rate. Molecular analysis of apo(a) immunoreactive material in urine revealed that the patterns of apo(a) fragments in nephrotic patients were distinct from those of control subjects. Full-length apo(a), large N-terminal apo(a) fragments similar in size to those present in plasma, as well as C-terminal fragments of apo(a) were detected in urine from nephrotic patients but not in urine from controls. All of these apo(a) forms were in addition to smaller N-terminal apo(a) fragments present in normal urine. This study also demonstrated the presence of Lp(a) in urine from nephrotic patients by ultracentrifugal fractionation. These data suggest that in nephrotic syndrome, Lp(a) and large fragments of apo(a) are passively filtered by the kidney through the glomerulus, whereas smaller apo(a) fragments are secreted into the urine.

scholarly journals Mid-term endothelial dysfunction post COVID-19

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
S Lampsas ◽  
E Oikonomou ◽  
G Siasos ◽  
N Souvaliotis ◽  
A Goliopoulou ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Hospital Discharge ◽  
Cardiovascular Complications ◽  
Endothelial Damage ◽  
Control Group ◽  
Post Discharge ◽  
Reference Limit ◽  
Coronary Syndrome ◽  
Control Subjects ◽  
History Of

Abstract Introduction Cardiovascular complications of Coronavirus disease (COVID-19), resulting from the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), have been documented. Endothelium-induced “cytokine storm” in critically ill COVID-19 patients is one of the leading causes of morbidity and mortality. Vascular endothelial damage caused by COVID-19 emphasizes the crucial role of endothelium in COVID-19 clinical impact. Purpose To examine the mid-term (1-month) impact of COVID-19 in endothelial function. Methods In this case control study, 20 consecutive patients who were hospitalized for COVID-19 either on Intensive Care Unit (ICU) or non-ICU were examined one month following hospital discharge. In the control group we recruited 12 consecutive subjects from the outpatient cardiology clinic. Demographic and clinical data were collected, and endothelial function was evaluated by brachial artery flow-mediated dilation (FMD). Results There was no difference in age between COVID-19 patients and control subjects (66±12 years vs. 71±5 years, p&lt;0.17), in male sex (63% vs. 54%, p=0.66) in history of diabetes mellitus (27% vs. 36%, p=0.64), hypertension (36% vs. 54%, p=0.39), cardiovascular disease (27% vs.18%, p=0.61). From the COVID-19 subjects 65% were overweight or obese. During their hospitalization [3 ICU (15%)/17 non-ICU (85%), mean days: 17±6.7], 4 (20%) of COVID-19 patients developed ARDS, while single cases of stress-induced cardiomyopathy, pulmonary embolism, and acute coronary syndrome were detected. One month post discharge D-dimers (0.71±0.55 μg/ml) levels were above upper reference limit. Importantly, FMD one month after hospital discharge date, was significantly impaired in the COVID-19 group (3.59±1.63% vs. 9.31±2.98%, p&lt;0.001) compared to control group. Conclusion Post COVID-19 subjects one month post discharge have significant impaired endothelial function compared to control subjects. These findings highlight the significant interaction of COVID-19 with arterial endothelium and merit further research to conclude on the exact impact of vascular endothelium in physical history of SARS-CoV-2 infection. FUNDunding Acknowledgement Type of funding sources: None.

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