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1.
Am J Respir Crit Care Med ; 203(3): 390-391, 2021 02 01.
Article in English | MEDLINE | ID: covidwho-1383573
2.
Arq Bras Cardiol ; 119(2): 319-325, 2022 08.
Article in English, Portuguese | MEDLINE | ID: covidwho-1893709

ABSTRACT

BACKGROUND: Inflammation is known to play a crucial role in many diseases, including COVID-19. OBJECTIVE: Using flow-mediated dilatation (FMD), we aimed to assess the effects of inflammation on endothelial function in COVID-19 patients. METHODS: This study was conducted with a total of 161 subjects, of whom 80 were diagnosed with COVID-19 within the last six months (comprising 48 women and 32 men with a mean age of 32.10 ± 5.87 years) and 81 were healthy controls (comprising 45 women and 36 men with a mean age of 30.51 ± 7.33 years). We analyzed the findings of transthoracic echocardiography and FMD in all subjects. All results were considered statistically significant at the level of p < 0.05. RESULTS: The echocardiography and FMD of the COVID-19 group were performed 35 days (range: 25-178) after diagnosis. There was no statistically significant difference in echocardiographic parameters. Differently, FMD (%) was significantly higher in the control group (9.52 ± 5.98 vs. 12.01 ± 6.18, p=0.01). In multivariate analysis with the forward stepwise model, FMD was significantly different in the control group compared to the COVID-19 group (1.086 (1.026 - 1.149), p=0.04). A Spearman's correlation test indicated that FMD (r=0.27, p=0.006) had a weak positive correlation with the presence of COVID-19. CONCLUSION: Our findings point to COVID-19-induced endothelial dysfunction, as assessed by FMD, in the early recovery phase.


FUNDAMENTO: Sabe-se que a inflamação desempenha um papel crucial em muitas doenças, incluindo a COVID-19. OBJETIVO: Utilizando a dilatação fluxo-mediada (DFM), objetivou-se avaliar os efeitos da inflamação na função endotelial de pacientes com COVID-19. MÉTODOS: Este estudo foi realizado com um total de 161 indivíduos, dos quais 80 foram diagnosticados com COVID-19 nos últimos seis meses (48 mulheres e 32 homens com idade média de 32,10±5,87 anos) e 81 eram controles saudáveis (45 mulheres e 36 homens com idade média de 30,51±7,33 anos). Os achados do ecocardiograma transtorácico e da DFM foram analisados em todos os indivíduos. Resultados com p<0,05 foram considerados estatisticamente significantes. RESULTADOS: O ecocardiograma e a DFM do grupo COVID-19 foram realizados 35 dias (intervalo: 25­178) após o diagnóstico. Não houve diferença estatisticamente significativa nos parâmetros ecocardiográficos. Em contraste, a DFM (%) foi significativamente maior no grupo controle (9,52±5,98 versus 12,01±6,18; p=0,01). Na análise multivariada com o modelo stepwise progressivo, a DFM foi significativamente diferente no grupo controle em relação ao grupo COVID-19 (1,086 (1,026­1,149), p=0,04). O teste de correlação de Spearman indicou que a DFM (r=0,27; p=0,006) apresentou correlação positiva fraca com a presença de COVID-19. CONCLUSÃO: Os achados deste estudo apontam para disfunção endotelial induzida por COVID-19, avaliada por DFM, na fase inicial de recuperação.


Subject(s)
COVID-19 , Vascular Diseases , Adult , Brachial Artery/diagnostic imaging , Dilatation , Dilatation, Pathologic/diagnostic imaging , Endothelium, Vascular , Female , Humans , Inflammation , Male , Vasodilation , Young Adult
3.
Am J Physiol Heart Circ Physiol ; 322(6): H906-H913, 2022 06 01.
Article in English | MEDLINE | ID: covidwho-1765169

ABSTRACT

Studies have suggested a potential role of endothelial dysfunction and atherosclerosis in the pathophysiology of COVID-19. Herein, we tested whether brachial flow-mediated dilation (FMD) and carotid intima-media thickness (cIMT) measured upon hospital admission are associated with acute in-hospital outcomes in patients hospitalized with COVID-19. A total of 211 patients hospitalized with COVID-19 were submitted to assessments of FMD and mean and maximum cIMT (cIMTmean and cIMTmax) within the first 72 h of hospital admission. Study primary outcome was a composite of intensive care unit admission, mechanical ventilation, or death during the hospitalization. These outcomes were also considered independently. Thrombotic events were included as a secondary outcome. Odds ratios (ORs) and confidence intervals (CIs) were calculated using unadjusted and adjusted multivariable logistic regression models. Eighty-eight (42%) participants demonstrated at least one of the composite outcomes. cIMTmean and cIMTmax were predictors of mortality and thrombotic events in the univariate analysis (cIMTmean and mortality: unadjusted OR 12.71 [95% CI 1.71-94.48]; P = 0.014; cIMTmean and thrombotic events: unadjusted OR 11.94 [95% CI 1.64-86.79]; P = 0.015; cIMTmax and mortality: unadjusted OR 8.47 [95% CI 1.41-51.05]; P = 0.021; cIMTmax and thrombotic events: unadjusted OR 12.19 [95% CI 2.03-73.09]; P = 0.007). However, these associations were no longer present after adjustment for potential confounders (P > 0.05). In addition, FMD% was not associated with any outcome. In conclusion, cIMT and FMD are not independent predictors of clinical outcomes in patients hospitalized with COVID-19. These results suggest that subclinical atherosclerosis and endothelial dysfunction may not be the main drivers of COVID-19 complications in patients hospitalized with COVID-19.NEW & NOTEWORTHY Studies have suggested a role of endothelial dysfunction and atherosclerosis in COVID-19 pathophysiology. In this prospective cohort study, we assessed the prognostic value of carotid intima-media thickness (IMT) and flow-mediated dilation (FMD) in patients with COVID-19. Carotid IMT and FMD were not independent predictors of major outcomes. These results suggest that other risk factors may be the main drivers of clinical outcomes in patients with COVID-19.


Subject(s)
Atherosclerosis , COVID-19 , Brachial Artery , Carotid Arteries/diagnostic imaging , Carotid Intima-Media Thickness , Dilatation , Endothelium, Vascular , Hospitalization , Hospitals , Humans , Prospective Studies , Risk Factors , Ultrasonography , Vasodilation/physiology
4.
Vascul Pharmacol ; 144: 106975, 2022 06.
Article in English | MEDLINE | ID: covidwho-1730153

ABSTRACT

BACKGROUND: Coronavirus disease-19 (COVID-19) is implicated by active endotheliitis, and cardiovascular morbidity. The long-COVID-19 syndrome implications in atherosclerosis have not been elucidated yet. We assessed the immediate, intermediate, and long-term effects of COVID-19 on endothelial function. METHODS: In this prospective cohort study, patients hospitalized for COVID-19 at the medical ward or Intensive Care Unit (ICU) were enrolled and followed up to 6 months post-hospital discharge. Medical history and laboratory examinations were performed while the endothelial function was assessed by brachial artery flow-mediated dilation (FMD). Comparison with propensity score-matched cohort (control group) was performed at the acute (upon hospital admission) and follow-up (1 and 6 months) stages. RESULTS: Seventy-three patients diagnosed with COVID-19 (37% admitted in ICU) were recruited. FMD was significantly (p < 0.001) impaired in the COVID-19 group (1.65 ± 2.31%) compared to the control (6.51 ± 2.91%). ICU-treated subjects presented significantly impaired (p = 0.001) FMD (0.48 ± 1.01%) compared to those treated in the medical ward (2.33 ± 2.57%). During hospitalization, FMD was inversely associated with Interleukin-6 and Troponin I (p < 0.05 for all). Although, a significant improvement in FMD was noted during the follow-up (acute: 1.75 ± 2.19% vs. 1 month: 4.23 ± 2.02%, vs. 6 months: 5.24 ± 1.62%; p = 0.001), FMD remained impaired compared to control (6.48 ± 3.08%) at 1 month (p < 0.001) and 6 months (p = 0.01) post-hospital discharge. CONCLUSION: COVID-19 patients develop a notable endothelial dysfunction, which is progressively improved over a 6-month follow-up but remains impaired compared to healthy controls subjects. Whether chronic dysregulation of endothelial function following COVID-19 could be accompanied by a residual risk for cardiovascular and thrombotic events merits further research.


Subject(s)
COVID-19 , COVID-19/complications , Cohort Studies , Endothelium, Vascular , Humans , Prospective Studies , Vasodilation/physiology
5.
Am J Physiol Heart Circ Physiol ; 322(2): H319-H327, 2022 02 01.
Article in English | MEDLINE | ID: covidwho-1613119

ABSTRACT

Vascular dysfunction has been reported in adults who have recovered from COVID-19. To date, no studies have investigated the underlying mechanisms of persistent COVID-19-associated vascular dysfunction. Our purpose was to quantify nitric oxide (NO)-mediated vasodilation in healthy adults who have recovered from SARS-CoV-2 infection. We hypothesized that COVID-19-recovered adults would have impaired NO-mediated vasodilation compared with adults who have not had COVID-19. In methods, we performed a cross-sectional study including 10 (5 men/5 women, 24 ± 4 yr) healthy control (HC) adults who were unvaccinated for COVID-19, 11 (4 men/7 women, 25 ± 6 yr) healthy vaccinated (HV) adults, and 12 (5 men/7 women, 22 ± 3 yr) post-COVID-19 (PC, 19 ± 14 wk) adults. COVID-19 symptoms severity (survey) was assessed. A standardized 39°C local heating protocol was used to assess NO-dependent vasodilation via perfusion (intradermal microdialysis) of 15 mM NG-nitro-l-arginine methyl ester during the plateau of the heating response. Red blood cell flux was measured (laser-Doppler flowmetry) and cutaneous vascular conductance (CVC = flux/mmHg) was expressed as a percentage of maximum (28 mM sodium nitroprusside + 43°C). In results, the local heating plateau (HC: 61 ± 20%, HV: 60 ± 19%, PC: 67 ± 19%, P = 0.80) and NO-dependent vasodilation (HC: 77 ± 9%, HV: 71 ± 7%, PC: 70 ± 10%, P = 0.36) were not different among groups. Neither symptom severity (25 ± 12 AU) nor time since diagnosis correlated with the NO-dependent vasodilation (r = 0.46, P = 0.13; r = 0.41, P = 0.19, respectively). In conclusion, healthy adults who have had mild-to-moderate COVID-19 do not have altered NO-mediated cutaneous microvascular function.NEW & NOTEWORTHY Healthy young adults who have had mild-to-moderate COVID-19 do not display alterations in nitric oxide-mediated cutaneous microvascular function. In addition, healthy young adults who have COVID-19 antibodies from the COVID-19 vaccinations do not display alterations in nitric oxide-mediated cutaneous microvascular function.


Subject(s)
COVID-19/physiopathology , Microcirculation/physiology , Skin/blood supply , Vasodilation/physiology , Adult , COVID-19/metabolism , COVID-19/prevention & control , COVID-19 Vaccines/therapeutic use , Case-Control Studies , Enzyme Inhibitors/pharmacology , Female , Humans , Laser-Doppler Flowmetry , Male , Microcirculation/drug effects , NG-Nitroarginine Methyl Ester/pharmacology , Nitric Oxide/metabolism , SARS-CoV-2 , Severity of Illness Index , Vasodilation/drug effects , Young Adult
6.
Obesity (Silver Spring) ; 30(1): 165-171, 2022 01.
Article in English | MEDLINE | ID: covidwho-1530202

ABSTRACT

OBJECTIVE: The aim of this study was to identify determinants of endothelial dysfunction in patients hospitalized with acute COVID-19. METHODS: A total of 109 hospitalized COVID-19 patients in noncritical status were cross-sectionally studied. Clinical data (age, sex, comorbidities, and medications) and BMI were assessed. Laboratory tests included serum hemoglobin, leukocytes, lymphocytes, platelets, C-reactive protein, ferritin, D-dimer, and creatinine. Physical status was evaluated using a handgrip dynamometer. Endothelial function was assessed noninvasively using the flow-mediated dilation (FMD) method. RESULTS: The sample average age was 51 years, 51% of patients were male, and the most frequent comorbidity was obesity (62%). Univariate analysis showed association of lower FMD with higher BMI, hypertension, use of oral antihypertensive, higher blood levels of creatinine, and larger baseline artery diameter. After adjusting for confounders, the multivariate analysis showed BMI (95% CI: -0.26 to -0.11; p < 0.001) as the major factor associated with FMD. Other factors associated with FMD were baseline artery diameter (95% CI: -1.77 to -0.29; p = 0.007) and blood levels of creatinine (95% CI: -1.99 to -0.16; p = 0.022). CONCLUSIONS: Increased BMI was the major factor associated with endothelial dysfunction in noncritically hospitalized COVID-19 patients. This may explain one of the pathways in which obesity may increase the risk for severe COVID-19.


Subject(s)
COVID-19 , Brachial Artery , Cross-Sectional Studies , Endothelium, Vascular , Hand Strength , Humans , Male , Middle Aged , SARS-CoV-2 , Vasodilation
7.
J Clin Hypertens (Greenwich) ; 24(2): 200-203, 2022 02.
Article in English | MEDLINE | ID: covidwho-1522731

ABSTRACT

SARS-CoV-2 is causing devastation both in human lives and economic resources. When the world seems to start overcoming the pandemics scourge, the threat of long-term complications of COVID-19 is rising. Reports show that some of these long-term effects may contribute to the main cause of morbimortality worldwide: the vascular diseases. Given the evidence of damage in the endothelial cells due to SARS-CoV-2 and that endothelial dysfunction precedes the development of arteriosclerosis, the authors propose to measure endothelial function around 6-12 months after acute disease in hypertensive patients, especially if they have other cardiovascular risk factors or overt vascular disease. The methods the authors propose are cost-effective and can be made available to any hypertension unit. These methods could be the "in vivo" assessment of endothelial function by flow mediated vasodilatation after ischemia by Laser-Doppler flowmetry and the measurement of plasma free circulating DNA and microparticles of endothelial origin.


Subject(s)
COVID-19 , Hypertension , Endothelial Cells , Endothelium, Vascular , Humans , Hypertension/epidemiology , SARS-CoV-2 , Vasodilation
9.
Am J Physiol Heart Circ Physiol ; 320(1): H404-H410, 2021 01 01.
Article in English | MEDLINE | ID: covidwho-1388544

ABSTRACT

While SARS-CoV-2 primarily affects the lungs, the virus may be inflicting detriments to the cardiovascular system, both directly through angiotensin-converting enzyme 2 receptor and initiating systemic inflammation. Persistent systemic inflammation may be provoking vascular dysfunction, an early indication of cardiovascular disease risk. To establish the potential effects of SARS-CoV-2 on the systemic vasculature in the arms and legs, we performed a cross-sectional analysis of young healthy adults (control: 5 M/15 F, 23.0 ± 1.3 y, 167 ± 9 cm, 63.0 ± 7.4 kg) and young adults who, 3-4 wk prior to testing, had tested positive for SARS-CoV-2 (SARS-CoV-2: 4 M/7 F, 20.2 ± 1.1 y, 172 ± 12 cm, 69.5 ± 12.4 kg) (means ± SD). Using Doppler ultrasound, brachial artery flow-mediated dilation (FMD) in the arm and single passive limb movement (sPLM) in the leg were assessed as markers of vascular function. Carotid-femoral pulse wave velocity (PWVcf) was asvsessed as a marker of arterial stiffness. FMD was lower in the SARS-CoV-2 group (2.71 ± 1.21%) compared with the control group (8.81 ± 2.96%) (P < 0.01) and when made relative to the shear stimulus (SARS-CoV-2: 0.04 ± 0.02 AU, control: 0.13 ± 0.06 AU, P < 0.01). The femoral artery blood flow response, as evidenced by the area under the curve, from the sPLM was lower in the SARS-CoV-2 group (-3 ± 91 mL) compared with the control group (118 ± 114 mL) (P < 0.01). PWVcf was higher in the SARS-CoV-2 group (5.83 ± 0.62 m/s) compared with the control group (5.17 ± 0.66 m/s) (P < 0.01). Significantly lower systemic vascular function and higher arterial stiffness are evident weeks after testing positive for SARS-CoV-2 among young adults compared with controls.NEW & NOTEWORTHY This study was the first to investigate the vascular implications of contracting SARS-CoV-2 among young, otherwise healthy adults. Using a cross-sectional design, this study assessed vascular function 3-4 wk after young adults tested positive for SARS-CoV-2. The main findings from this study were a strikingly lower vascular function and a higher arterial stiffness compared with healthy controls. Together, these results suggest rampant vascular effects seen weeks after contracting SARS-CoV-2 in young adults.


Subject(s)
Blood Vessels/physiopathology , Brachial Artery/physiopathology , COVID-19/physiopathology , Carotid-Femoral Pulse Wave Velocity , Femoral Artery/physiopathology , Hyperemia/physiopathology , Vascular Stiffness/physiology , Vasodilation/physiology , Adolescent , Angiotensin-Converting Enzyme 2/metabolism , Area Under Curve , Blood Vessels/metabolism , Brachial Artery/diagnostic imaging , COVID-19/diagnostic imaging , Case-Control Studies , Cross-Sectional Studies , Female , Humans , Hyperemia/diagnostic imaging , Male , SARS-CoV-2 , Severity of Illness Index , Ultrasonography, Doppler , Young Adult
10.
Am J Physiol Heart Circ Physiol ; 321(3): H479-H484, 2021 09 01.
Article in English | MEDLINE | ID: covidwho-1322856

ABSTRACT

Recent findings suggest that COVID-19 causes vascular dysfunction during the acute phase of the illness in otherwise healthy young adults. To date, to our knowledge, no studies have investigated the longer-term effects of COVID-19 on vascular function. Herein, we hypothesized that young, otherwise healthy adults who are past the acute phase of COVID-19 would exhibit blunted peripheral [brachial artery flow-mediated dilation (FMD) and reactive hyperemia] and cerebral vasodilator function (cerebral vasomotor reactivity to hypercapnia; CVMR) and increased central arterial stiffness. Sixteen young adults who were at least 4 wk past a COVID-19 diagnosis and 12 controls who never had COVID-19 were studied. Eight subjects with COVID-19 were symptomatic (SYM) and eight were asymptomatic (ASYM) at the time of testing. FMD and reactive hyperemia were not different between COVID and control groups. However, FMD was lower in SYM (3.8 ± 0.6%) compared with ASYM (6.8 ± 0.9%; P = 0.007) and control (6.8 ± 0.6%; P = 0.003) with no difference between ASYM and control. Similarly, peak blood velocity following cuff release was lower in SYM (47 ± 8 cm/s) compared with ASYM (64 ± 19 cm/s; P = 0.025) and control (61 ± 14 cm/s; P = 0.036). CVMR and arterial stiffness were not different between any groups. In summary, peripheral macrovascular and microvascular function, but not cerebral vascular function or central arterial stiffness were blunted in young adults symptomatic beyond the acute phase of COVID-19. In contrast, those who were asymptomatic had similar vascular function compared with controls who never had COVID-19.NEW & NOTEWORTHY This study was the first to investigate the persistent effects of COVID-19 on vascular function in otherwise healthy young adults. We demonstrated that peripheral macrovascular and microvascular vasodilation was significantly blunted in young adults still symptomatic from COVID-19 beyond the acute phase (>4 wk from diagnosis), whereas those who become asymptomatic have similar vascular function compared with controls who never had COVID-19. In contrast, cerebral vascular function and central arterial stiffness were unaffected irrespective of COVID-19 symptomology.


Subject(s)
COVID-19/complications , Cerebrovascular Circulation , Regional Blood Flow , Vasodilation , Adult , Blood Flow Velocity , COVID-19/diagnosis , COVID-19/physiopathology , Female , Humans , Male , Vascular Stiffness
11.
Int J Cardiovasc Imaging ; 38(1): 25-32, 2022 Jan.
Article in English | MEDLINE | ID: covidwho-1318779

ABSTRACT

The systemic effects of COVID-19 disease are still largely uncertain and needs to be scrutinized with further trials. Endothelial dysfunction (ED) is responsible for the majority of adverse cardiovascular events. Flow-mediated dilation (FMD) is easily obtainable method to assess ED accurately. It is aimed to evaluate ED by measuring FMD following COVID-19 disease. Patients diagnosed with COVID-19 disease were recruited to the hospital two month after the discharge. Sex and age-matched healthy subjects were determined as the control group. Blood samples and FMD measurements were obtained from each participant. All subjects were divided into two groups according to the presence of ED determined by FMD measurements. These two groups were compared in terms of demographic features and the presence of recovered COVID-19 disease. A total of 92 subjects consisting of 59 without ED and 33 with ED were included in the study. ED (+) group was older (p = 0.015) and more likely to have hypertension (p = 0.044) and COVID-19 rate was higher in ED (+) group (p = 0.009). While neutrophil count (p = 0.047) and CRP (p = 0.036) were higher, eGFR (p = 0.044) was lower in ED (+) group. In the backward multivariable regression analysis, COVID-19 disease [OR = 3.611, 95% CI 1.069-12.198, p = 0.039] and BMI [OR = 1.122, 95% CI 1.023-1.231, p = 0.015] were independent predictors of ED. COVID-19 disease may cause ED which is the major underlying factor of cardiovascular diseases. Furthermore, COVID-19 disease may deteriorate the existing cardiovascular disease course. Detecting ED in the early phase or preventing by new treatment modalities may improve short and long-term outcome.


Subject(s)
COVID-19 , Hypertension , Brachial Artery/diagnostic imaging , Dilatation , Endothelium, Vascular , Humans , Predictive Value of Tests , SARS-CoV-2 , Vasodilation
12.
Respir Med ; 185: 106469, 2021.
Article in English | MEDLINE | ID: covidwho-1240603

ABSTRACT

BACKGROUND: The prothrombotic phenotype and diffuse intravascular coagulation observed in COVID-19 reflect endothelial dysfunction, which is linked to blood flow delivery deficiencies and cardiovascular risk. Assessments of detect vascular deficiencies among newly diagnosed and hospitalized patients due to COVID-19 have yet to be determined. OBJECTIVE: To assess endothelial function characteristics in relation to length of hospitalization and mortality in patients diagnosed with COVID-19 and compare to patients without COVID-19. METHODS: A prospective observational study involving 180 patients with confirmed COVID-19 (COVID-19 group) or suspected and ruled out COVID-19 (Non-COVID-19 group). Clinical evaluation and flow mediated vasodilation (FMD) were performed between the first 24-48 h of hospitalization. Patients were followed until death or discharge. RESULTS: We evaluated 98 patients (COVID-19 group) and 82 (Non-COVID-19 group), COVID-19 group remained hospitalized longer and more deaths occurred compared to the Non-COVID-19 group (p = 0.01; and p < 0.01). Patients in COVID-19 group also had a significantly greater reduction in both FMDmm and FMD% (p < 0.01 in both). We found that absolute FMD≤0.26 mm and relative FMD≤3.43% were the ideal cutoff point to predict mortality and longer hospital stay. In Kaplan Meyer's analysis patients had a high probability of death within a period of up to 10 days of hospitalization. CONCLUSION: Patients hospitalized for COVID-19 present endothelial vascular dysfunction early, remained hospitalized longer and had a higher number of deaths, when compared with patients without COVID-19.


Subject(s)
Brachial Artery/physiopathology , COVID-19/epidemiology , Cardiovascular Diseases/physiopathology , Endothelium, Vascular/physiopathology , Regional Blood Flow/physiology , Vasodilation/physiology , Cardiovascular Diseases/epidemiology , Comorbidity , Female , Follow-Up Studies , Humans , Male , Middle Aged , Prospective Studies , SARS-CoV-2 , United States/epidemiology
13.
Shock ; 56(6): 964-968, 2021 12 01.
Article in English | MEDLINE | ID: covidwho-1220083

ABSTRACT

BACKGROUND: Endothelial and microvascular dysfunction may be a key pathogenic feature of severe COVID-19. The aim of this study was to investigate endothelial-dependent and endothelial-independent skin microvascular reactivity in patients with critical COVID-19. METHODS: Twelve patients with COVID-19 treated with non-invasive or invasive mechanical ventilation were included in the study. We investigated skin microvascular reactivity on 2 separate days during hospitalization (study day 1 and 2) and at least 3 months after disease onset (study day 3). Twelve controls with no confirmed or suspected COVID-19 infection during 2020 were also examined. Skin perfusion was investigated through Laser Speckle Contrast Imaging before and after iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP) to determine the endothelial-dependent and the endothelial-independent vasodilation, respectively. RESULTS: Compared to controls, patients with critical COVID-19 had higher basal skin perfusion and reduced responses to endothelial-dependent (ACh, P = 0.002) and endothelial-independent (SNP, P = 0.01) vasodilator drugs on study day 1. In addition, the ACh/SNP ratio was significantly reduced in patients (0.50 ±â€Š0.36 vs. 0.91 ±â€Š0.49 in controls, P = 0.02). Three months after disease onset, surviving patients tended to have reduced ACh-mediated vasodilation compared to controls (P = 0.08). CONCLUSIONS: This small-sized pilot study demonstrates that critical COVID-19 infection is associated with microvascular impairment and, in particular, a markedly reduced endothelial function. Our results also suggest that microvascular function may not be fully recovered 3 months after disease onset.


Subject(s)
COVID-19/epidemiology , Critical Illness/epidemiology , Endothelium, Vascular/physiopathology , Microcirculation/physiology , Regional Blood Flow/physiology , Vasodilation/physiology , Aged , COVID-19/physiopathology , Comorbidity , Female , Follow-Up Studies , Humans , Male , Microvessels/physiopathology , Middle Aged , Pilot Projects , Prospective Studies , SARS-CoV-2
14.
J Med Virol ; 93(1): 573-575, 2021 01.
Article in English | MEDLINE | ID: covidwho-1206803

ABSTRACT

Patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may present a significant hypoxemia. The exactly mechanism of such hypoxemia in patients with coronavirus disease 2019 (COVID-19) is not well described. It has been suggested that microthrombosis contributes to this mechanism, increasing pulmonary dead space. However, dead spaces would not be sensible to oxygen supplementation, and also, enlargement of pulmonary vessels it has been evidenced. Shunt mechanism by vasodilatation, instead, could explain decubitus dependence in oxygenation by blood redistribution as observed in these patients, and moreover, would be more sensible to oxygen supplementation than dead spaces. We hypothesized that SARS-CoV-2 causes an intrapulmonary vascular dilatation (IPVD), determining a shunt mechanism by vasodilatation. We performed contrast-enhanced transthoracic echocardiography to search IPVD shunt in patients with confirmed COVID-19, hospitalized in an intensive care unit. Ten patients were recruited; one patient was excluded due to low quality of echocardiographic image, and nine patients were included. IPVD was found in seven (78%) patients, with different grades, including patient with normal compliance and the one without invasive ventilation. We demonstrated that shunt by IPVD is present among patients with COVID-19, and this mechanism is probably implicated in significant hypoxemia observed.


Subject(s)
COVID-19/pathology , Lung/blood supply , SARS-CoV-2 , Vasodilation , Adult , Aged , Female , Humans , Male , Middle Aged
15.
Int J Mol Sci ; 22(5)2021 Mar 03.
Article in English | MEDLINE | ID: covidwho-1129730

ABSTRACT

According to the World Health Organization, cardiovascular diseases are the main cause of death worldwide. They may be caused by various factors or combinations of factors. Frequently, endothelial dysfunction is involved in either development of the disorder or results from it. On the other hand, the endothelium may be disordered for other reasons, e.g., due to infection, such as COVID-19. The understanding of the role and significance of the endothelium in the body has changed significantly over time-from a simple physical barrier to a complex system encompassing local and systemic regulation of numerous processes in the body. Endothelium disorders may arise from impairment of one or more signaling pathways affecting dilator or constrictor activity, including nitric oxide-cyclic guanosine monophosphate activation, prostacyclin-cyclic adenosine monophosphate activation, phosphodiesterase inhibition, and potassium channel activation or intracellular calcium level inhibition. In this review, plants are summarized as sources of biologically active substances affecting the endothelium. This paper compares individual substances and mechanisms that are known to affect the endothelium, and which subsequently may cause the development of cardiovascular disorders.


Subject(s)
Endothelium, Vascular/drug effects , Endothelium, Vascular/physiology , Plants/chemistry , Secondary Metabolism , Endothelium, Vascular/cytology , Humans , Plant Extracts/chemistry , Plant Extracts/pharmacology , Plants/metabolism , Vasodilation/drug effects , Vasodilation/physiology , Vasodilator Agents/chemistry , Vasodilator Agents/pharmacology
16.
Am J Respir Crit Care Med ; 203(3): 390-391, 2021 02 01.
Article in English | MEDLINE | ID: covidwho-1127636
18.
Free Radic Biol Med ; 163: 153-162, 2021 02 01.
Article in English | MEDLINE | ID: covidwho-1065088

ABSTRACT

Nitric oxide (NO) is a free radical playing an important pathophysiological role in cardiovascular and immune systems. Recent studies reported that NO levels were significantly lower in patients with COVID-19, which was suggested to be closely related to vascular dysfunction and immune inflammation among them. In this review, we examine the potential role of NO during SARS-CoV-2 infection from the perspective of the unique physical, chemical and biological properties and potential mechanisms of NO in COVID-19, as well as possible therapeutic strategies using inhaled NO. We also discuss the limits of NO treatment, and the future application of this approach in prevention and therapy of COVID-19.


Subject(s)
Anti-Inflammatory Agents/therapeutic use , Anticoagulants/therapeutic use , Antiviral Agents/therapeutic use , COVID-19/drug therapy , Lung/drug effects , Nitric Oxide/therapeutic use , Administration, Inhalation , Anti-Inflammatory Agents/blood , Anticoagulants/blood , Antiviral Agents/blood , COVID-19/blood , COVID-19/pathology , COVID-19/virology , Endothelial Cells/drug effects , Endothelial Cells/pathology , Endothelial Cells/virology , Humans , Inflammation , Lung/blood supply , Lung/virology , Mitochondria/drug effects , Mitochondria/virology , Nitric Oxide/blood , SARS-CoV-2/drug effects , SARS-CoV-2/pathogenicity , Severity of Illness Index , Vasodilation/drug effects
19.
Rev Cardiovasc Med ; 21(3): 339-344, 2020 09 30.
Article in English | MEDLINE | ID: covidwho-875134

ABSTRACT

There is emerging evidence to suggest that vitamin D deficiency is associated with adverse outcomes in COVID-19 patients. Conversely, vitamin D supplementation protects against an initial alveolar diffuse damage of COVID-19 becoming progressively worse. The mechanisms by which vitamin D deficiency exacerbates COVID-19 pneumonia remain poorly understood. In this review we describe the rationale of the putative role of endothelial dysfunction in this event. Herein, we will briefly review (1) anti-inflammatory and anti-thrombotic effects of vitamin D, (2) vitamin D receptor and vitamin D receptor ligand, (3) protective role of vitamin D against endothelial dysfunction, (4) risk of vitamin D deficiency, (5) vitamin D deficiency in association with endothelial dysfunction, (6) the characteristics of vitamin D relevant to COVID-19, (7) the role of vitamin D on innate and adaptive response, (8) biomarkers of endothelial cell activation contributing to cytokine storm, and (9) the bidirectional relationship between inflammation and homeostasis. Finally, we hypothesize that endothelial dysfunction relevant to vitamin D deficiency results from decreased binding of the vitamin D receptor with its ligand on the vascular endothelium and that it may be immune-mediated via increased interferon 1 α. A possible sequence of events may be described as (1) angiotensin II converting enzyme-related initial endothelial injury followed by vitamin D receptor-related endothelial dysfunction, (2) endothelial lesions deteriorating to endothelialitis, coagulopathy and thrombosis, and (3) vascular damage exacerbating pulmonary pathology and making patients with vitamin D deficiency vulnerable to death.


Subject(s)
Betacoronavirus , Coronavirus Infections/epidemiology , Endothelium, Vascular/physiopathology , Pneumonia, Viral/epidemiology , Vasodilation/physiology , Vitamin D Deficiency/epidemiology , COVID-19 , Comorbidity , Coronavirus Infections/physiopathology , Humans , Pandemics , Pneumonia, Viral/physiopathology , SARS-CoV-2 , Vitamin D Deficiency/physiopathology
20.
Rev Cardiovasc Med ; 21(3): 315-319, 2020 09 30.
Article in English | MEDLINE | ID: covidwho-875132

ABSTRACT

Great attention has been paid to endothelial dysfunction (ED) in coronavirus disease 2019 (COVID-19). There is growing evidence to suggest that the angiotensin converting enzyme 2 receptor (ACE2 receptor) is expressed on endothelial cells (ECs) in the lung, heart, kidney, and intestine, particularly in systemic vessels (small and large arteries, veins, venules, and capillaries). Upon viral infection of ECs by severe acute respiratory syndrome coronarvirus 2 (SARS-CoV-2), ECs become activated and dysfunctional. As a result of endothelial activation and ED, the levels of pro-inflammatory cytokines (interleukin -1, interleukin-6 (IL-6), and tumor necrosis factor-α), chemokines (monocyte chemoattractant protein-1), von Willebrand factor (vWF) antigen, vWF activity, and factor VIII are elevated. Higher levels of acute phase reactants (IL-6, C-reactive protein, and D-dimer) are also associated with SARS-CoV-2 infection. Therefore, it is reasonable to assume that ED contributes to COVID-19-associated vascular inflammation, particularly endotheliitis, in the lung, heart, and kidney, as well as COVID-19-associated coagulopathy, particularly pulmonary fibrinous microthrombi in the alveolar capillaries. Here we present an update on ED-relevant vasculopathy in COVID-19. Further research for ED in COVID-19 patients is warranted to understand therapeutic opportunities.


Subject(s)
Betacoronavirus , Blood Coagulation Disorders/etiology , Coronavirus Infections/complications , Endothelium, Vascular/physiopathology , Pneumonia, Viral/complications , Vascular Diseases/etiology , Vasodilation/physiology , Blood Coagulation Disorders/physiopathology , COVID-19 , Coronavirus Infections/epidemiology , Humans , Inflammation/etiology , Inflammation/physiopathology , Pandemics , Pneumonia, Viral/epidemiology , SARS-CoV-2 , Vascular Diseases/physiopathology
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