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Background: COVID-19 survivors can experience lingering symptoms known as PASC that appear in different phenotypes. The etiology remains elusive and endothelial dysfunction has been postulated as a main driver of PASC. Method(s): Prospective cohort including COVID- and COVID+ with (COVID+PASC+) or without (COVID+PASC-) PASC. We measured endothelial function using Endopat, an FDA approved test, with derived reactive hyperemic index RHI (endothelial dysfunction<=1.67) and arterial elasticity (augmentation index standardized at 75 bpm or AI@75;(lower =better). PASC symptoms were categorized into three non-exclusive phenotypes: Cardiopulmonary CP (postexertional malaise, shortness of breath, cough, palpitations), Neurocognitive N (change in smell/taste, neuropathy, 'brain fog', headache), and General G (fatigue, gastrointestinal or bladder problems). Result(s): We included 491 participants with 109 of the 186 with confirmed COVID+ experiencing PASC. Median number of days between COVID diagnosis and study visit was 249 days (IQR: 144, 510). Among COVID+PASC+, the median number of symptoms was 7.0 (IQR: 3.0,13.0);97 experienced symptoms categorized as G, 90 as N, and 87 as CP. COVID+ PASC+ had the lowest RHI (1.77+/-0.47) and the largest proportion [46.79% (n=51)] with RHI<=1.67 (Figure). AI@75 was the lowest in COVID- (3.11+/-15.97) followed by COVID+PASC- (3.57 +/- 16.34). Within COVID+PASC+, the mean AI@75 among G was 10.11+/-14.85, 11.36+/-14.67 with N, and highest (12.01 +/- 14.48) with CP. Symptoms' number was positively associated with AI@75 (p=0.01). The estimated mean difference in AI@75 between COVID+ PASC+ with CP and COVID+ PASC- was 8.44+/-2.46 (p=0.001), between COVID+ PASC+ with CP phenotype and COVID- was 8.9+/-1.91 (p< .0001), and between COVID+ PASC+ with CP phenotype and COVID+ PASC without CP phenotype was 7.51+/-3.75 (p=0.04) Conclusion(s): PASC was associated with worse arterial elasticity and within PASC, the cardiopulmonary phenotype had the highest arterial stiffness. (Figure Presented).
ABSTRACT
Post-COVID-syndromes have a high impact on incapacity for work: a mean of over 100 days has been reported in Germany [1]. Magnesium deficiency is documented as a riskincreasing factor for fatal outcome of acute covid disease [2, 3]. A first case report of post-COVID treatment with hybrid magnesium parenteral/ oral was presented in February 2021 during the Global Magnesium COVID 19 online conference. As of yet, there is no established explanation for post-COVID or long-COVID syndrome as well as there being no established treatment. In recourse to the hypothesis that magnesiumdepletion might favour microvascular early-aging and so favour neuro- degenerative prozesses [4] now preliminary observations of these parameters in post-covid patients in our primary care office result. This is done in connection with long years documentation of pulsewave-analysis (pwv), magnesium and Mg/Caprofiles in patients who suffered covid- disease. Figure 1 shows an over 6-year series of pulse-wave-analyses in a 59-year-old female patient who suffered from post-COVID syndrome. Her augmentation index (AIX) as an indicator of the actual microvascular condition increased from favorable 8% (2020) to highly pathological 39% in the post-COVID disease period - corresponding with the mean value of an 80-year-old person [5]. Another 67-year-old female post-COVID patient recovered clinically very well and quickly with high-dosed magnesium therapy and showed coincident positive decrease of AIX to 4%. Further case reports in the context of magnesium pretests and AIX are presented. Late controlled studies concerning magnesium supplementation and PWV focus on the other parameter - the (macrovascular determined) pulse-wave-velocity (PWV) and found no association of PWV with several months of magnesium supplementation [6]. Therefore, it must be emphasized that all our observations of the last years where not based on PWV but rather focused on AIX as a volatile but more magnesium-dependent parameter. Furthermore, our patients where mostly supplemented over years and not only 24 weeks. Evident is the overall small number of clinically manifesting post-COVID cases among our COVID patients (n= 10 when writing the ) among actually 470 Corona-context treatment cases. We have two working hypotheses for this. I: Persistently high magnesium levels may contrib- ute to reducing the number of post- COVID cases - and II: In the case of post-COVID syndrome, high-dose possibly hybrid magnesium therapy might favorably influence the course of the disease. The Corona pandemic and its microvascular consequences are possibly and unfortunately a non-intended turbo-experiment for microvascular early aging in a great number of undetected magnesium- depletion patients. Facing the burden of disease for individuals - and society as a whole - this justifies not only controlled studies but also the increased attention of medical doctors to the optimal magnesium status of these patients.
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Background: Sex differences in immunological responses to COVID-19 infection and mechanisms that may contribute towards post-acute sequelae of SARS-Co-V2 (PASC) have been reported. However, evidence on the effects of COVID infection on vascular dysfunction and PASC are limited. Method(s): FDA approved EndoPAT device was used to measure endothelial function [Reactive Hyperemia Index (RHI)] and arterial stiffness [Augmentation Index standardized at 75 beats/min (AI@75;higher AI = worse arterial elasticity)] in an adult cohort (age >=18 years) with a history of COVID-19 infection (COVID+) or confirmed SARS-CoV2 antibody negative (COVID-). Generalized linear regression was used to compute estimates of RHI and AI@75. Adjusted models included age, sex, race, blood pressure, lipids, body mass index (BMI), smoking status, and pre-existing comorbidities. Two-way interactions were used to determine if the effects of COVID or PASC status on endothelial function depends on age, sex, race, smoking status, or prevalent comorbidities. Result(s): 61.99% (n=305) of study participants were COVID- and 187 (38.01%) were COVID+. Among COVID+, 57.22% (n=107) were female, 31.72% (n=59) were non-white race, and the average age was 46.64+/-13.79 years. COVIDparticipants had a smaller proportion (38.03%) of female sex (p< .0001), lower BMI [COVID+ (30.79+/-8.95 kg/m2) vs. COVID- (27.76+/-5.89 kg/m2);p< .0001], and higher proportion of smokers [COVID+ (17.78%) vs. COVID- (58.22%);p< .0001]. The average follow-up was 349.68+/-276.76 days and 109 (22.15%) COVID+ experienced PASC. 42.48% (n=80) of COVID+ and 41.64% (n=127) of COVID- had RHI<= 1.67 (p=0.8). The average AI@75 among COVID+ without PASC was 3.63+/-16.24, with PASC was 10.5+/-14.72, and 3.11+/-15.97 among COVID- (p=0.0001). Male sex had the lowest AI@75 (-0.08+/-14.9) compared to female sex (10.75+/-15.3;< .0001). In adjusted models, PASC, female sex had 8.14+/-2.95 higher AI@75 compared to PASC, male sex (p=0.006), 18.58+/-2.99 higher AI@75 compared to COVID+ without PASC, male sex (p< .0001), 13.81+/-2.11 higher AI@75 compared to COVID-, male sex (p< .0001), and 4.97+/-2.28 higher AI@75 compared to COVID-, female sex (p=0.03). Sex was not associated with RHI or modified the effect of COVID or PASC status on endothelial function Conclusion(s): The effect of COVID and PASC status on arterial stiffness depends on sex. Female sex is associated with increased arterial stiffness (worse arterial elasticity) in the post-acute phase of COVID-19. (Figure Presented).
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Objective. To study the changes in the vascular wall, vascular age and metabolic parameters in polymorbid COVID-19 conva-lescents. Material and methods. The study included 62 patients with hypertension who reached the target blood pressure (BP) with dual an-tihypertensive therapy after severe and extremely severe COVID-19. The following examinations were performed: laboratory tests of metabolic parameters, assessment of changes in the vessel elasticity indices (pulse-wave velocity (PWV), augmentation index (AI), central systolic BP (cSBP), 24-hour BP monitoring, and non-invasive markers of liver fibrosis. Results. According to office BP measurements, after the coronavirus infection, an increase in systolic BP (SBP) by 29.6% and di-astolic BP (DBP) by 23.6%, as well as heart rate (HR) by 11.8% (p<0.05) was reported during regular antihypertensive therapy. In addition, 24-hour BP monitoring data indicated an increase in the average daily SBP, DBP, and heart rate. After the coronavirus infection, an increase in PWV by 35.4% (p<0.05), AI by 24.4% (p<0.05), cSBP by 22.1% were reported. Carbohydrate and lipid metabolism parameters deteriorated. A pronounced adverse effect of coronavirus infection on liver function was observed. The vascular age (according to the modified SCORE scale) increased by 6 years (p<0.05). Conclusion. Our study showed that patients after severe and extremely severe COVID-19 have a high risk of liver fibrosis, hypertension and lipid metabolism control worsening and accelerating vascular aging.Copyright © 2023, Media Sphera Publishing Group. All rights reserved.
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Objective. To study the changes in the vascular wall, vascular age and metabolic parameters in polymorbid COVID-19 conva-lescents. Material and methods. The study included 62 patients with hypertension who reached the target blood pressure (BP) with dual an-tihypertensive therapy after severe and extremely severe COVID-19. The following examinations were performed: laboratory tests of metabolic parameters, assessment of changes in the vessel elasticity indices (pulse-wave velocity (PWV), augmentation index (AI), central systolic BP (cSBP), 24-hour BP monitoring, and non-invasive markers of liver fibrosis. Results. According to office BP measurements, after the coronavirus infection, an increase in systolic BP (SBP) by 29.6% and di-astolic BP (DBP) by 23.6%, as well as heart rate (HR) by 11.8% (p<0.05) was reported during regular antihypertensive therapy. In addition, 24-hour BP monitoring data indicated an increase in the average daily SBP, DBP, and heart rate. After the coronavirus infection, an increase in PWV by 35.4% (p<0.05), AI by 24.4% (p<0.05), cSBP by 22.1% were reported. Carbohydrate and lipid metabolism parameters deteriorated. A pronounced adverse effect of coronavirus infection on liver function was observed. The vascular age (according to the modified SCORE scale) increased by 6 years (p<0.05). Conclusion. Our study showed that patients after severe and extremely severe COVID-19 have a high risk of liver fibrosis, hypertension and lipid metabolism control worsening and accelerating vascular aging.Copyright © 2023, Media Sphera Publishing Group. All rights reserved.
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Objective. To study the changes in the vascular wall, vascular age and metabolic parameters in polymorbid COVID-19 conva-lescents. Material and methods. The study included 62 patients with hypertension who reached the target blood pressure (BP) with dual an-tihypertensive therapy after severe and extremely severe COVID-19. The following examinations were performed: laboratory tests of metabolic parameters, assessment of changes in the vessel elasticity indices (pulse-wave velocity (PWV), augmentation index (AI), central systolic BP (cSBP), 24-hour BP monitoring, and non-invasive markers of liver fibrosis. Results. According to office BP measurements, after the coronavirus infection, an increase in systolic BP (SBP) by 29.6% and di-astolic BP (DBP) by 23.6%, as well as heart rate (HR) by 11.8% (p<0.05) was reported during regular antihypertensive therapy. In addition, 24-hour BP monitoring data indicated an increase in the average daily SBP, DBP, and heart rate. After the coronavirus infection, an increase in PWV by 35.4% (p<0.05), AI by 24.4% (p<0.05), cSBP by 22.1% were reported. Carbohydrate and lipid metabolism parameters deteriorated. A pronounced adverse effect of coronavirus infection on liver function was observed. The vascular age (according to the modified SCORE scale) increased by 6 years (p<0.05). Conclusion. Our study showed that patients after severe and extremely severe COVID-19 have a high risk of liver fibrosis, hypertension and lipid metabolism control worsening and accelerating vascular aging.Copyright © 2023, Media Sphera Publishing Group. All rights reserved.
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Objective. Evaluation of the possibility of a fixed combination of azilsartan medoxomil + chlorthalidone in additional angioprotection in patients with arterial hypertension (HTN) and high pulse wave velocity (PWV) after confirmed severe or extremely severe COVID-19 (bilateral polysegmental viral pneumonia)treated by genetically engineered biological drugs, who had not previously received combined antihypertensive therapy. Design and methods. An open observational study lasting 12 weeks included 30 patients, 28-31 days after discharge from the hospital after a severe and extremely severe COVID-19, who received or had not previously received antihypertensive therapy. Patients underwent 24-hour blood pressure (BP) monitoring, applanation tonometry (augmentation index and central BP), measurement of PWV, laboratory tests before and after prescription of a fixed combination of azilsartan medoxomil + chlorthalidone. Results. At baseline, patients showed an increase in office blood pressure to 153,06/92,2 mmHg. After treatment with a fixed combination of azilsartan medoxomil + chlorthalidone, a decrease in systolic BP by 18,47 % and diastolic BP by 16,24 % was observed. According to ambulatory BP monitoring, the decrease in systolic BP was 19,65 % and diastolic BP - 24,68 %, PWV decreased by 34,4 %, augmentation index - by 9,42 %, central systolic BP - by 15,48 % (p < 0,05). At baseline, vascular age (VA) was increased to 44,96 years compared to the passport age of 35,03 years. After treatment, there was a significant decrease in VA to 38,74 years (p < 0,01). In addition, the levels of C-reactive protein, fibrinogen, D-dimer, glucose, blood urea nitrogen and uric acid significantly decreased. Conclusions. The fixed combination of azilsartan medoxomil + chlorthalidone provides better control of BP. It also helps to improve vascular elasticity (augmentation index, PWV, central systolic BP, decrease in VA) and to reduce post-infectious inflammation in HTN patients after a severe coronavirus infection. Copyright © 2021 All-Russian Public Organization Antihypertensive League. All rights reserved.
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Background: Cardiac Rehabilitation (CR) is a supervised exercise and risk factor modification program for patients with cardiac conditions. Endothelial dysfunction is often present and is associated with worsening cardiac prognosis, and several studies have indicated that standard onsite CR has improved endothelial function in heart disease patients. However, during the COVID-19 pandemic, many CR programs transitioned to a virtual or hybrid model of care to increase safety of CR programs. Objective(s): The objective of this study was to determine vascular function of patients with coronary artery disease (CAD) measured before and after 4 months of outpatient CR using a virtual model of care. Method(s): Virtual CR included 1 virtual group session/week by videoconferencing and hybrid CR included 1 session/week (4 on-site and 12 virtual group sessions) for a total of 16 weeks. CAD patients (6 females, 4 males) mean age 68.1+/-7.5 years rested in a supine position to measure 1) brachial artery flow-mediated dilation (FMD), 2) microvascular function, and 3) augmentation index (AI) using ultrasound sonography (n=8) and an EndoPAT 2000 (n=9). Two patients completed virtual CR and the rest underwent hybrid CR. These measurements were obtained concurrently using an ultrasound transducer at the brachial artery proximal to a blood pressure cuff on the forearm with EndoPAT cuffs on the index fingers during 5-minute intervals of baseline, occlusion, and recovery. FMD results were analyzed using automated Cardiovascular Suite software. AI and Reactive Hyperemia Index (LnRHI) were determined using automatic analysis via the EndoPAT 2000. Anthropometrics, blood pressure, and food intake were recorded at each visit. Patients were advised to refrain from strenuous exercise, alcohol, caffeine, and highly saturated foods at least 12 hours prior to the study appointment. One tailed paired t-tests were conducted between baseline and completion. Result(s): Adherence to CR averaged 10.3+/-3.2 out of 16 sessions. FMD improved from (2.75+/-1.71% to 5.63+/-4.37%, p=0.048) while there was no improvement in AI (14.2+/-18.8 to 13.2+/-19.6, p=0.45) or LnRHI (0.56+/-0.12 to 0.52+/-0.20, p=0.24). Conclusion(s): While there was no improvement in LnRHI or AI after CR, FMD improved in CAD patients after 4 months of adapted CR. Our results indicate that while virtual and hybrid models of CR may not be sufficient for improving microvascular function and aortic stiffness in CAD, there is an improvement of endothelial function. Future studies should examine the effects of adherence, duration and exercise intensity within these alternative models of CR on aortic and microvascular improvements.
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Objective: Evaluation of the capability of a fixed combination of lisinopril + amlodipine + rosuvastatin (ECWAMER) in achieving additional angioprotection in patients with arterial hypertension (AH) and high pulse wave velocity (PWV) in patients after confirmed COVID-19 had 75 - 95% lung involvement, complicated by bilateral polysegmental viral pneumonia, with genetically engineered biological drugs (GIBD) therapy, who had not previously received combined antihypertensive therapy (AHT). Design and method: An open-label observational study with a duration of 12 weeks has been carried out. 30 patients who not previously received combined AHT was included. Patients underwent daily monitoring of blood pressure (ABPM), applanation tonometry (determination of the augmentation index (IA) and central blood pressure (CSAD)), measurement of PWV, laboratory tests (lipid composition of blood, fasting glucose, C-reactive protein - CRP, OAC, ferritin, fibrinogen, D-dimer, ALT, AST, creatinine, uric acid) before and after prescribing a fixed combination of lisinopril + amlodipine + rosuvastatin (ECVAMER). Results: At baseline, the patients had an increase in office blood pressure to 152.6 / 89.1 mm Hg. After prescribing a fixed combination of lisinopril + amlodipine + rosuvastatin, there was a decrease in systolic blood pressure (SBP) by 15.8% and diastolic blood pressure (DBP) by 12.2%. According to ABPM data, the decrease in SBP was 15% and DBP - 9%, decreased PWV by 23.8%, IA by 9%, CSAP by 12.4% (p < 0.05 for all comparisons with the baseline value). Vascular age (SV) was initially increased to 41.9 years with a passport age of 35.03 years. After the end of therapy, there was a significant decrease in CO up to 36.5 years, LDL by 46.8%, triglycerides by 16.8% and an increase in HDL by 10.7% (p < 0.05 for all comparisons with the baseline value). In addition, the levels of CRP, fibrinogen, D-dimer, glucose, and uric acid significantly decreased. Conclusions: The fixed combination of lisinopril + amlodipine + rosuvastatin provides better blood pressure control, improved vascular elasticity, and also improves lipid and carbohydrate metabolism in patients, reduces inflammation in patients with hypertension and hyperlipidemia after suffering from severe and extremely severe COVID-19.
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Objective: Endothelial dysfunction is thought to underlie many of the complications of COVID-19 but to what degree this persists after recovery is unknown. Here we examine endothelial function in subjects previously hospitalized with COVID- 19, those with mild symptoms who were not hospitalized and negative controls (absence of SARS-CoV-2-antibodies). Endothelial function was measured as pulse wave response to the β2 adrenergic agonist salbutamol (PWRS) which is mediated through the nitric oxide - cyclic guanosine monophosphate pathway (NO-cGMP). Design and method: Echocardiography was used to exclude subjects with cardiac abnormalities. Tonometry of the radial artery (SphygmoCor, AtCor Medical, Sydney, Australia) was performed in duplicate by a single operator before and after inhalation of 200 mcg of salbutamol using a spacer device. The PWRS was taken as the change from baseline in augmentation index (Aix) as calculated by the SphygmoCor system. In a sub-sample, PWRS was assessed in the presence and absence of the phosphodiesterase type 5 inhibitor sildenafil which inhibits the breakdown of cGMP. Results: We recruited 88 subjects (49 men) aged 47.9 ± 14.3 (mean ± SD) years of whom 32 were previously hospitalized with COVID-19 (~6 months). Subjects previously hospitalized with COVID-19 were all previously assessed in a dedicated pulmonary clinic. Age, gender, BMI, smoking status, diabetes and estimated 10-year cardiovascular risk (Q-RISKâ3) were similar between the groups. Administration of salbutamol reduced AIx in controls and those with mild COVID-19 but produced an increase in AIx in previously hospitalized COVID-19 cases (mean [95% CI]): -2.85 [-5.52, -0.188] %, -2.32 [-5.17,0.54] %, and 3.03 [0.06, 6.00] % respectively, P = 0.017 between the groups. In a sub-sample (11 hospitalized and 11 non-hospitalized) the PWRS was measured again 30 minutes after oral administration of sildenafil 25 mg. This produced a greater reduction in AIx: -5.28 [-9.00, -1.54] % in non-hospitalized and a reduction: -3.90 [-7.60, -0.21] % in hospitalized patients, and an overall improvement in the PWRS (P = 0.006). Conclusions: In subjects previously hospitalized with severe COVID-19, endothelial function is impaired for many months after hospital discharge and the impaired NO-cGMP mediated vasodilation may be reversed by sildenafil.
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Objective: To fight the COVID-19 pandemic, messenger RNA (mRNA) vaccines were the first to be adopted by vaccination programs worldwide. We sought to investigate the short-term effect of mRNA vaccine administration on endothelial function and arterial stiffness. Design and method: Thirty-two participants (mean age 37 ± 8 years, 20 men) that received the BNT162b2 mRNA COVID-19 vaccine were studied in 3 sessions in a sequence-randomized, sham-controlled, assessor-blinded, cross-over design. The primary outcome was endothelial function assessed by brachial artery flow-mediated dilatation (FMD), and secondary outcomes were aortic stiffness, evaluated with carotid-femoral pulse wave velocity (PWV) and augmentation index (AIx@75), and inflammation measured by high-sensitivity C-reactive protein (hsCRP) in blood samples. The outcomes were assessed prior to, and at 8 h, 24 h post the 1st dose of vaccination, and 8 h, 24 h, and 48 h post the 2nd. Results: There was an increase in hsCRP that was apparent at 24 h after both the 1st dose (-0.60 [95% Confidence intervals [CI]: -1.60 to -0.20], p = 0.013) and the 2nd dose (max median difference at 48 h -6.60 [95% CI: -9.80 to -3.40], p < 0.001) compared to sham. The vaccine did not change PWV or AIx@75. FMD remained unchanged during the 1st dose but decreased significantly by 1.5% (95% CI: 0.1% to 2.9%, p = 0.037) at 24 h post the 2nd dose. FMD values returned towards baseline at 48 h. Conclusions: Our study shows that the mRNA vaccine causes a prominent increase in inflammatory markers, especially after the 2nd dose, and a transient deterioration of endothelial function at 24 h that returns towards baseline at 48 h. These results confirm the short-term cardiovascular safety of the vaccine.
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BACKGROUND AND AIMS: Adverse weight gain within the first year of receiving a kidney transplant is associated with adverse health outcomes. Kidney transplant recipients (KTRs) have asked for support with physical activity and following healthy lifestyles. There is no recognised intervention to address weight gain prevention for new KTRs. Usability of an online intervention to prevent weight gain in new KTRs has recently been reported. The aim of this study was to examine the feasibility of undertaking a randomised controlled trial of an online intervention group (IG) compared with usual care UC) to address weight gain prevention in new KTRs. METHOD: Participants were recruited from two south-London transplant sites, had a kidney transplant within 3 months, and had access to an internet compatible device. Exclusion criteria included history of an unstable medical condition, non- English speaking or <18 years. At baseline assessment participants were randomized to either UC or IG. The UC group received standard dietary and physical activity education. The IG received access to a 12-week password-protected website, weekly email reminders, and could contact the research physiotherapist via a secure message function. Primary feasibility outcomes included screening rates, consent rates, adherence to study visits, acceptability of outcomes, engagement with the intervention, retention, willingness to be randomized, adverse events, hospitalizations, experience using the online intervention and experience taking part in the trial. Secondary outcomes were recorded at baseline, 3- and 12-months. These included body weight, body mass index (BMI), bioimpedance (BIA), pulse wave velocity (PWV), augmentation index (AI) and six-minute walk distance (6MWD). RESULTS: Seventeen new KTRs (median age 49 years, 10 males, median 62 days post-transplant) were randomized to the IG (n = 9) or UC (n = 8). Screening rate was 84.2% (95% CI: 68.8-94.0), recruitment 62.5% (95% CI: 43.7-79.0) and intervention adherence at 12 months was 76.4% (95% CI: 50.0-93.2). All pre-set progression criteria for feasibility were achieved. There were no associated adverse events. Qualitative analysis revealed four themes;optimizing participation and recruitment, impact of Coronavirus disease 2019 (COVID-19), engagement is a choice (technical and personal factors) and mechanisms of action (assessment and intervention factors). The IG appeared to stabilize median body weight across the study;94.5 kg, (IQR: 63.0, 102.0), 95.0 kg, (IQR: 66.7, 105.3) and 94.7 kg (IQR: 77.2, 117.3). Whereas UC participants increased [81.3 kg, (IQR: 73.6,94.6), 86.2 kg (75.4, 96.5) and 93.3 kg (70.3, 101.9)]. IG increased 6MWD [450 m, (IQR: 450, 540), 525 m (IQR: 472.5, 615) and 495 m (IQR: 465, 615)] and UC decreased 6MWD [517.5 m (IQR: 436, 570), 507.5 m (IQR: 442.5, 605) and 435 m (IQR 435, 555)]. All other outcomes were comparable across the sample. CONCLUSION: Limitations include inadequate power and small sample size, and it was a single-centre study. Integrated mixed methods analysis demonstrate congruency of both qualitative and quantitative data. Participant attitudes, experiences and engagement with the study and intervention provide insight for future trial design. A future definitive trial is warranted and welcomed by KTRs.
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Aim. To evaluate the potential of a fixed-dose combination of lisinopril+amlodi-pine+rosuvastatin (Equamer® ) in achieving additional vascular protection in patients with hypertension and high pulse wave velocity (PWV) after severe and very severe coronavirus disease 2019 (COVID-19), complicated by bilateral multisegmental viral pneumonia, with the use of biological therapy, who had not previously received combination antihypertensive therapy. Material and methods. This 12-week open-label observational study included 30 patients with or without antihypertensive therapy. The patients underwent 24-hour blood pressure monitoring, applanation tonometry (determination of the augmentation index (AI) and central blood pressure (CBP)), PWV measurement, blood laboratory tests (lipid profile, fasting glucose, C-reactive protein, complete blood count, ferritin, fibrinogen, D-dimer, alanine aminotransferase, aspartate aminotransferase, creatinine, uric acid) before and after switch to a fixed-dose combination of lisinopril+amlodipine+rosuvastatin. Results. At baseline, the patients had an increase in office blood pressure (BP) up to 152,6/89,1 mm Hg. After prescribing a fixed-dose combination of lisinopril+amlo dipine+rosuvastatin, there was a decrease in systolic blood pressure (SBP) by 15,8% and diastolic blood pressure (DBP) by 12,2%. According to 24-hour blood pressure monitoring, the decrease in SBP was 15%, DBP — by 9%, PWV — by 23,8%, AI — by 9%, CBP — by 12,4% (p<0,05 for all compared to baseline values). Vascular age (VA) was initially increased to 41,9 years with a chronological age of 35,03 years. After the end of therapy, there was a significant decrease in VA to 36,5 years, low-density lipoproteins by 46,8%, triglycerides by 16,8% and an increase in high-density lipoproteins by 10,7% (p<0,05 for all compared to baseline values). In addition, the levels of C-reactive protein, fibrinogen, D-dimer, glucose, and uric acid significantly decreased. Conclusion. The fixed-dosed combination of lisinopril+amlodipine+rosuvastatin provides better blood pressure control, improved vascular elasticity parameters (AI, PWV, CBP, decrease in VA), and also improves lipid and carbohydrate metabolism, reduces inflammation in patients with hypertension and hyperlipidemia after severe COVID-19.
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NEW FINDINGS: What is the central question of this study? We sought to investigate whether carotid stiffness, carotid intima-media thickness and the aortic augmentation index are altered in young adults 3-4 weeks after contraction of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) compared with young healthy adults. What is the main finding and its importance? We found that carotid stiffness, Young's modulus and the aortic augmentation index were greater in young adults who tested positive for SARS-CoV-2 compared with healthy young adults. These findings provide additional evidence for detrimental effects of SARS-CoV-2 on young adult vasculature, which might have implications for cardiovascular health. ABSTRACT: Contracting severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been observed to cause decrements in vascular function of young adults. However, less is known about the impact of SARS-CoV-2 on arterial stiffness and structure, which might have additional implications for cardiovascular health. The purpose of this study was to assess the carotid artery stiffness and structure using ultrasound and the aortic augmentation index (AIx) using applanation tonometry in young adults after they tested positive for SARS-CoV-2. We hypothesized that carotid artery stiffness, carotid intima-media thickness (cIMT) and aortic AIx would be elevated in young adults with SARS-CoV-2 compared with healthy young adults. We evaluated 15 young adults (six male and nine female; 20 ± 1 years of age; body mass index, 24 ± 3 kg m-2 ) 3-4 weeks after a positive SARS-CoV-2 test result compared with young healthy adults (five male and 10 female; 23 ± 1 years of age; body mass index, 22 ± 2 kg m-2 ) who were evaluated before the coronavirus 2019 pandemic. Carotid stiffness, Young's modulus and cIMT were assessed using ultrasound, whereas aortic AIx and aortic AIx standardized to 75 beats min-1 (AIx@HR75) were assessed from carotid pulse wave analysis using SphygmoCor. Group differences were observed for carotid stiffness (control, 5 ± 1 m s-1 ; SARS-CoV-2, 6 ± 1 m s-1 ), Young's modulus (control, 396 ± 120 kPa; SARS-CoV-2, 576 ± 224 kPa), aortic AIx (control, 3 ± 13%; SARS-CoV-2, 13 ± 9%) and aortic AIx@HR75 (control, -3 ± 16%; SARS-CoV-2, 10 ± 7%; P < 0.05). However, cIMT was similar between groups (control, 0.42 ± 0.06 mm; SARS-CoV-2, 0.44 ± 0.08 mm; P > 0.05). This cross-sectional analysis revealed higher carotid artery stiffness and aortic stiffness among young adults with SARS-CoV-2. These results provide further evidence of cardiovascular impairments among young adults recovering from SARS-CoV-2 infection, which should be considered for cardiovascular complications associated with SARS-CoV-2.