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      Long-term cardiovascular health status and physical functioning of nonhospitalized patients with COVID-19 compared with non-COVID-19 controls

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          Abstract

          Coronavirus disease 2019 (COVID-19) is reported to have long-term effects on cardiovascular health and physical functioning, even in the nonhospitalized population. The physiological mechanisms underlying these long-term consequences are however less well described. We compared cardiovascular risk factors, arterial stiffness, and physical functioning in nonhospitalized patients with COVID-19, at a median of 6 mo postinfection, versus age- and sex-matched controls. Cardiovascular risk was assessed using blood pressure and biomarker concentrations (amino-terminal pro-B-type-natriuretic-peptide, high-sensitive cardiac troponin I, C-reactive protein), and arterial stiffness was assessed using carotid-femoral pulse wave velocity. Physical functioning was evaluated using accelerometry, handgrip strength, gait speed and questionnaires on fatigue, perceived general health status, and health-related quality of life (hrQoL). We included 101 former patients with COVID-19 (aged 59 [interquartile range, 55–65] yr, 58% male) and 101 controls. At 175 [126–235] days postinfection, 32% of the COVID-19 group reported residual symptoms, notably fatigue, and 7% required post-COVID-19 care. We found no differences in blood pressure, biomarker concentrations, or arterial stiffness between both groups. Former patients with COVID-19 showed a higher handgrip strength (43 [33–52] vs. 38 [30–48] kg, P = 0.004) and less sleeping time (8.8 [7.7–9.4] vs. 9.8 [8.9–10.3] h/day, P < 0.001) and reported fatigue more often than controls. Accelerometry-based habitual physical activity levels, gait speed, perception of general health status, and hrQoL were not different between groups. In conclusion, one in three nonhospitalized patients with COVID-19 reports residual symptoms at a median of 6 mo postinfection, but we were unable to relate these symptoms to increases in cardiovascular risk factors, arterial stiffness, or physical dysfunction.

          NEW & NOTEWORTHY We examined cardiovascular and physical functioning outcomes in nonhospitalized patients with COVID-19, at a median of 6 mo postinfection. When compared with matched controls, minor differences in physical functioning were found, but objective measures of cardiovascular risk and arterial stiffness did not differ between groups. However, one in three former patients with COVID-19 reported residual symptoms, notably fatigue. Follow-up studies should investigate the origins of residual symptoms and their long-term consequences in former, nonhospitalized patients with COVID-19.

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          Most cited references52

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          Post-acute COVID-19 syndrome

          Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the pathogen responsible for the coronavirus disease 2019 (COVID-19) pandemic, which has resulted in global healthcare crises and strained health resources. As the population of patients recovering from COVID-19 grows, it is paramount to establish an understanding of the healthcare issues surrounding them. COVID-19 is now recognized as a multi-organ disease with a broad spectrum of manifestations. Similarly to post-acute viral syndromes described in survivors of other virulent coronavirus epidemics, there are increasing reports of persistent and prolonged effects after acute COVID-19. Patient advocacy groups, many members of which identify themselves as long haulers, have helped contribute to the recognition of post-acute COVID-19, a syndrome characterized by persistent symptoms and/or delayed or long-term complications beyond 4 weeks from the onset of symptoms. Here, we provide a comprehensive review of the current literature on post-acute COVID-19, its pathophysiology and its organ-specific sequelae. Finally, we discuss relevant considerations for the multidisciplinary care of COVID-19 survivors and propose a framework for the identification of those at high risk for post-acute COVID-19 and their coordinated management through dedicated COVID-19 clinics.
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            EuroQol - a new facility for the measurement of health-related quality of life

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              Is Open Access

              Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel

              Abstract Aims To appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD). Methods and results We assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized trials of LDL-lowering therapies. In clinical studies, plasma LDL burden is usually estimated by determination of plasma LDL cholesterol level (LDL-C). Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. Both the naturally randomized genetic studies and the randomized intervention trials consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects. Conclusion Consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD.
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                Author and article information

                Journal
                Am J Physiol Heart Circ Physiol
                Am J Physiol Heart Circ Physiol
                AJPHEART
                American Journal of Physiology - Heart and Circulatory Physiology
                American Physiological Society (Rockville, MD )
                0363-6135
                1522-1539
                1 January 2023
                2 December 2022
                2 December 2022
                : 324
                : 1
                : H47-H56
                Affiliations
                [1] 1Department of Physiology, Radboud Institute for Health Sciences, Radboud University Medical Center , Nijmegen, The Netherlands
                [2] 2Clinical Chemistry and Hematology Laboratory, Hospital Gelderse Vallei Ede , Ede, The Netherlands
                [3] 3Department of Electrical Engineering, Indian Institute of Technology Madras , Chennai, India
                [4] 4Department of Epidemiology, Erasmus Medical Center, University Medical Center Rotterdam , Rotterdam, The Netherlands
                [5] 5Department of General Practice, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht University , Utrecht, The Netherlands
                Author notes
                Correspondence: T. M. H. Eijsvogels ( thijs.eijsvogels@ 123456radboudumc.nl ).
                Author information
                https://orcid.org/0000-0001-6330-4157
                https://orcid.org/0000-0003-3899-471X
                https://orcid.org/0000-0003-0747-4471
                Article
                H-00335-2022 H-00335-2022
                10.1152/ajpheart.00335.2022
                9870581
                36459448
                3faa79d4-9a4e-4b98-a411-ecaad81d3a72
                Copyright © 2023 the American Physiological Society.
                History
                : 5 July 2022
                : 4 November 2022
                : 22 November 2022
                Funding
                Funded by: Hartstichting (Heart Foundation), doi 10.13039/501100002996;
                Award ID: 2020T063
                Award Recipient : Koen M. van der Sluijs Award Recipient : Maryam Kavousi Award Recipient : Geert-Jan Geersing Award Recipient : Frans H. Rutten Award Recipient : Thijs M.H. Eijsvogels
                Categories
                Research Article
                Cardiovascular Consequences of COVID
                Custom metadata
                True

                Cardiovascular Medicine
                cardiovascular health,covid-19,long-term effects,nonhospitalized,physical functioning

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