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1.
Am J Hypertens ; 35(11): 948-954, 2022 Nov 02.
Article in English | MEDLINE | ID: covidwho-2097304

ABSTRACT

BACKGROUND: Although hypertension is a risk factor for severe Coronavirus Disease 2019 (COVID-19) illness, little is known about the effects of COVID-19 on blood pressure (BP). Central BP measures taken over a 24-hour period using ambulatory blood pressure monitoring (ABPM) adds prognostic value in assessing cardiovascular disease (CVD) risk compared with brachial BP measures from a single time point. We assessed CVD risk between adults with and without a history of COVID-19 via appraisal of 24-hour brachial and central hemodynamic load from ABPM. METHODS: Cross-sectional analysis was performed on 32 adults who tested positive for COVID-19 (29 ± 13 years, 22 females) and 43 controls (28 ± 12 years, 26 females). Measures of 24-hour hemodynamic load included brachial and central systolic and diastolic BP, pulse pressure, augmentation index (AIx), pulse wave velocity (PWV), nocturnal BP dipping, the ambulatory arterial stiffness index (AASI), and the blood pressure variability ratio (BPVR). RESULTS: Participants who tested positive for COVID-19 experienced 6 ± 4 COVID-19 symptoms, were studied 122 ± 123 days after testing positive, and had mild-to-moderate COVID-19 illness. The results from independent samples t-tests showed no significant differences in 24-hour, daytime, or nighttime measures of central or peripheral hemodynamic load across those with and without a history of COVID-19 (P > 0.05 for all). CONCLUSIONS: No differences in 24-hour brachial or central ABPM measures were detected between adults recovering from mild-to-moderate COVID-19 and controls without a history of COVID-19. Adults recovering from mild-to-moderate COVID-19 do not have increased 24-hour central hemodynamic load.


Subject(s)
COVID-19 , Hypertension , Vascular Stiffness , Adult , Female , Humans , Blood Pressure Monitoring, Ambulatory/methods , Pulse Wave Analysis/methods , Cross-Sectional Studies , Blood Pressure , Vascular Stiffness/physiology , Hemodynamics
2.
J Cardiopulm Rehabil Prev ; 41(3): 199-201, 2021 05 01.
Article in English | MEDLINE | ID: covidwho-1072449

ABSTRACT

INTRODUCTION: Both inflammation and cardiorespiratory fitness (CRF) are associated with the risk of respiratory infections. To clarify the hypothesis that CRF attenuates the incident risk of pneumonia due to inflammation, we conducted a prospective study examining the independent and joint associations of inflammation and CRF on the risk of pneumonia in a population sample of 2041 middle-aged men. METHODS: Cardiorespiratory fitness was directly measured as peak oxygen uptake (V˙o2peak) during progressive exercise testing to volitional fatigue, and categorized into tertiles. Inflammation was defined by high-sensitivity C-reactive protein (hsCRP). Pneumonia cases were identified by internal medicine physicians using the International Classification of Diseases codes in clinical practice. RESULTS: During a median follow-up of 27 yr, 432 pneumonia cases were recorded. High hsCRP and CRF were associated with a higher risk (HR = 1.38; 95% CI, 1.02-1.88) and a lower risk of pneumonia (HR = 0.55; CI, 0.39-0.76) after adjusting for potential confounders, respectively. Compared with normal hsCRP-Fit, moderate to high hsCRP-Unfit had an increased risk of pneumonia (HR = 1.63; CI, 1.21-2.20), but moderate to high hsCRP-Fit was not associated with an increased risk of pneumonia (HR = 1.25; CI, 0.93-1.68). CONCLUSIONS: High CRF attenuates the increased risk of pneumonia due to inflammation. These findings have potential implications for the prevention of respiratory infection characterized by systemic inflammation, such as coronavirus disease-2019 (COVID-19).


Subject(s)
Cardiorespiratory Fitness/physiology , Inflammation/epidemiology , Inflammation/physiopathology , Pneumonia/epidemiology , Pneumonia/physiopathology , Adult , C-Reactive Protein/metabolism , Causality , Cohort Studies , Comorbidity , Exercise Test , Finland/epidemiology , Follow-Up Studies , Humans , Incidence , Inflammation/blood , Male , Middle Aged , Pneumonia/blood , Prospective Studies , Risk Factors
3.
Med Hypotheses ; 143: 110197, 2020 Oct.
Article in English | MEDLINE | ID: covidwho-716873

ABSTRACT

Coronavirus disease 2019 (COVID-19) may have a metabolic origin given strong links with risk factors such as lipids and glucose and co-morbidities such as obesity and type 2 diabetes mellitus. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein mediates viral cellular entry via the ACE2 receptor. The cytoplasmic tail of this spike protein is heavily palmitoylated. Emerging studies suggest that SARS-CoV-2 alters lipid metabolism in the lung epithelial cells by modulating peroxisome proliferator-activated receptor alpha (PPARα), possibly contributing to lipotoxicity, inflammation and untoward respiratory effects. Disruption of this process may affect palmitoylation of SARS-CoV spike protein and thus infectivity and viral assembly. COVID-19 is also increasingly being recognized as a vascular disease, with several studies noting prominent systemic endothelial dysfunction. The pathogenesis of endothelial dysfunction may also be linked to COVID-19-mediated metabolic and inflammatory effects. Herein, exercise will be compared to fenofibrate as a possible therapeutic strategy to bolster resilience against (and help manage recovery from) COVID-19. This paper will explore the hypothesis that exercise may be a useful adjuvant in a setting of COVID-19 management/rehabilitation due to its effects on PPARα and vascular endothelial function.


Subject(s)
Coronavirus Infections/therapy , Exercise Therapy/methods , PPAR alpha/metabolism , Pneumonia, Viral/therapy , Spike Glycoprotein, Coronavirus/metabolism , Betacoronavirus , COVID-19 , Comorbidity , Coronavirus Infections/drug therapy , Cytoplasm/metabolism , Diabetes Mellitus, Type 2/complications , Exercise , Fenofibrate/chemistry , Humans , Inflammation , Lipid Metabolism , Lipoylation , Lung/metabolism , Obesity/complications , Pandemics , SARS-CoV-2
4.
JAMA Cardiol ; 5(10): 1198, 2020 10 01.
Article in English | MEDLINE | ID: covidwho-636343
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