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      Serum Level of Lactate Dehydrogenase is Associated with Cardiovascular Disease Risk as Determined by the Framingham Risk Score and Arterial Stiffness in a Health-Examined Population in China

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          Abstract

          Introduction

          Lactate dehydrogenase (LDH) is an important oxidoreductase in the anaerobic metabolic pathway. The role of LDH in arterial stiffness (AS) and 10-year cardiovascular disease (CVD10) risk has not been established.

          Methods

          This retrospective, cross-sectional, and observational study evaluated the relationships between the LDH level and AS and CVD10 risk in 12,597 health-examined people (6988 men and 5609 women; mean age, 49.49 years) in China. Brachial–ankle pulse wave velocity (baPWV) was used to estimate AS. The Framingham CVD 10-year risk prediction model was used to calculate the CVD10 risk score.

          Results

          In both sexes, an increased LDH level was associated with increased AS and CVD10 (men: β = 0.032, P < 0.001; women: β = 0.025, P < 0.001). Half of the population with a high LDH level ( 172 U/L) showed significantly increased AS and CVD10 risk score. Men and women with baPWV ≥1400 cm/s had a higher LDH level, and the latter was significantly different from that of the group with baPWV <1400 cm/s (men: 176.93±30.99 vs 173.00±33.36, P < 0.001; women: 189.10±34.20 vs 171.39±31.08, P < 0.001). In both sexes, a higher level of LDH was noted in groups with higher CVD10 risk score (men: 176.65±32.51 vs 172.94±32.46, P < 0.001; women: 202.51±44.05 vs 175.73±32.39, P < 0.001).

          Discussion

          An increased LDH level may be associated with AS and CVD10 risk. The LDH level could be a new predictor of AS and CVD10 risk in health-examined populations.

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          Most cited references24

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          2013 ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.

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            Arterial Stiffness and Cardiovascular Risk in Hypertension

            Arterial stiffness, a leading marker of risk in hypertension, can be measured at material or structural levels, with the latter combining effects of the geometry and composition of the wall, including intramural organization. Numerous studies have shown that structural stiffness predicts outcomes in models that adjust for conventional risk factors. Elastic arteries, nearer to the heart, are most sensitive to effects of blood pressure and age, major determinants of stiffness. Stiffness is usually considered as an index of vascular aging, wherein individuals excessively affected by risk factor exposure represent early vascular aging, whereas those resistant to risk factors represent supernormal vascular aging. Stiffness affects the function of the brain and kidneys by increasing pulsatile loads within their microvascular beds, and the heart by increasing left ventricular systolic load; excessive pressure pulsatility also decreases diastolic pressure, necessary for coronary perfusion. Stiffness promotes inward remodeling of small arteries, which increases resistance, blood pressure, and in turn, central artery stiffness, thus creating an insidious feedback loop. Chronic antihypertensive treatments can reduce stiffness beyond passive reductions due to decreased blood pressure. Preventive drugs, such as lipid-lowering drugs and antidiabetic drugs, have additional effects on stiffness, independent of pressure. Newer anti-inflammatory drugs also have blood pressure independent effects. Reduction of stiffness is expected to confer benefit beyond the lowering of pressure, although this hypothesis is not yet proven. We summarize different steps for making arterial stiffness measurement a keystone in hypertension management and cardiovascular prevention as a whole.
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              Height and body-mass index trajectories of school-aged children and adolescents from 1985 to 2019 in 200 countries and territories: a pooled analysis of 2181 population-based studies with 65 million participants

              Summary Background Comparable global data on health and nutrition of school-aged children and adolescents are scarce. We aimed to estimate age trajectories and time trends in mean height and mean body-mass index (BMI), which measures weight gain beyond what is expected from height gain, for school-aged children and adolescents. Methods For this pooled analysis, we used a database of cardiometabolic risk factors collated by the Non-Communicable Disease Risk Factor Collaboration. We applied a Bayesian hierarchical model to estimate trends from 1985 to 2019 in mean height and mean BMI in 1-year age groups for ages 5–19 years. The model allowed for non-linear changes over time in mean height and mean BMI and for non-linear changes with age of children and adolescents, including periods of rapid growth during adolescence. Findings We pooled data from 2181 population-based studies, with measurements of height and weight in 65 million participants in 200 countries and territories. In 2019, we estimated a difference of 20 cm or higher in mean height of 19-year-old adolescents between countries with the tallest populations (the Netherlands, Montenegro, Estonia, and Bosnia and Herzegovina for boys; and the Netherlands, Montenegro, Denmark, and Iceland for girls) and those with the shortest populations (Timor-Leste, Laos, Solomon Islands, and Papua New Guinea for boys; and Guatemala, Bangladesh, Nepal, and Timor-Leste for girls). In the same year, the difference between the highest mean BMI (in Pacific island countries, Kuwait, Bahrain, The Bahamas, Chile, the USA, and New Zealand for both boys and girls and in South Africa for girls) and lowest mean BMI (in India, Bangladesh, Timor-Leste, Ethiopia, and Chad for boys and girls; and in Japan and Romania for girls) was approximately 9–10 kg/m2. In some countries, children aged 5 years started with healthier height or BMI than the global median and, in some cases, as healthy as the best performing countries, but they became progressively less healthy compared with their comparators as they grew older by not growing as tall (eg, boys in Austria and Barbados, and girls in Belgium and Puerto Rico) or gaining too much weight for their height (eg, girls and boys in Kuwait, Bahrain, Fiji, Jamaica, and Mexico; and girls in South Africa and New Zealand). In other countries, growing children overtook the height of their comparators (eg, Latvia, Czech Republic, Morocco, and Iran) or curbed their weight gain (eg, Italy, France, and Croatia) in late childhood and adolescence. When changes in both height and BMI were considered, girls in South Korea, Vietnam, Saudi Arabia, Turkey, and some central Asian countries (eg, Armenia and Azerbaijan), and boys in central and western Europe (eg, Portugal, Denmark, Poland, and Montenegro) had the healthiest changes in anthropometric status over the past 3·5 decades because, compared with children and adolescents in other countries, they had a much larger gain in height than they did in BMI. The unhealthiest changes—gaining too little height, too much weight for their height compared with children in other countries, or both—occurred in many countries in sub-Saharan Africa, New Zealand, and the USA for boys and girls; in Malaysia and some Pacific island nations for boys; and in Mexico for girls. Interpretation The height and BMI trajectories over age and time of school-aged children and adolescents are highly variable across countries, which indicates heterogeneous nutritional quality and lifelong health advantages and risks. Funding Wellcome Trust, AstraZeneca Young Health Programme, EU.
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                Author and article information

                Journal
                Int J Gen Med
                Int J Gen Med
                ijgm
                International Journal of General Medicine
                Dove
                1178-7074
                04 January 2022
                2022
                : 15
                : 11-17
                Affiliations
                [1 ]Department of Health Management Center, The First Affiliated Hospital of Nanjing Medical University , Nanjing, 210029, People’s Republic of China
                [2 ]Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University , Nanjing, 210029, People’s Republic of China
                Author notes
                Correspondence: Qun Zhang Tel +86 25 68303925 Fax +86 25 68303925 Email lucyqzhang@126.com
                [*]

                These authors contributed equally to this work

                Article
                337517
                10.2147/IJGM.S337517
                8742599
                35018110
                f2b3b26f-6b71-49cc-baec-fba67407aa0e
                © 2022 Zhu et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                : 07 September 2021
                : 16 November 2021
                Page count
                Figures: 1, Tables: 4, References: 25, Pages: 7
                Funding
                Funded by: Social Development Project of Jiangsu Province;
                This study was funded by the Social Development Project of Jiangsu Province (BE2016787), Social Development Project of Jiangsu Province (BE2016787), and Natural Science Foundation of the Jiangsu Higher Education Institutions of China (19KJB320010).
                Categories
                Original Research

                Medicine
                lactate dehydrogenase,arterial stiffness,10-year cardiovascular disease risk,brachial–ankle pulse wave velocity,framingham cvd 10-year risk prediction model

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