Serum adenosine deaminase activity and coronary artery disease: a
retrospective case-control study based on 9929 participants

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Abstract

Background:

Adenosine deaminase (ADA) regulates purine metabolism through the conversion of adenosine to uric acid (UA). Adenosine and UA are closely associated with cardiovascular events, but the correlation between serum ADA activity and coronary artery disease (CAD) has not been defined.

Methods:

We performed a hospital-based retrospective case-control study that included a total of 5212 patients with CAD and 4717 sex- and age-matched controls. The serum activity of ADA was determined by peroxidase assays in an automatic biochemistry analyzer.

Results:

Serum ADA activity in the CAD group (10.08 ± 3.57 U/l) was significantly lower than that of the control group (11.71 ± 4.20 U/l, p < 0.001). After adjusting for conventional factors, serum ADA activity negatively correlated with the presence of CAD (odds ratio = 0.852, 95% confidence interval: 0.839–0.865, p < 0.001). Among the patients with CAD, serum ADA activity was lowest in patients with myocardial infarction (MI; 9.77 ± 3.80 U/l). Diabetes mellitus and hypertension increased the serum ADA activity in CAD patients.

Conclusions:

Serum ADA activity is significantly attenuated in patients with CAD, particularly in MI. We propose a mechanism by which the body maintains adenosine levels to protect the cardiovascular system in the event of CAD.

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Most cited references 37

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Nitric oxide synthase inhibition and oxidative stress in cardiovascular diseases: possible therapeutic targets?

Luc Lorgis, Catherine Vergely, Jean-Claude Guilland … (2013)

Nitric oxide (NO) is synthetized enzymatically from l-arginine (l-Arg) by three NO synthase isoforms, iNOS, eNOS and nNOS. The synthesis of NO is selectively inhibited by guanidino-substituted analogs of l-Arg or methylarginines such as asymmetric dimethylarginine (ADMA), which results from protein degradation in cells. Many disease states, including cardiovascular diseases and diabetes, are associated with increased plasma levels of ADMA. The N-terminal catalytic domain of these NOS isoforms binds the heme prosthetic group as well as the redox cofactor, tetrahydrobiopterin (BH(4)) associated with a regulatory protein, calmodulin (CaM). The enzymatic activity of NOS depends on substrate and cofactor availability. The importance of BH(4) as a critical regulator of eNOS function suggests that BH(4) may be a rational therapeutic target in vascular disease states. BH(4) oxidation appears to be a major contributor to vascular dysfunction associated with hypertension, ischemia/reperfusion injury, diabetes and other cardiovascular diseases as it leads to the increased formation of oxygen-derived radicals due to NOS uncoupling rather than NO. Accordingly, abnormalities in vascular NO production and transport result in endothelial dysfunction leading to various cardiovascular disorders. However, some disorders including a wide range of functions in the neuronal, immune and cardiovascular system were associated with the over-production of NO. Inhibition of the enzyme should be a useful approach to treat these pathologies. Therefore, it appears that both a lack and excess of NO production in diseases can have various important pathological implications. In this context, NOS modulators (exogenous and endogenous) and their therapeutic effects are discussed. © 2013.

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Adenosine: physiology, pharmacology, and clinical applications.

Jamie Layland, David Carrick, Matthew Lee … (2014)

Adenosine is a ubiquitous extracellular signaling molecule with essential functions in human physiology. Due to the widespread expression of adenosine receptors, it has far-reaching effects across many different organ systems. With a prominent role in the cardiovascular system, it has been extensively studied for both its therapeutic and diagnostic abilities. One of the key areas of use is in the coronary circulation whereby adenosine produces a hyperemic response. An important target of adenosine is the coronary microcirculation whereby adenosine acts as a prominent vasodilator with many of the beneficial effects of adenosine reflected in its capacity to affect the microvessels. Adenosine also has an important role in the pre-conditioned state and also in the attenuation of ischemia-reperfusion injury. This review examines the physiology, pharmacology, and therapeutic applications of adenosine in the human cardiovascular system and provides a brief overview of important aspects of the adenosine-cardiac interaction. It also examines the role of adenosine in the coronary hyperemic response and discusses the use of adenosine for this purpose. After recent concerns about the use of adenosine, a discussion regarding safety of this drug is provided. A brief review of novel agents used to initiate coronary hyperemia is also provided.

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The role of uric acid in the pathogenesis of human cardiovascular disease.

Mehmet Kanbay, Hee-Kyoung Kang, Mark Segal … (2013)

Hyperuricaemia is common in subjects with cardiovascular disease, but is not commonly considered a true risk factor. Recent studies suggest that uric acid is biologically active and can stimulate oxidative stress, endothelial dysfunction, inflammation and vasoconstriction. Epidemiological studies have found that uric acid can independently predict the development of hypertension, as well as stroke and heart failure. Experimentally raising uric acid in animals increases blood pressure, and pilot studies suggest that lowering uric acid in humans can reduce blood pressure in hypertensive individuals. Uric acid may also have emerging roles in the pathogenesis of kidney disease, metabolic syndrome and diabetes. More studies need to be performed on the pathophysiology and clinical consequences of hyperuricaemia in cardiovascular disease.

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Author and article information

Contributors

Chao Xuan:

ORCID: https://orcid.org/0000-0001-8273-0178

Qing-Wu Tian

Shao-Yan Zhang

Hui Li

Ting-Ting Tian

Peng Zhao

Kang Yue

Yan-Yan Ling

Guo-Wei He

Li-Min Lun

Journal

Journal ID (nlm-ta): Ther Adv Chronic Dis

Journal ID (iso-abbrev): Ther Adv Chronic Dis

Journal ID (publisher-id): TAJ

Journal ID (hwp): sptaj

Title: Therapeutic Advances in Chronic Disease

Publisher: SAGE Publications (Sage UK: London, England )

ISSN (Print): 2040-6223

ISSN (Electronic): 2040-6231

Publication date (Electronic): 6 December 2019

Publication date Collection: 2019

Volume: 10

Electronic Location Identifier: 2040622319891539

Affiliations

[1-2040622319891539]Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, 59, Haier Road, Qingdao 266101, China

[2-2040622319891539]Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China

[3-2040622319891539]Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China

[4-2040622319891539]Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China

[5-2040622319891539]Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China

[6-2040622319891539]Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China

[7-2040622319891539]Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China

[8-2040622319891539]Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, China

[9-2040622319891539]Department of Cardiovascular Surgery, TEDA International Cardiovascular Hospital, Tianjin, China

[10-2040622319891539]Academy of Medical Sciences and Peking Union Medical College, Tianjin, China

[11-2040622319891539]Department of Surgery, Oregon Health and Science University, Portland, Oregon, USA

[12-2040622319891539]Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, 59, Haier Road, Qingdao 266101, China

Author notes

[*] lunlmqd@ 123456163.com

[*] bio-x.c@ 123456hotmail.com

Author information

Chao Xuan https://orcid.org/0000-0001-8273-0178

Article

Publisher ID: 10.1177_2040622319891539

DOI: 10.1177/2040622319891539

PMC ID: 6900608

PubMed ID: 31839921

SO-VID: 2f17553e-7007-4fac-a637-01b4a47d04d4

License:

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( http://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

History

Date received : 7 August 2019

Date accepted : 30 October 2019

Funding

Funded by: National Natural Science Foundation of China, FundRef https://doi.org/10.13039/501100001809;

Award ID: 81672073

Funded by: China Postdoctoral Science Foundation, FundRef https://doi.org/10.13039/501100002858;

Award ID: 2016M590620

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cover-date January-December 2019

typesetter ts1

Keywords: adenosine,adenosine deaminase,coronary artery disease

Data availability:

Keywords: adenosine, adenosine deaminase, coronary artery disease

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Serum adenosine deaminase activity and coronary artery disease: a retrospective case-control study based on 9929 participants

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Abstract

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Cardiovascular Innovations and Applications

Most cited references 37

Nitric oxide synthase inhibition and oxidative stress in cardiovascular diseases: possible therapeutic targets?

Adenosine: physiology, pharmacology, and clinical applications.

The role of uric acid in the pathogenesis of human cardiovascular disease.

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