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      Prognostic significance of serum albumin in patients with stable coronary artery disease treated by percutaneous coronary intervention

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          Abstract

          Background

          Stable coronary artery disease (CAD) is known to have an increased risk of cardiovascular events. Serum albumin (Alb) is reported as a useful risk-stratification tool in cardiovascular diseases such as acute coronary syndrome or heart failure. However, the association between Alb and stable CAD is unclear. Thus, we aimed to investigate the prognostic significance of Alb in patients with stable CAD.

          Methods and results

          We analyzed the data of all patients admitted to Shinonoi General Hospital between October 2014 and October 2017 for newly diagnosed stable CAD, treated via elective percutaneous coronary intervention, with the exception of old myocardial infarction. We collected data, including Alb, at admission. The primary endpoint was major adverse cardiac events (MACE; defined as all-cause death, non-fatal myocardial infarction, non-fatal stroke). In 204 enrolled patients (median age, 73 years), during a median follow-up of 783 days, 28 experienced MACE. Alb was significantly lower in patients with MACE than in those without (p<0.001). In Kaplan-Meier analysis, low Alb predicted worse prognosis in MACE (p<0.001). In multivariate Cox regression analysis, low Alb levels independently predicted MACE (p<0.001) after adjusting for age and sex (HR 4.128 [95% CI 1.632–10.440], p = 0.003), or, age and C-reactive protein (HR 3.373 [95% CI 1.289–8.828], p = 0.013).

          Conclusions

          Low Alb levels predicted MACE in patients with stable CAD.

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          Most cited references22

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          Inflammation in atherosclerosis: from pathophysiology to practice.

          Peter Libby, Paul M Ridker, Göran K Hansson (2009)
          Until recently, most envisaged atherosclerosis as a bland arterial collection of cholesterol, complicated by smooth muscle cell accumulation. According to that concept, endothelial denuding injury led to platelet aggregation and release of platelet factors which would trigger the proliferation of smooth muscle cells in the arterial intima. These cells would then elaborate an extracellular matrix that would entrap lipoproteins, forming the nidus of the atherosclerotic plaque. Beyond the vascular smooth muscle cells long recognized in atherosclerotic lesions, subsequent investigations identified immune cells and mediators at work in atheromata, implicating inflammation in this disease. Multiple independent pathways of evidence now pinpoint inflammation as a key regulatory process that links multiple risk factors for atherosclerosis and its complications with altered arterial biology. Knowledge has burgeoned regarding the operation of both innate and adaptive arms of immunity in atherogenesis, their interplay, and the balance of stimulatory and inhibitory pathways that regulate their participation in atheroma formation and complication. This revolution in our thinking about the pathophysiology of atherosclerosis has now begun to provide clinical insight and practical tools that may aid patient management. This review provides an update of the role of inflammation in atherogenesis and highlights how translation of these advances in basic science promises to change clinical practice.
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            Serum albumin: relationship to inflammation and nutrition.

            Burl R Don, George Kaysen (2004)
            Hypoalbuminemia is the result of the combined effects of inflammation and inadequate protein and caloric intake in patients with chronic disease such as chronic renal failure. Inflammation and malnutrition both reduce albumin concentration by decreasing its rate of synthesis, while inflammation alone is associated with a greater fractional catabolic rate (FCR) and, when extreme, increased transfer of albumin out of the vascular compartment. A vicious cascade of events ensues in which inflammation induces anorexia and reduces the effective use of dietary protein and energy intake and augments catabolism of the key somatic protein, albumin. Hypoalbuminemia is a powerful predictor of mortality in patients with chronic renal failure, and the major cause of death in this population is due to cardiovascular events. Inflammation is associated with vascular disease and likely causes injury to the vascular endothelium, and hypoalbuminemia as two separate expressions of the inflammatory process. Albumin has a myriad of important physiologic effects that are essential for normal health. However, simply administering albumin to critically ill patients with hypoalbuminemia has not been shown to improve survival or reduce morbidity. Thus the inference from these clinical studies suggests that the cause of hypoalbuminemia, rather than low albumin levels specifically, is responsible for morbidity and mortality.
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              One-year cardiovascular event rates in outpatients with atherothrombosis.

              Ph. Steg, Deepak Bhatt, Peter Wilson … (2007)
              Few data document current cardiovascular (CV) event rates in stable patients with atherothrombosis in a community setting. Differential event rates for patients with documented coronary artery disease (CAD), cerebrovascular disease (CVD), or peripheral arterial disease (PAD) or those at risk of these diseases have not been previously evaluated in a single international cohort. To establish contemporary, international, 1-year CV event rates in outpatients with established arterial disease or with multiple risk factors for atherothrombosis. The Reduction of Atherothrombosis for Continued Health (REACH) Registry is an international, prospective cohort of 68 236 patients with either established atherosclerotic arterial disease (CAD, PAD, CVD; n = 55 814) or at least 3 risk factors for atherothrombosis (n = 12 422), who were enrolled from 5587 physician practices in 44 countries in 2003-2004. Rates of CV death, myocardial infarction (MI), and stroke. As of July 2006, 1-year outcomes were available for 95.22% (n = 64 977) of participants. Cardiovascular death, MI, or stroke rates were 4.24% overall: 4.69% for those with established atherosclerotic arterial disease vs 2.15% for patients with multiple risk factors only. Among patients with established disease, CV death, MI, or stroke rates were 4.52% for patients with CAD, 6.47% for patients with CVD, and 5.35% for patients with PAD. The incidences of the end point of CV death, MI, or stroke or of hospitalization for atherothrombotic event(s) were 15.20% for CAD, 14.53% for CVD, and 21.14% for PAD patients with established disease. These event rates increased with the number of symptomatic arterial disease locations, ranging from 5.31% for patients with risk factors only to 12.58% for patients with 1, 21.14% for patients with 2, and 26.27% for patients with 3 symptomatic arterial disease locations (P<.001 for trend). In this large, contemporary, international study, outpatients with established atherosclerotic arterial disease, or at risk of atherothrombosis, experienced relatively high annual CV event rates. Multiple disease locations increased the 1-year risk of CV events.
              Article 0 comments Cited 258 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Sho Suzuki:
                ORCID: http://orcid.org/0000-0001-9058-9258
                Role: ConceptualizationRole: Data curationRole: Formal analysisRole: InvestigationRole: MethodologyRole: VisualizationRole: Writing – original draftRole: Writing – review & editing
                Naoto Hashizume: Role: MethodologyRole: Resources
                Yusuke Kanzaki: Role: Data curationRole: Project administrationRole: Resources
                Takuya Maruyama: Role: Resources
                Ayako Kozuka: Role: Resources
                Kumiko Yahikozawa: Role: Resources
                Chiara Lazzeri: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, CA USA )
                ISSN (Electronic): 1932-6203
                Publication date (Electronic): 3 July 2019
                Publication date Collection: 2019
                Volume: 14
                Issue: 7
                Electronic Location Identifier: e0219044
                Affiliations
                [001]Department of Cardiovascular Medicine, Minaminagano Medical Center, Shinonoi General Hospital, Nagano, Japan
                Azienda Ospedaliero Universitaria Careggi, ITALY
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Author information
                http://orcid.org/0000-0001-9058-9258
                Article
                Publisher ID: PONE-D-19-07902
                DOI: 10.1371/journal.pone.0219044
                PMC ID: 6608965
                PubMed ID: 31269058
                SO-VID: e4f9d991-7b15-470b-9e63-49ecbbb7588c
                Copyright © © 2019 Suzuki et al
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 19 March 2019
                Date accepted : 16 June 2019
                Page count
                Figures: 1, Tables: 4, Pages: 9
                Funding
                The authors received no specific funding for this work.
                Categories
                Subject: Research Article
                Subject: Medicine and Health Sciences
                Subject: Vascular Medicine
                Subject: Coronary Heart Disease
                Subject: Stable Coronary Artery Disease
                Subject: Medicine and Health Sciences
                Subject: Cardiology
                Subject: Coronary Heart Disease
                Subject: Stable Coronary Artery Disease
                Subject: Medicine and Health Sciences
                Subject: Cardiology
                Subject: Myocardial Infarction
                Subject: Medicine and Health Sciences
                Subject: Vascular Medicine
                Subject: Coronary Heart Disease
                Subject: Medicine and Health Sciences
                Subject: Cardiology
                Subject: Coronary Heart Disease
                Subject: Biology and Life Sciences
                Subject: Biochemistry
                Subject: Proteins
                Subject: Albumins
                Subject: Serum Albumin
                Subject: Biology and Life Sciences
                Subject: Immunology
                Subject: Immune Response
                Subject: Inflammation
                Subject: Medicine and Health Sciences
                Subject: Immunology
                Subject: Immune Response
                Subject: Inflammation
                Subject: Medicine and Health Sciences
                Subject: Diagnostic Medicine
                Subject: Signs and Symptoms
                Subject: Inflammation
                Subject: Medicine and Health Sciences
                Subject: Pathology and Laboratory Medicine
                Subject: Signs and Symptoms
                Subject: Inflammation
                Subject: Medicine and Health Sciences
                Subject: Cardiology
                Subject: Heart Failure
                Subject: Biology and Life Sciences
                Subject: Biochemistry
                Subject: Proteins
                Subject: Albumins
                Subject: Biology and Life Sciences
                Subject: Biochemistry
                Subject: Proteins
                Subject: Hemoglobin
                Custom metadata
                Data Availability All relevant data are within the manuscript, Supporting Information files, and on Dryad (doi: 10.5061/dryad.fn6730j).

                ScienceOpen disciplines: Uncategorized
                Data availability:
                ScienceOpen disciplines: Uncategorized

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