|Year : 2018 | Volume
| Issue : 1 | Page : 28-34
Serum selenium level in acute myocardial infarction
Abdallah I Ali Kelani1, Hanan S El-Deen Mohammed1, Mona M Soliman1, Marwa Sayed2, Hala M El-Badre3, Mai A Fathi1
1 Department of Internal Medicine, Faculty of Medicine, Assiut University Hospital, Assiut, Egypt
2 Department of Cardiology, Faculty of Medicine, Assiut University Hospital, Assiut, Egypt
3 Department of Biochemistry, Faculty of Medicine, Assiut University Hospital, Assiut, Egypt
|Date of Submission||09-Oct-2017|
|Date of Acceptance||16-Nov-2017|
|Date of Web Publication||20-Mar-2018|
Mai A Fathi
Assiut, El Azhar Street, El HARMIN Tower, 71111
Source of Support: None, Conflict of Interest: None
Introduction Although remarkable developments have been made in the management of cardiovascular disease, myocardial infarction (MI) remains the most common cause of death worldwide. MI is an acute condition of myocardial cell death that occurs as a result of imbalance between the coronary blood supply and myocardial requirements. Lipid peroxidation and excessive production of reactive oxygen species (ROS), such as superoxide anions (O2•−) and hydrogen peroxide, play a major role in the mechanism of MI. ROS directly damage the cell membrane and cause cell necrosis. However, ROS also stimulate signal transfer to upregulate inflammatory cytokines, for example, tumor necrosis factor-α in the ischemic area and the neighboring myocardium.
Aim The aims of this article were: (a) to determine serum selenium (Se) and the cut-off value in acute MI patients and the correlation between serum Se and other cardiac biomarkers such as troponin, creatine kinase (CK), creatine kinase myocardial brand (CK-MB), C-reactive protein, and lipogram; and (b) to determine the most predictor risk factor of MI.
Materials and methods The study was carried out on 120 individuals (60 patients and 60 controls). The patients presented to the Internal Medicine Department and Coronary Care Unit at Assiut University Hospital. The healthy controls were selected and matched for age and sex, and only those who were found to be in good health and free from any signs of chronic diseases or disorders were included.
Results The main finding of this analysis that there is a statistical difference between patients and controls in serum Se as the mean Se level in patients was 80.3±20.5 and in controls it was 97.2±14.0 and P value of less than 0.001, Thus, serum Se is significantly low in MI patients. Also, there was no statistical difference in serum Se in terms of sex, smoking, accompanying diseases (diabetes or hypertension), or type of infarction.
Conclusion This study supports a significant association between deficient serum Se concentration with cut-off value of up to 84 ng/ml and MI. Strikingly, the most predictor of MI is serum Se, followed by total cholesterol, diabetes mellitus, low-density lipoprotein, and hypertension.
Keywords: myocardial infarction, selenium, trace elements
|How to cite this article:|
Ali Kelani AI, El-Deen Mohammed HS, Soliman MM, Sayed M, El-Badre HM, Fathi MA. Serum selenium level in acute myocardial infarction. Egypt J Intern Med 2018;30:28-34
|How to cite this URL:|
Ali Kelani AI, El-Deen Mohammed HS, Soliman MM, Sayed M, El-Badre HM, Fathi MA. Serum selenium level in acute myocardial infarction. Egypt J Intern Med [serial online] 2018 [cited 2018 Aug 14];30:28-34. Available from: http://www.esim.eg.net/text.asp?2018/30/1/28/227963
| Introduction|| |
Selenium (Se) is a unique essential element as it replaces sulfur in cysteine to form the 21st amino acid selenocysteine and is, thereby, directly attached to proteins, compared with other metals that act as cofactors or prosthetic groups . This unique biology necessitates a complex metabolic fate for dietary sources of Se before the Se structure becomes biologically active.
Several selenoproteins have antioxidant functions; however, the full biological repertoire of selenoproteins is still incompletely known. Hence, the action of Se is complex and interlinked with many metabolic pathways. Selenoprotein expression in tissues shows a hierarchical relation, with the liver and the heart affected more than the endocrine organs and the brain by Se deficiency .
The antioxidant effects have led to investigations into the link of Se deficiency to pro-oxidant pathologic states such as atherothrombotic cardiovascular disease and heart failure .
Numerous investigations have examined the relation of plasma Se, a simple and likely inadequate measure of body Se status, with cardiovascular disease. Although several studies have shown that low Se status is associated with cardiovascular disease and mortality, other studies have shown a lack of a relationship. Furthermore, recent studies of Se supplementation in the generally Se-replete population of the USA have shown an increased risk of diabetes mellitus (DM) in patients administered Se in modest supplemental doses .
Hence, even though Se is an attractive nutraceutical because of its significant effects on many biological functions relevant to cardiovascular disease prevention, an incomplete understanding of its biology in health and disease prevents its routine use in humans .
Moreover, Benstoem et al.  consider Se a marker in coronary heart disease.
Reductions in the circulating levels of the essential trace elements, Se , zinc, and chromium , are found in patients and experimental models of MI. Reduction of serum levels of zinc and Se was found in patients with high levels of cardiac markers, which implies that trace element levels are associated with the degree of myocardial injury and may play a role in the pathological process of ischemic heart disease .
Being essential metals integral to the activity of antioxidant enzymes, this nutrient imbalance favors the progression of oxidative stress and the generation of reactive oxygen species (ROS) that overwhelm the internal antioxidant defenses . Hence, the supplementation of microminerals could be useful for the prevention of MI through antioxidant mechanisms.
The results from previous clinical trials indicate no overall benefit of supplementation with Se only in the prevention of cardiovascular disease. Thus, a combination of Se with trace elements such as zinc and chromium was used to evaluate the possible synergistic effects. Se supplements are available in two forms: inorganic mineral salts, typically sodium selenite or selenate, and organic forms such as Se-enriched yeasts . Among the different types of Se, Se yeast has been found to be the best bioavailable form, being more effective than sodium selenite and selenate in increasing tissue Se retention .
| Materials and methods|| |
The study was carried out on 120 individuals (60 patients and 60 controls). The patients presented to the Internal Medicine Department and Coronary Care Unit at Assiut University Hospital. The healthy controls were selected and matched for age and sex, and only those who were found to be in good health and free from any signs of chronic diseases or disorders were included.
Eligibility for enrollment in the current study was defined by the following inclusion and exclusion criteria:
Acute myocardial infarction (MI) patients diagnosed by assessment of history, clinical examination, determination of cardiac biomarkers [troponin, creatine kinase (CK), creatine kinase myocardial brand (CK-MB)], ECG, and echocardiography.
Patients on Se supplementations were excluded from the study.
| Methods|| |
An informed consent was obtained for all patients and the approval of the Research Ethics Committee of Assiut Faculty of Medicine was obtained before the study.
- All studied patients were subjected to the following:
- Assessment of history.
- Physical examination.
- Laboratory investigations including the following: serum Se, troponin, CK, CK-MB, C-reactive protein (CRP), and lipid profile.
- ECG and echocardiography.
The data were tested for normality using the Anderson–Darling test and for homogeneity variances before further statistical analysis. Categorical variables were described by number and percent, where continuous variables were described by mean and SD. χ2-Test and the Fisher exact test were used to compare between categorical variables; continuous variables were compared using a t-test and analysis of variance. Receiver operating characteristic curve was used to predict the cut-off value. Multiple linear regression analysis was carried out to detect the most important predictor of MI. A two-tailed P value of less than 0.05 was considered statistically significant. All analyses were carried out using the IBM SPSS 20.0 software (IBM Corporation, Armonk, NY, USA).
| Results|| |
Results are shown in [Table 1],[Table 2],[Table 3],[Table 4],[Table 5],[Table 6],[Table 7],[Table 8],[Table 9] and [Figure 1] and [Figure 2].
|Table 2 Comparison between patients and control in terms of serum selenium|
Click here to view
|Table 5 Range, mean, and SD of the studied parameters in the patient group|
Click here to view
|Figure 2 Receiver operating characteristic curve to detect the cut-off value of selenium between patients and controls.|
Click here to view
[Table 2] shows that there is a statistical difference between the patients and the controls in serum Se as the mean Se in patients was 80.3±20.5 and in controls it was 97.2±14.0 and P value of less than 0.001. Thus, serum Se is significantly low in MI patients.
Among the 36 cases of our study who were diagnosed with acute MI, four (11.1%) only had low Se (below the cut-off value <84 ng/ml) as a risk factor for MI and were nondiabetic, nonhypertensive, and nonsmokers.
Also, among these 36 cases, five (13.9%) had low Se and were smokers, which represent two risk factors for MI.
Five (13.9%) of these 36 cases had low Se and were diabetic.
Also, four (11.1%) cases had low serum Se and were hypertensive, which represent two risk factors for MI.
As three risk factors for MI in four (11.1%) cases were diabetes, smoking habit, and low Se levels.
In contrast, only two (5.6%) cases were hypertensive, smokers, and had low serum Se.
Also, four (11.1%) cases were diabetic, hypertensive, and had low Se levels.
On combining the four risk factors of MI (DM, hypertension, smoking, and low Se), we found that eight (22.2%) cases had these four risk factors ([Table 10]).
|Table 10 Multivariate analysis using multiple binary logistic regressions to assess the predictors of myocardial infarction|
Click here to view
| Discussion|| |
Atherosclerosis is a well-known precursor of ischemic heart disease because of accumulation of lipids and fibrous elements in the arteries . Development of atherosclerosis depends on a balance between proinflammatory stimuli, anti-inflammatory, and antioxidant defense mechanisms . The disturbance of Se may cause MI because of a direct effect on the vascular system or indirectly by lipoprotein metabolism .
Lipoprotein oxidation is inhibited by enzymatic antioxidants, such as glutathione peroxidase and selenoenzyme glutathione peroxidase, the activities of which depend on an adequate Se supply. Se-binding antioxidants are designed to prevent the occurrence of free radical-induced injury under normal conditions .
This study found that there is no correlation between serum Se and high-density lipoprotein (HDL) cholesterol. This is in agreement with the result obtained by Christensen et al. , who found that HDL cholesterol did not vary with Se.
This study shows that serum Se has a significant negative correlation with the low-density lipoprotein cholesterol level . In addition, the authors found a significant reduction in non-HDL cholesterol levels. Nonetheless, the effects of Se substitution on the lipid profile remain partially understood .
Moreover, previous studies have shown that Se supplementation may affect and thus control the migration, adherence, and phagocytosis of leukocytes .
Se influences the inflammatory signaling pathways that modulate ROS by inhibiting the nuclear factor-κB cascade, resulting in a suppressed production of interleukins and tumor necrosis factor-α .
Also, Stranges et al.  concluded that there was no association of HDL cholesterol with biomarkers of Se status. Nawrot et al.  found that elevated baseline Se levels were associated with a lower risk for hypertension in men, but data from the Lipid Analytic Cologne cohort suggested that higher serum Se concentrations were associated with higher blood pressure levels and a higher prevalence of hypertension .
This result is in agreement with that reported by Zhuravlyova and Filonenko , who found that Se levels were related to the extent of myocardial injury during infarction. It was also reported that Se level in the acute phase of MI is closely correlated with the peak number of cardiac biomarkers, as well as the activity of metabolic oxygen-dependent reactions .
This result is in agreement with that reported by Li et al. , who concluded that there is a significant correlation between serum Se and MI, and they concluded that although Se deficiency is plausibly linked to an increased risk of MI, the inconsistency among the findings of previous studies precludes definitive recommendations at present .
The present study found a significant negative correlation between serum Se and CRP as serum Se plays a role in the regulation of the inflammatory response as reported by Benstoem .
This result is in agreement with that reported by Ghashut et al. , who found that the magnitude of systemic inflammatory response as evidenced by CRP is a major factor associated with lower Se.
The present study found no correlation between serum Se and the site of MI; this result is in agreement with that reported by Radchenko et al. , who found no difference in Se concentration depending on the location of MI.
The present study found no statistical difference in serum Se in terms of age, sex, smoking, diabetes, or hypertension. This result is in agreement with that reported by Radchenko et al. , who found no difference in Se concentration depending on age, sex, smoking, and accompanying diseases.
Trace elements, for example Se, are increasingly being recognized as essential mediators in the development and progression of MI . The discrepancy between the studies of the association between Se levels and coronary heart disease risk could be explained by the fact that most studies have been carried out in European countries with markedly lower Se intake compared with that in the USA. Epidemiological studies support the possibility that the deficiency of certain essential elements may increase the risk of MI. Afridi et al.  found that there was a significant relationship between Se deficiency and MI risk.
In another study aimed to estimate alterations in serum Se levels in the acute phase of MI. Serum Se levels were measured at admission and after 24 h in 60 consecutive patients with acute coronary syndrome. A positive correlation was also found between the peak TnI and the difference from baseline to 24 h. Moreover, a close negative correlation was observed between baseline Se levels and the difference from baseline to 24 h. These results suggest that alterations in serum Se may be related to the extent of MI .
However, some studies suggest that there is no correlation between Se levels and MI risk. Xun et al.  found no association between Se levels and measures of subclinical atherosclerosis among young American adults.
MI occurs when myocardial ischemia, diminished blood supply to the heart, exceeds a critical threshold and overwhelms myocardial cellular repair mechanisms designed to maintain normal operating function and homeostasis .
Tang et al.  found that the genetic variant in glutathione peroxidase 1 gene is associated with an increased risk of coronary artery disease in a Chinese population.
Hassanzadeh et al.  found that patients with acute MI have lower plasma concentrations of Se and higher concentrations of proinflammatory cytokines of tumor necrosis factor-α and interleukin-6.
The present study found no correlation between serum Se and serum triglycerides; this result is in agreement with that reported by Wells et al. .
A meta-analysis of 14 prospective cohort studies found a modest but statistically significant inverse association between Se levels and coronary heart disease .
Also, Altekin et al.  found that Se deficiency is plausibly linked to an increased risk of MI. Also, Se deficiency in acute coronary syndrome is associated with increased other cardiac biomarkers and CRP.
Alanne et al.  have shown that polymorphisms in the Selenoprotein S gene have significant effects on cardiovascular morbidity, especially in women.
Lubos et al.  concluded that low Se concentrations were associated with the risk of future cardiovascular death in patients with acute coronary syndrome.
Moreover, the Se content of grains and vegetables generally depends on the Se content in the corresponding soils .
The atmosphere plays an important role in the biogeochemical cycling of Se. It influences the transport and transformation of Se .
The present study found that serum Se is significantly low in MI patients.
The present study found a negative correlation between serum Se and peak troponin as reported by Kutil et al. , who found a negative correlation between peak troponin level and serum Se.
The present study found no correlation between serum Se and CK or CK-MB.
The present study found a positive correlation between serum Se and ejection fraction, but the correlation was insignificant.
No statistical difference was found in our study between serum Se in ST-segment MI and non-ST-segment MI.
Strikingly, using multivariate analysis with multiple binary logistic regressions to assess the predictor of MI, we found that the most important risk factor to predict of MI is serum Se, followed by total cholesterol, DM, low-density lipoprotein, and hypertension, respectively. This supports the result found in this study as no statistical difference was found in serum Se in terms of age, sex, smoking, diabetes, or hypertension.
From the above data, it can be stated that low serum Se with a cut-off value of up to 84 ng/ml is an important risk factor for MI. Se acts as an antioxidant that protects the cardiac muscle against the damaging effects of free radicals.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Stadtman TC. Selenoproteins – tracing the role of a trace element in protein function. PLoS Biol 2005; 3:e421.
Bermano G, Nicol F, Dyer JA, Sunde RA, Beckett GJ, Arthur JR, Hesketh JE. Tissue-specific regulation of selenoenzyme gene expression during selenium deficiency in rats. Biochem J 1995; 311:425–430.
Joseph J, Loscalzo J. Selenistasis: epistatic effects of selenium on cardiovascular phenotype. Nutrients 2013; 5:340–358.
Benstoem C, Goetzenich A, Kraemer S, Borosch S, Manzanares W, Hardy G, Stoppe C. Selenium and its supplementation in cardiovascular disease – What do we know? Nutrients 2015; 7:3094–3118.
Panicker S, Swathy SS, John F, Madambath I. Impact of selenium on NFkappaB translocation in isoproterenol-induced myocardial infarction in rats. Biol Trace Elem Res 2010; 138:202–211.
Afridi HI, Kazi TG, Kazi N, Sirajuddin , Kandhro GA, Baig JA et al.
Chromium and manganese levels in biological samples of Pakistani myocardial infarction patients at different stages as related to controls. Biol Trace Elem Res 2011; 142:259–273.
Altekin E, Coker C, Sisman AR, Onvural B, Kuralay F, Kirimli O. The relationship between trace elements and cardiac markers in acute coronary syndromes. J Trace Elem Med Biol 2005; 18:235–242.
Weber KT, Weglicki WB, Simpson RU. Macroand micronutrient dyshomeostasis in the adverse structural remodeling of myocardium. Cardiovasc Res 2009; 81:500–508.
Alimohamady R, Aliarabi H, Bahari A, Dezfoulian AH. Influence of different amounts and sources of selenium supplementation on performance, some blood parameters, and nutrient digestibility in lambs. Biol Trace Elem Res 2013; 154:45–54.
Thiry C, Schneider YJ, Pussemier L, De Temmerman L, Ruttens A. Selenium bioaccessibility and bioavailability in Se-enriched food supplements. Biol Trace Elem Res 2013; 152:152–160.
Dutta P, Courties G, Wei Y, Leuschner F, Gorbatov R, Robbins CS et al.
Myocardial infarction accelerates atherosclerosis. Nature 2012; 487:325–329.
Li F, Gao1 J, Zhang B. Association between deficient selenium levels and myocardial infarction: a meta-analysis. Int J Clin Exp Med 2016; 9:6086–6609.
Nomoto A, Higuchi Y, Kobiki Y, Ogawa A. Synthesis of selenium compounds by free radical addition based on visible-light-activated sese bond cleavage. Mini Rev Med Chem 2013; 13:814–823.
Christensen K, Werner M, Malecki K. Serum selenium and lipid levels association observed in the national health and nutrition examination survey (NHANES); 2011–2012. Environ Res 2015; 140:76–84.
Navas-Acien A, Bleys J, Guallar E. Selenium intake and cardiovascular risk: What is new? Curr Opin Lipidol 2008; 19:43–49.
Ahrens I, Ellwanger C, Smith BK, Bassler N, Chen YC, Neudorfer I et al.
Selenium supplementation induces metalloproteinase-dependent L-selectin shedding from monocytes. J Leukoc Biol 2008; 83:1388–1395.
Forman HJ, Torres M. Reactive oxygen species and cell signaling: Respiratory burst in macrophage signaling. Am J Respir Crit Care Med 2002; 166:S4–S8.
Stranges S, Laclustra M, Ji C, Cappuccio FP, Navas-Acien A, Ordovas JM et al.
Higher selenium status is associated with adverse blood lipid profile in British adults. J Nutr 2010; 140:81–87.
Nawrot TS, Staessen JA, Roels HA, Den Hond E, Thijs L, Fagard RH et al.
Blood pressure and blood selenium: a cross-sectional and longitudinal population study. Eur Heart J 2007; 28:628–633.
Berthold HK, Michalke B, Krone W, Guallar E, Gouni-Berthold I. Influence of serum selenium concentrations on hypertension: the lipid analytic cologne cross-sectional study. J Hypertens 2012; 30:1328–1335.
Zhuravlyova L, Filonenko M. The correlation between serum selenium level and cardiac biomarkers in patients with acute myocardial infarction. Arch Cardiovasc Dis Suppl 2016; 8:12.
Ghashut RA, Mc Millan DC, Kinsella J, Vasilaki AT, Talwar D, Duncan A. The effect of the systemic inflammatory response on plasma zinc and selenium adjusted for albumin. Clin Nutr 2016; 2:381–387.
Radchenko EN, Nizov AA, Ivanova AY, Sidorova YS. The content of selen in blood plasma in patients with acute Q-wave myocardial infarction. Vopr Pitan 2015; 84:64–69.
Chen A, Li G, Liu Y. Association between copper levels and myocardial infarction: a meta-analysis. Inhal Toxicol 2015; 27:237–246.
Afridi HI, Kazi TG, Talpur FN, Kazi A, Arain SS, Arain SA et al.
Interaction between selenium and mercury in biological samples of Pakistani myocardial infarction patients at different stages as related to controls. Biol Trace Elem Res 2014; 158:143–151.
Kutil B, Ostadal P, Vejvoda J, Kukacka J, Cepova J, Alan D et al.
Alteration in serum selenium levels and their relation to troponin I in acute myocardial infarction. Mol Cell Biochem 2010; 345:23–27.
Xun P, Liu K, Morris JS, Daviglus ML, He K. Longitudinal association between toenail selenium levels and measures of subclinical atherosclerosis: The CARDIA trace element study. Atherosclerosis 2010; 210:662–667.
Li S, Zheng MQ, Rozanski GJ. Glutathione homeostasis in ventricular myocytes from rat hearts with chronic myocardial infarction. Exp Physiol 2009; 94:815–824.
Tang NP, Wang LS, Yang L, Gu HJ, Sun QM, Cong RH et al.
Genetic variant in glutathione peroxidase 1 gene is associated with an increased risk of coronary artery disease in a Chinese population. Clin Chim Acta 2008; 395:89–93.
Hassanzadeh M, Faridhosseini R, Mahini M, Faridhosseini F, Ranjbar A. Serum levels of TNF-, IL-6, and selenium in patients with acute and chronic coronary artery disease. Iran J Immunol 2006; 3:142–145.
Wells EM, Navas-Acien A, Apelberg BJ, Herbstman JB. Association of selenium and copper with lipids in umbilical cord blood. J Dev Orig Health Dis 2014; 281:281–287.
Flores-Mateo G, Navas-Acien A, Pastor-Barriuso R, Guallar E. Selenium and coronary heart disease: a meta-analysis. Am J Clin Nutr 2006; 84:762–773.
Alanne M, Kristiansson K, Auro K, Silander K, Kuulasmaa K, Peltonen L et al.
Variation in the selenoprotein s gene locus is associated with coronary heart disease and ischemic stroke in two independent finnish cohorts. Hum Genet 2007; 122:355–365.
Lubos E, Sinning CR, Schnabel RB, Wild PS, Zeller T, Rupprecht HJ et al.
Serum selenium and prognosis in cardiovascular disease: results from the AtheroGene study. Atherosclerosis 2010; 209:271–277.
Navarro-Alarcon M, Cabrera-Vique C. Selenium in food and the human body: a review. Sci Total Environ 2008; 400:115–141.
Wen H, Carignan J. Reviews on atmospheric selenium: emissions, speciation and fate. Atmospheric Environ 2007; 41:7151–7165.
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10]