Effect of stress hyperglycaemia on monocyte chemoattractant protein‑1 levels and the short‑term prognosis of patients with acute ST‑segment elevation myocardial infarction undergoing primary percutaneous coronary intervention

  • Authors:
    • Nina Liu
    • Jianlong Sheng
    • Youmin Wang
  • View Affiliations

  • Published online on: March 4, 2019     https://doi.org/10.3892/etm.2019.7338
  • Pages: 3823-3829
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Abstract

The present study prospectively investigated the effect of blood glucose level at admission on monocyte chemoattractant protein‑1 levels at different time points before and after primary percutaneous coronary intervention, and the postoperative 1‑year prognosis of patients with acute ST‑segment elevation myocardial infarction. The 146 patients with acute ST‑segment elevation myocardial infarction undergoing primary percutaneous coronary intervention were divided into three groups: Group 1, non‑diabetic, non‑hyperglycemic group; group 2, stress hyperglycemia group; and group 3, diabetic group. Serum monocyte chemoattractant protein‑1 levels before and after percutaneous coronary intervention (PCI), and the incidence of major adverse cardiovascular events 1‑year post PCI were observed. The increase in monocyte chemoattractant protein‑1 levels 24 h after percutaneous coronary intervention, compared with those before percutaneous coronary intervention, was significantly correlated with the blood glucose level at admission. Furthermore, the 1‑year postoperative major adverse cardiovascular events rates were significantly higher in groups 2 and 3 compared with group 1. Logistic regression analysis demonstrated that a high blood glucose level at admission, diabetes, and high preoperative monocyte chemoattractant protein‑1 levels were risk factors for major adverse cardiovascular events 1‑year post‑percutaneous coronary intervention. Stress hyperglycemia and diabetes may contribute to high monocyte chemoattractant protein‑1 levels and prolonged inflammation. These symptoms are associated with poor prognosis of acute ST‑segment elevation myocardial infarction in patients undergoing primary percutaneous coronary intervention.

Introduction

Primary percutaneous coronary intervention (PCI) rapidly and completely restores blood flow in occluded coronary arteries in patients with acute myocardial infarction (AMI), thus effectively enabling the reperfusion of the infarcted myocardium, reducing the mortality rate and the incidence of cardiac endpoint events in AMI patients (1,2). However, for diabetic and non-diabetic patients, a high blood glucose level during AMI is associated with a poor AMI prognosis and somewhat affects the benefits of primary PCI (36). A random high blood glucose level at admission in non-diabetic patients with AMI is known as stress hyperglycemia (3).

It is not fully understood how stress hyperglycemia affects the prognosis of primary PCI (4,6,7). Previous studies have demonstrated that inflammation serves an important role in this process (810). Monocyte chemoattractant protein 1 (MCP-1) is an important inflammatory cytokine during the inflammatory response. MCP-1 serves roles in chemotaxis and the activation of monocytes/macrophages, the upregulation of the expression of monocyte/macrophage adhesion molecules and the production of inflammatory cytokines including interleukin (IL) 1 and 6, chemotaxis and the activation of basophils (1113). These result in the release of histamine and inflammatory responses that may be associated with vascular injury, the development of atherosclerosis, plaque instability and restenosis following coronary stenting (14,15). MCP-1 may serve an important role in the mechanism by which stress hyperglycemia affects the prognosis of AMI, but limited data are available regarding these associations and further studies are required to confirm this.

A prospective study was conducted to investigate MCP-1 levels at different time points before and after primary PCI, and the prognosis of patients with acute ST-segment elevation myocardial infarction (ASTEMI) 1-year post-PCI. Blood glucose levels were also measured at admission to explore how stress hyperglycemia affects the prognosis of primary PCI.

Materials and methods

Subjects

A total of 146 patients (age range, 35–80 years; average age, 60.1 years) with ASTEMI who successfully underwent primary PCI within 12 h of onset at the Second Affiliated Hospital of Anhui Medical University between December 2014 and December 2016 were included in the present study. Each patient and/or his/her family provided informed consent for PCI and written informed consent for the present study. Ethics approval for the study was granted from the Second Affiliated Hospital of Anhui Medical University Ethics Committee. ASTEMI was diagnosed according to the Third Universal Definition of the myocardial infarction document, as described previously (16). ASTEMI was defined as complaints of chest pain with ECG signs compatible with AMI (ST-segment elevation >2 mm in precordial leads and >1 mm in limb leads). Patients were included in the current study if they were diagnosed with ASTEMI, over the age of 18 years and were successfully treated with PCI. Patients with the following conditions were excluded: Severe peripheral vascular disease, peptic ulcer, coagulation disorders, severe infections, tumors, and connective tissue diseases, along with patients who succumbed within 48 h of admission or did not successfully undergo PCI (as the study required monitoring of MCP-1 levels for 48 h post-operatively).

Group assignment

Eligible patients with ASTEMI were divided into three groups (groups 1, 2 and 3), according to history of diabetes, blood glucose level at admission, and glycated hemoglobin A1c (HbA1c) level. The glucose oxidase method by automated analyzer was utilized to measure blood glucose levels (17). Group 1 was the non-diabetic, non-hyperglycemic group (blood glucose at admission <8.0 mmol/l); group 2 was the stress hyperglycemia group (non-diabetic, hyperglycemic group; blood glucose at admission ≥8.0 mmol/l); and group 3 was the diabetic group. Non-diabetic patients were defined by having no history of diabetes, with fasting blood glucose levels 24 h after admission, 2-h postprandial blood glucose levels and HbA1c levels that were incompatible with the diagnostic criteria of diabetes. Diabetes was diagnosed according to the Standards of Medical Care in Diabetes (2014) from the American Diabetes Association (18).

Perioperative medications

Prior to PCI, patients were routinely given 300 mg aspirin (Bayer AG, Leverkusen, Germany) and 300 mg clopidogrel (Sanofi S.A., Paris, France) by oral administration. Upon successful puncture, 3,000 IU unfractionated heparin was given via an arterial sheath. After coronary angiography and before PCI, additional unfractionated heparin was given via an arterial sheath (until 100 IU/kg). Additionally, 2,000 IU heparin was given each additional hour during PCI to maintain an activated clotting time ≥300 sec. Following PCI, aspirin, clopidogrel, angiotensin-converting enzyme inhibitors (Perindopril, 2–8 mg daily according to patient blood pressure; Servier, Suresnes, France) and β-blockers (Metoprolol succinate, 23.75–95 mg daily according to patient heart rate; Astrazeneca, Cambridge, UK) were routinely administered, unless otherwise contraindicated.

Cardiovascular events

The incidence of cardiovascular events during hospitalization (severe arrhythmias intra-PCI, severe heart failure and mortality) and of major adverse cardiovascular events (MACEs), including cardiogenic death, non-fatal myocardial infarction, target vessel revascularization, and severe heart failure occurring within one year after PCI were observed. Severe arrhythmia was defined as sinus arrest for ≥3 sec, grade 2 (or above) type II atrioventricular block, ventricular tachycardia and ventricular fibrillation. Severe heart failure was defined as class IV, according to the criteria of the New York Heart Association (19).

MCP-1 sample collection and testing

Blood samples (3 ml) were collected from the cubital vein prior to PCI (at admission), 24 and 48 h after PCI into a standard serum tube (no anticoagulant), followed by centrifugation at 1,006.2 × g for 10 min at room temperature. The upper layer of serum was collected into a test tube, which was sealed and stored at −80°C for later use. The MCP-1 level was measured by ELISA (cat. no. SEA087Hu; Cloud-Clone Corp., Wuhan, China).

Statistical analysis

Data are expressed as the mean ± standard deviation. A Kolmogorov-Smirnov test was performed to verify the normality of the distribution. For normally distributed data, one-way analysis of variance was performed to analyze differences among the groups and the least significant difference was calculated to analyze between-group differences. Non-normally distributed measurement data or measurement data with heterogeneous variance were analyzed using the K independent samples method. Count data were analyzed with a χ2 test. Correlations of measurement data with a normal distribution were analyzed with Pearson's correlation analysis. For non-normally distributed measurement data, Spearman's rank correlation analysis was used. Partial correlation analysis was applied to eliminate the influence of certain factors. P<0.05 was considered to indicate a statistically significant difference. Risk factors for MACEs 1-year post-PCI were analyzed using binary logistic regression analysis. SPSS V19.0 (IBM Corp., Armonk, NY, USA) was used for statistical analysis.

Results

General information

A total of 146 patients with ASTEMI were eligible to participate, of which 128 were men and 18 women, with an average age of 60.1±11.0 years. Groups 1, 2, and 3 included 56, 50 and 40 patients, respectively. No significant differences among the groups were observed in age, sex, peak creatine kinase level, blood lipid profile, smoking history, history of hypertension or history of cerebrovascular disease. Blood glucose level at admission was significantly higher in group 3 (diabetic group) compared with groups 1 and 2 (P<0.05; Table I).

Table I.

Baseline clinical characteristics.

Table I.

Baseline clinical characteristics.

VariablesGroup 1 (n=56)Group 2 (n=50)Group 3 (n=40)
Male sex (%)52 (92.9)40 (80.0)36 (90.0)
Female sex (%)4 (7.1)10 (20)4 (10)
Age (years)58.9±11.061.2±10.160.5±12.0
Smoking history (%)26 (46.4)26 (52.0)20 (50.0)
Hypertensive disease (%)22 (39.3)24 (48.0)24 (60.0)
Cerebrovascular disease (%)  6 (10.7)  6 (12.0)  4 (10.0)
Blood glucose on admission (mmol/l)6.73±0.92 9.61±1.40a 12.78±3.32a,b
Total cholesterol (mmol/l)4.31±0.904.59±0.964.52±0.85
TG (mmol/l)1.52±0.701.61±0.911.79±0.78
HDL (mmol/l)1.05±0.350.99±0.251.02±0.30
LDL (mmol/l)2.66±0.702.89±0.722.73±0.65
VLDL (mmol/l)0.42±0.270.44±0.270.46±0.21
LP-a (mmol/l)0.19±0.160.17±0.110.18±0.09
CK (U/l)2699±14192744±15102866±1323

a P<0.05 vs. group 1

b P<0.05 vs. group 2. CK, creatine kinase; HDL-C, high-density lipoprotein cholesterol; LDL-C, Low-density lipoprotein cholesterol; TG, triglyceride; VLDL, very-low-density lipoprotein; LP-a, lipoprotein-a.

Coronary intervention-associated data

The comparison of coronary angiography results of each group during primary PCI reveled that more patients had multivessel lesions in group 3 (diabetic group) compared with groups 1 and 2 (P<0.05). No significant among-group differences were observed in infarction-related artery, from AMI onset to reperfusion treatment, or maximum dilating pressure during PCI (P<0.05; Table II). This indicates that these factors do not affect the differences in MCP-1 levels among groups.

Table II.

Characteristics of primary PCI.

Table II.

Characteristics of primary PCI.

Infarction-related artery

GroupnLADRCALCXMultivessel disease (%)Time of onset to reperfusion (h)Maximum pressure of expansion (kPa)
Group 1562662430 (53.6)5.61±2.01 1,432.75±256.32
Group 2503061428 (56.0)5.83±1.61 1,408.25±262.38
Group 3402021836 (90.0)a,b5.97±1.791,418.4±256.26

a P<0.05 vs. group 1

b P<0.05 vs. group 2. LAD, left anterior descending artery; LCX, left circumflex artery; PCI, percutaneous coronary intervention; RCA, right coronary artery.

MCP-1 levels

The MCP-1 levels were higher 24 h following PCI compared with prior to PCI in all three groups (P<0.05), particularly in group 2 (stress hyperglycaemia group) and group 3 (diabetic group; P<0.001; Fig. 1). High MCP-1 levels 48 h after PCI were sustained, whereas the MCP-1 levels significantly decreased 48 h after PCI compared with 24 h after PCI in group 1 (non-diabetic, non-hyperglycemic group; P<0.05; Fig. 1).

Significant differences were observed in MCP-1 levels at different time points: MCP-1 levels were significantly higher in groups 2 and 3 compared with group 1, both before PCI and 24 and 48 h after PCI (P<0.05; Fig. 1).

Cardiovascular events during hospitalization

No patients with ASTEMI succumbed during hospitalization. The incidences of intraoperative severe arrhythmias and severe heart failure during hospitalization were higher in groups 2 and 3 compared with group 1, but the differences did not reach statistical significance (P>0.05; Fig. 2).

One-year post-PCI MACEs

The 1-year postoperative MACE rate was higher in groups 2 and 3 compared with group 1 (P<0.05), with no significant difference between groups 2 and 3 (Table III). Variables including blood glucose level at admission, age, diabetes, hypertension, smoking history, history of cerebrovascular diseases, infarction-related artery, multivessel lesions, time from AMI onset to reperfusion treatment, MCP-1 levels before PCI and 24 and 48 h after PCI, and blood lipids were incorporated into binary logistic regression analysis. The results demonstrated that blood glucose level at admission (Wald=4.286, β=2.146, P=0.038), diabetes (Wald=9.165, β=58.086, P=0.002), and preoperative MCP-1 levels (Wald=15.991, β=1.024, P<0.001) were risk factors for MACEs occurring within 1 year after PCI. This indicates that the increased level of blood glucose and MCP-1 at admission, as well as diabetes, were the risk factors for the occurrence of MACE 1 year following primary PCI in patients with ASTEMI.

Table III.

MACE in the 1-year postoperative period.

Table III.

MACE in the 1-year postoperative period.

GroupnMACE (%)Cardiac deaths (%)Non-death AMI (%)Target vessel revascularization (%)Severe heart failure (%)
Group 15614 (25.0)5 (8.9)6 (10.7)4 (7.1)9 (16.1)
Group 25022 (44.0)a6 (12.0)8 (16.0)8 (16.0)12 (24.0)
Group 34020 (50.0)a5 (12.5)8 (20.0)6 (15.0)14 (35.0)

a P<0.05 vs. group 1. AMI, acute myocardial infarction; MACE, major adverse cardiovascular events.

Discussion

The present study demonstrated that the blood glucose level can be higher at admission not only for patients with ASTEMI with diabetes, but also for certain patients with ASTEMI without diabetes. The latter condition is called stress hyperglycaemia (3), which is defined as the first random blood glucose level tested post-admission being no less than 8.0 mmol/l. Among non-diabetic patients, patients with stress hyperglycaemia had higher preoperative and postoperative MCP-1 levels compared with those without hyperglycaemia at admission. Furthermore, patients with stress hyperglycaemia and diabetes had a higher rate of MACEs occurring within 1 year after PCI compared with non-hyperglycemic patients. This result indicated that for patients with ASTEMI, stress hyperglycaemia and diabetes are associated with a poor prognosis post-PCI.

Diabetes is an independent risk factor for coronary heart disease (20). Patients with coronary heart disease and diabetes frequently have multiple, severe and complicated coronary artery lesions (21). The present study also demonstrated that the incidence of multivessel lesions was significantly higher in diabetic patients with AMI compared with non-diabetic patients with AMI. Furthermore, patients with diabetes are characterized by chronic hyperglycaemia; during AMI, glucose metabolism disorders may worsen, resulting in a further increase in the blood glucose level at admission (3,4). It is known that patients with AMI and diabetes have a poor prognosis following PCI (2224). However, in the case of AMI, not only patients with diabetes have elevated blood glucose, but patients who have not been previously diagnosed with diabetes may have elevated blood glucose at admission (46). This is termed stress hyperglycaemia.

During AMI, this stress hyperglycaemia is usually transient and is eliminated as AMI is stabilized. However, certain patients may develop diabetes in the future due to insulin resistance (25,26), while a previous study reported that high blood glucose at admission is unrelated to diabetes in the future (27). Regardless of the association between stress hyperglycaemia and diabetes, a number of studies have demonstrated that stress hyperglycaemia is associated with a poor prognosis in AMI (4,6,7).

Researchers continue to debate whether stress hyperglycaemia indicates the severity of the condition of patients with AMI or if hyperglycaemia itself may damage cardiac function (28,29). The mechanism by which stress hyperglycaemia affects the prognosis of AMI is not fully understood (6,7). Studies have shown that inflammation serves an important role in this process (810,30,31). The study of Marfella et al (31) demonstrated that during AMI, hyperglycaemia was associated with increased levels of inflammatory markers, enhanced expression of cytotoxic T-cells, and reduced expression of suppressor T-cells. There was a positive correlation between stress hyperglycaemia and poor cardiac outcomes in patients with AMI (31). The study primarily confirmed the involvement of lymphocytes in the effects of stress hyperglycaemia on cardiac function in AMI. However, monocytes/macrophages are important immune cells in the body, similar to lymphocytes. Following AMI, monocytes/macrophages are rapidly recruited to the infarct zone, where they promote wound healing and ventricular remodeling (32,33). MCP-1 is an important inflammatory cytokine during the process of monocyte/macrophage activation. To the best of our knowledge, there is a lack of studies investigating the effect of stress hyperglycaemia on perioperative MCP-1 levels in patients with AMI undergoing PCI and the associated dynamic changes, thus the present study focused on this.

Patients with diabetes frequently have high baseline levels of MCP-1 (34,35). The present study also demonstrated that for patients with ASTEMI, the MCP-1 levels pre-PCI were significantly higher in patients with diabetes compared with non-diabetic patients. Furthermore, due to AMI and PCI, the MCP-1 levels increased more significantly following PCI in patients with diabetes, indicating that patients with diabetes were more sensitive to certain inflammatory stimuli.

In addition, the present study indicated that MCP-1 levels at different time points before and after PCI were higher. It also demonstrated that high MCP-1 levels lasted longer (maintained for 48 h after PCI) in patients with stress hyperglycaemia compared with non-diabetic and non-hyperglycemic patients, with no significant difference from the trend observed in patients with diabetes. Stress hyperglycaemia is usually transient; the blood glucose level usually returns to normal at discharge, indicating that stress hyperglycaemia is unrelated to the sustained expression of inflammatory cytokines due to chronic hyperglycaemia (36). El-Osta et al (37) described that transient hyperglycaemia induces long-lasting activating epigenetic alterations in the promoter of nuclear factor-κ B subunit p65 in aortic endothelial cells, which causes p65 gene expression to increase. The epigenetic and gene expression alterations persist for at least 6 days after normal physiological glucose levels are restored, inducing increases in MCP-1 and vascular cell adhesion molecule 1 expression. The study of El-Osta et al (37) reported that hyperglycaemia in patients with stress hyperglycaemia, although transient, may still result in days of activation of the upstream signaling pathway of MCP-1 expression. This observation was confirmed by the serum MCP-1 levels in the patients with ASTEMI in the present study.

Furthermore, the present study demonstrated that for non-diabetic patients, the increase in MCP-1 levels after PCI compared with those prior to PCI was significantly associated with blood glucose level at admission in a dose-dependent manner, indicating that hyperglycaemia itself may be associated with elevated chemokine levels and may prolong the effects of chemokines. Hyperglycaemia may increase the expression levels of MCP-1 and MCP-1-induced protein, thereby enhancing the effects of reactive oxygen species, endoplasmic reticulum and autophagy, resulting in myocardial apoptosis (30). This enhancement may increase the incidence of no-reperfusion during primary PCI in patients with AMI, resulting in myocardial microcirculation thrombosis (3840), an increase in the area of AMI (41). It could also have an effect on the post-PCI cardiac recovery of patients with AMI (42), and subsequently higher post-PCI MACE rate in patients with hyperglycemia compared with non-hyperglycemic patients. These effect of hyperglycaemia on the expression of MCP-1 may represent one of the mechanisms by which stress hyperglycaemia affects the prognosis of AMI.

In conclusion, the present study demonstrated that stress hyperglycaemia was associated with elevated serum MCP-1 levels in patients with ASTEMI undergoing primary PCI and may enhance and prolong MCP-1-associated inflammatory responses resulting in a poor prognosis post-PCI. This indicates that stress hyperglycaemia may affect the prognosis of patients with ASTEMI undergoing primary PCI via elevated MCP-1 levels. Thus, blocking excessively high MCP-1 levels may become a potential option for improving the prognosis of patients with ASTEMI following primary PCI, though further research is required to validate these results.

In the present study, patients with unsuccessful PCI or those who succumbed within 48 h of admission were excluded, as this study required monitoring of MCP-1 levels for 48 h after PCI; this exclusion may result in selection bias. As for ethical considerations, no interventions were given for MCP-1 levels to further verify the association between MCP-1 levels and poor prognosis. In addition, the sample size was small, and the study period was short. Thus, the long-term prognoses of the subjects in this study should be monitored and large multicenter studies are required to further validate these results. The current study revealed that stress hyperglycemia and high monocyte chemoattractant protein-1 levels at admission are risk factors for the adverse prognosis of patients with ASTEMI undergoing primary PCI. Therefore, patients with ASTEMI exhibiting such biochemical abnormalities should have more medical attention paid to them.

Acknowledgements

Not applicable.

Funding

No funding was received.

Availability of data and materials

The datasets used and/or analyzed during the present study are available from the corresponding author on reasonable request.

Authors' contributions

YW conceived and designed the current study, and revised the manuscript critically for important intellectual content. NL and JS collected, analyzed and interpreted the data. NL wrote the manuscript. All authors read and approved the final version of the manuscript.

Ethics approval and consent to participate

Ethics approval for the study was granted from the Second Affiliated Hospital of Anhui Medical University Ethics Committee. Each patient and/or his/her family provided written informed consent for the study.

Patient consent for publication

Not applicable.

Competing interests

The authors declare that they have no competing interests.

References

1 

Task Force on Myocardial Revascularization of The European Society of Cardiology (ESC), the European Association for Cardio-Thoracic Surgery (EACTS)1; European Association for Percutaneous Cardiovascular Interventions (EAPCI), ; Wijns W, Kolh P, Danchin N, Di Mario C, Falk V, Folliguet T, Garg S, Huber K, et al: Guidelines on myocardial revascularization. Eur Heart J. 31:2501–2555. 2010. View Article : Google Scholar : PubMed/NCBI

2 

Keeley EC, Boura JA and Grines CL: Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: A quantitative review of 23 randomised trials. Lancet. 361:13–20. 2003. View Article : Google Scholar : PubMed/NCBI

3 

Capes SE, Hunt D, Malmberg K and Gerstein HC: Stress hyperglycaemia and increased risk of death after myocardial infarction in patients with and without diabetes: A systematic overview. Lancet. 355:773–778. 2000. View Article : Google Scholar : PubMed/NCBI

4 

Straumann E, Kurz DJ, Muntwyler J, Stettler I, Furrer M, Naegeli B, Frielingsdorf J, Schuiki E, Mury R, Bertel O and Spinas GA: Admission glucose concentrations independently predict early and late mortality in patients with acute myocardial infarction treated by primary or rescue percutaneous coronary intervention. Am Heart J. 150:1000–1006. 2005. View Article : Google Scholar : PubMed/NCBI

5 

Timmer JR, Hoekstra M, Nijsten MW, van der Horst IC, Ottervanger JP, Slingerland RJ, Dambrink JH, Bilo HJ, Zijlstra F and van't Hof AW: Prognostic value of admission glycosylated hemoglobin and glucose in nondiabetic patients with ST-segment-elevation myocardial infarction treated with percutaneous coronary intervention. Circulation. 124:704–711. 2011. View Article : Google Scholar : PubMed/NCBI

6 

Yang Y, Kim TH, Yoon KH, Chung WS, Ahn Y, Jeong MH, Seung KB, Lee SH and Chang K: The stress hyperglycaemia ratio, an index of relative hyperglycaemia, as a predictor of clinical outcomes after percutaneous coronary intervention. Int J Cardiol. 241:57–63. 2017. View Article : Google Scholar : PubMed/NCBI

7 

Kim EJ, Jeong MH, Kim JH, Ahn TH, Seung KB, Oh DJ, Kim HS, Gwon HC, Seong IW, Hwang KK, et al: KAMIR-NIH registry investigators: Clinical impact of admission hyperglycaemia on in-hospital mortality in acute myocardial infarction patients. Int J Cardiol. 236:9–15. 2017. View Article : Google Scholar : PubMed/NCBI

8 

Kosuge M, Kimura K, Kojima S, Sakamoto T, Matsui K, Ishihara M, Asada Y, Tei C, Miyazaki S, Sonoda M, et al: Effects of glucose abnormalities on in-hospital outcome after coronary intervention for acute myocardial infarction. Circ J. 69:375–379. 2005. View Article : Google Scholar : PubMed/NCBI

9 

Worthley MI, Holmes AS, Willoughby SR, Kucia AM, Heresztyn T, Stewart S, Chirkov YY, Zeitz CJ and Horowitz JD: The deleterious effects of hyperglycaemia on platelet function in diabetic patients with acute coronary syndromes mediation by superoxide production, resolution with intensive insulin administration. J Am Coll Cardiol. 49:304–310. 2007. View Article : Google Scholar : PubMed/NCBI

10 

Ray KK, Cannon CP, Morrow DA, Kirtane AJ, Buros J, Rifai N, McCabe CH, Gibson CM and Braunwald E: Synergistic relationship between hyperglycaemia and inflammation with respect to clinical outcomes in non-ST-elevation acute coronary syndromes: Analyses from OPUS-TIMI 16 and TACTICS-TIMI 18. Eur Heart J. 28:806–813. 2007. View Article : Google Scholar : PubMed/NCBI

11 

Ikeda U, Matsui K, Murakami Y and Shimada K: Monocyte chemoattractant protein-1 and coronary artery disease. Clin Cardiol. 25:143–147. 2002. View Article : Google Scholar : PubMed/NCBI

12 

de Léséleuc L, Orlova M, Cobat A, Girard M, Huong NT, Ba NN, Thuc NV, Truman R, Spencer JS, Adams L, et al: PARK2 mediates interleukin 6 and monocyte chemoattractant protein 1 production by human macrophages. PLoS Negl Trop Dis. 7:e20152013. View Article : Google Scholar : PubMed/NCBI

13 

Liu L, Gao XJ, Ren CG, Hu JH, Liu XW, Zhang P, Zhang ZW and Fu ZJ: Monocyte chemoattractant protein-1 contributes to morphine tolerance in rats with cancer-induced bone pain. Exp Ther Med. 13:461–466. 2017. View Article : Google Scholar : PubMed/NCBI

14 

Cipollone F, Marini M, Fazia M, Pini B, Iezzi A, Reale M, Paloscia L, Materazzo G, D'Annunzio E, Conti P, et al: Elevated circulating levels of monocyte chemoattractant protein-1 in patients with restenosis after coronary angioplasty. Arterioscler Thromb Vasc Biol. 21:327–334. 2001. View Article : Google Scholar : PubMed/NCBI

15 

Heil M, Ziegelhoeffer T, Wagner S, Fernández B, Helisch A, Martin S, Tribulova S, Kuziel WA, Bachmann G and Schaper W: Collateral artery growth (arteriogenesis) after experimental arterial occlusion is impaired in mice lacking CC-chemokine receptor-2. Circ Res. 94:671–677. 2004. View Article : Google Scholar : PubMed/NCBI

16 

Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, White HD, Thygesen K, Alpert JS, White HD; Writing Group on the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction, ; et al: Third universal definition of myocardial infarction. Eur Heart J. 33:2551–2567. 2012. View Article : Google Scholar : PubMed/NCBI

17 

Yuen VG and McNeill JH: Comparison of the glucose oxidase method for glucose determination by manual assay and automated analyzer. J Pharmacol Toxicol Methods. 44:543–546. 2000. View Article : Google Scholar : PubMed/NCBI

18 

American Diabetes Association: Standards of medical care in diabetes-2014. Diabetes Care. 37 (Suppl 1):S14–S80. 2014. View Article : Google Scholar : PubMed/NCBI

19 

Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland JGF, Coats AJS, Falk V, González-Juanateyr JR, Harjola VP, Jankowska EA, et al: 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail. 18:891–975. 2016. View Article : Google Scholar : PubMed/NCBI

20 

Wang C, Li F, Guo J, Li C, Xu D and Wang B: Insulin resistance, blood glucose and inflammatory cytokine levels are risk factors for cardiovascular events in diabetic patients complicated with coronary heart disease. Exp Ther Med. 15:1515–1519. 2018.PubMed/NCBI

21 

Xu W, Tian M and Zhou Y: The relationship between insulin resistance, adiponectin and C-reactive protein and vascular endothelial injury in diabetic patients with coronary heart disease. Exp Ther Med. 16:2022–2026. 2018.PubMed/NCBI

22 

Antoniucci D, Valenti R, Migliorini A, Parodi G, Moschi G, Memisha G, Santoro GM and Cerisano G: Impact of insulin-requiring diabetes mellitus on effectiveness of reperfusion and outcome of patients undergoing primary percutaneous coronary intervention for acute myocardial infarction. Am J Cardiol. 93:1170–1172. 2004. View Article : Google Scholar : PubMed/NCBI

23 

Timmer JR, van der Horst IC, de Luca G, Ottervanger JP, Hoorntje JC, de Boer MJ, Suryapranata H, Dambrink JH, Gosselink M, Zijlstra F, et al: Zwolle Myocardial Infarction Study Group: Comparison of myocardial perfusion after successful primary percutaneous coronary intervention in patients with ST-elevation myocardial infarction with versus without diabetes mellitus. Am J Cardiol. 95:1375–1377. 2005. View Article : Google Scholar : PubMed/NCBI

24 

Prasad A, Stone GW, Stuckey TD, Costantini CO, Zimetbaum PJ, McLaughlin M, Mehran R, Garcia E, Tcheng JE, Cox DA, et al: Impact of diabetes mellitus on myocardial perfusion after primary angioplasty in patients with acute myocardial infarction. J Am Coll Cardiol. 45:508–514. 2005. View Article : Google Scholar : PubMed/NCBI

25 

Knudsen EC, Seljeflot I, Abdelnoor M, Eritsland J, Mangschau A, Arnesen H and Andersen GO: Abnormal glucose regulation in patients with acute ST-elevation myocardial infarction-a cohort study on 224 patients. Cardiovasc Diabetol. 8:62009. View Article : Google Scholar : PubMed/NCBI

26 

Terlecki M, Bryniarski L, Bednarek A, Kocowska M, Kawecka-Jaszcz K and Czarnecka D: The risk of diabetes development in long-term observation of patients with acute hyperglycaemia during myocardial infarction. Kardiol Pol. 73:606–612. 2015. View Article : Google Scholar : PubMed/NCBI

27 

Ishihara M, Inoue I, Kawagoe T, Shimatani Y, Kurisu S, Hata T, Nakama Y, Kijima Y and Kagawa E: Is admission hyperglycaemia in non-diabetic patients with acute myocardial infarction a surrogate for previously undiagnosed abnormal glucose tolerance? Eur Heart J. 27:2413–2419. 2006. View Article : Google Scholar : PubMed/NCBI

28 

Ishihara M: Acute hyperglycemia in patients with acute myocardial infarction. Circ J. 76:563–571. 2012. View Article : Google Scholar : PubMed/NCBI

29 

Roberts GW, Quinn SJ, Valentine N, Alhawassi T, O'Dea H, Stranks SN, Burt MG and Doogue MP: Relative hyperglycemia, a marker of critical illness: Introducing the stress hyperglycemia ratio. J Clin Endocrinol Metab. 100:4490–4497. 2015. View Article : Google Scholar : PubMed/NCBI

30 

Younce CW, Wang K and Kolattukudy PE: Hyperglycaemia-induced cardiomyocyte death is mediated via MCP-1 production and induction of a novel zinc-finger protein MCPIP. Cardiovasc Res. 87:665–674. 2010. View Article : Google Scholar : PubMed/NCBI

31 

Marfella R, Siniscalchi M, Esposito K, Sellitto A, De Fanis U, Romano C, Portoghese M, Siciliano S, Nappo F, Sasso FC, et al: Effects of stress hyperglycemia on acute myocardial infarction: Role of inflammatory immune process in functional cardiac outcome. Diabetes Care. 26:3129–3135. 2003. View Article : Google Scholar : PubMed/NCBI

32 

Birdsall HH, Green DM, Trial J, Youker KA, Burns AR, MacKay CR, LaRosa GJ, Hawkins HK, Smith CW, Michael LH, et al: Complement C5a, TGF-beta 1, and MCP-1, in sequence, induce migration of monocytes into ischemic canine myocardium within the first one to five hours after reperfusion. Circulation. 95:684–692. 1997. View Article : Google Scholar : PubMed/NCBI

33 

Niu J, Jin Z, Kim H and Kolattukudy PE: MCP-1-induced protein attenuates post-infarct cardiac remodeling and dysfunction through mitigating NF-κB activation and suppressing inflammation-associated microRNA expression. Basic Res Cardiol. 110:262015. View Article : Google Scholar : PubMed/NCBI

34 

Zietz B, Büchler C, Herfarth H, Müller-Ladner U, Spiegel D, Schölmerich J and Schäffler A: Caucasian patients with type 2 diabetes mellitus have elevated levels of monocyte chemoattractant protein-1 that are not influenced by the −2518 A->G promoter polymorphism. Diabetes Obes Metab. 7:570–578. 2005. View Article : Google Scholar : PubMed/NCBI

35 

Piemonti L, Calori G, Lattuada G, Mercalli A, Ragogna F, Garancini MP, Ruotolo G, Luzi L and Perseghin G: Association between plasma monocyte chemoattractant protein-1 concentration and cardiovascular disease mortality in middle-aged diabetic and nondiabetic individuals. Diabetes Care. 32:2105–2110. 2009. View Article : Google Scholar : PubMed/NCBI

36 

Tenerz A, Norhammar A, Silveira A, Hamsten A, Nilsson G, Rydén L and Malmberg K: Diabetes, insulin resistance, and the metabolic syndrome in patients with acute myocardial infarction without previously known diabetes. Diabetes Care. 26:2770–2776. 2003. View Article : Google Scholar : PubMed/NCBI

37 

El-Osta A, Brasacchio D, Yao D, Pocai A, Jones PL, Roeder RG, Cooper ME and Brownlee M: Transient high glucose causes persistent epigenetic changes and altered gene expression during subsequent normoglycemia. J Exp Med. 205:2409–2417. 2008. View Article : Google Scholar : PubMed/NCBI

38 

Ishihara M, Kojima S, Sakamoto T, Asada Y, Tei C, Kimura K, Miyazaki S, Sonoda M, Tsuchihashi K, Yamagishi M, et al: Acute hyperglycemia is associated with adverse outcome after acute myocardial infarction in the coronary intervention era. Am Heart J. 150:814–820. 2005. View Article : Google Scholar : PubMed/NCBI

39 

Iwakura K, Ito H, Ikushima M, Kawano S, Okamura A, Asano K, Kuroda T, Tanaka K, Masuyama T, Hori M and Fujii K: Association between hyperglycemia and the no-reflow phenomenon in patients with acute myocardial infarction. J Am Coll Cardiol. 41:1–7. 2003. View Article : Google Scholar : PubMed/NCBI

40 

Ota S, Tanimoto T, Orii M, Hirata K, Shiono Y, Shimamura K, Matsuo Y, Yamano T, Ino Y, Kitabata H, et al: Association between hyperglycemia at admission and microvascular obstruction in patients with ST-segment elevation myocardial infarction. J Cardiol. 65:272–277. 2015. View Article : Google Scholar : PubMed/NCBI

41 

Pak S, Yatsynovich Y and Markovic JP: A meta-analysis on the correlation between admission hyperglycemia and myocardial infarct size on CMRI. Hellenic J Cardiol. 59:174–178. 2018. View Article : Google Scholar : PubMed/NCBI

42 

Ishihara M, Inoue I, Kawagoe T, Shimatani Y, Kurisu S, Nishioka K, Umemura T, Nakamura S and Yoshida M: Impact of acute hyperglycemia on left ventricular function after reperfusion therapy in patients with a first anterior wall acute myocardial infarction. Am Heart J. 146:674–678. 2003. View Article : Google Scholar : PubMed/NCBI

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May-2019
Volume 17 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Liu N, Sheng J and Wang Y: Effect of stress hyperglycaemia on monocyte chemoattractant protein‑1 levels and the short‑term prognosis of patients with acute ST‑segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. Exp Ther Med 17: 3823-3829, 2019
APA
Liu, N., Sheng, J., & Wang, Y. (2019). Effect of stress hyperglycaemia on monocyte chemoattractant protein‑1 levels and the short‑term prognosis of patients with acute ST‑segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. Experimental and Therapeutic Medicine, 17, 3823-3829. https://doi.org/10.3892/etm.2019.7338
MLA
Liu, N., Sheng, J., Wang, Y."Effect of stress hyperglycaemia on monocyte chemoattractant protein‑1 levels and the short‑term prognosis of patients with acute ST‑segment elevation myocardial infarction undergoing primary percutaneous coronary intervention". Experimental and Therapeutic Medicine 17.5 (2019): 3823-3829.
Chicago
Liu, N., Sheng, J., Wang, Y."Effect of stress hyperglycaemia on monocyte chemoattractant protein‑1 levels and the short‑term prognosis of patients with acute ST‑segment elevation myocardial infarction undergoing primary percutaneous coronary intervention". Experimental and Therapeutic Medicine 17, no. 5 (2019): 3823-3829. https://doi.org/10.3892/etm.2019.7338