Free IGF-1, Intact IGFBP-4, and PicoPAPP-A are Altered in Acute Myocardial Infarction Compared to Stable Coronary Artery Disease and Healthy Controls

2018 ◽  
Vol 51 (02) ◽  
pp. 112-119 ◽  
Author(s):  
Athanasios Anastasilakis ◽  
Dimitrios Koulaxis ◽  
Jagriti Upadhyay ◽  
Eirini Pagkalidou ◽  
Nikoleta Kefala ◽  
...  

AbstractInsulin-like growth factor-1 (IGF-1) and its binding proteins have been implicated in the pathophysiology of coronary artery disease (CAD) and myocardial infarction (MI). We investigated components of the IGF-1 system in circulation at the time of acute MI and following reperfusion in relation to levels of stable CAD patients and controls. Patients with MI (MI Group, n=31) treated with percutaneous coronary intervention (PCI) were compared to patients with stable CAD subjected to scheduled PCI (CAD Group, n=40) and controls with symptoms mimicking CAD without stenosis in angiography (Control Group, n=43). The number and extent of stenosis were recorded. Total and free IGF-1, total and intact IGF binding protein (IGFBP)-3 and -4, pico-Pregnancy Associated Plasma Protein-A (PAPP-A), and the known markers ALT, AST, CK and CK-MB were measured at baseline and 6 or 24 h after the intervention. Patients with MI had higher free IGF-1 (p=0.003) and PAPP-A (p=0.011), but lower intact IGFBP-4 (p=0.006) compared with patients with stable CAD or healthy controls. None of the investigated molecules changed following reperfusion or correlated with the extent of stenosis. AST (p<0.001), CK (p<0.001) and CK-MB (p<0.001), were also higher. Free IGF-1, intact IGFBP-4 and PAPP-A could predict MI, but with lower accuracy than CK-MB. In conclusion, free IGF-1 levels are higher in MI compared to CAD patients and controls and this could result from increased cleavage of its binding protein IGFBP-4 by the higher PAPP-A levels. Free IGF-1, intact IGFBP-4, and/or PAPP-A are inferior to CK-MB as predictors or markers of myocardial damage.

2016 ◽  
Vol 39 (3) ◽  
pp. 79 ◽  
Author(s):  
Mehmet N Akkus ◽  
Adil Ormam ◽  
Sabri Seyis ◽  
Çagdas Baran ◽  
Aysegül Görür ◽  
...  

Purpose: The purpose of this study was to determine whether the plasma levels of soluble extracellular matrix metalloproteinase inducer (EMMPRIN) differed among the patients with ST-elevation myocardial infarction (STEMI), non-STEMI (NSTEMI) and stable coronary artery disease (CAD) and the healthy controls, and to identify the factors associated with the differences in plasma levels of this this protein among patients in these groups. Methods: Plasma EMMPRIN levels were compared among four age- and sex-matched groups of patients with STEMI, NSTEMI and stable CAD and healthy controls (n=44 per group), then logistic regression and correlation analyses were conducted for the whole acute myocardial infarction (AMI) patients group. Results: EMMPRIN levels were significantly higher in the STEMI (39.4±9.2ng/mL) and NSTEMI (37.1±10.5ng/mL) groups than in either the stable CAD (27.5±4.7ng/mL) or control (24.5±5.8ng/mL) groups (p


2010 ◽  
Vol 104 (11) ◽  
pp. 1029-1037 ◽  
Author(s):  
Naglaa Idriss ◽  
Gregory Lip ◽  
Balu Balakrishnan ◽  
Rumi Jaumdally ◽  
Christopher Boos ◽  
...  

SummaryIt was the aim of this study to determine plasma haemoxygenase-1 (HO-1) across the spectrum of health, angina but normal coronary arteries (NCA), stable coronary artery disease (CAD), and acute coronary syndromes (ACS), and relationships with angiogenin, matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1, and vascular endothelial growth factor. Plasma markers were measured (ELISA) in peripheral venous citrated plasma from 50 healthy subjects, 30 with NCA, 70 with stable CAD and 24 with an ACS, and from patient’s aortic root, coronary ostium, coronary sinus and femoral artery. Human umbilical vein endothelial cells (HUVECs) were cultured with or without tumour necrosis factor (TNF), and platelets were probed. HO-1 was raised in stable CAD (p<0.05) and increased further in ACS (p<0.01) compared to healthy controls and NCA. HO-1 correlated only with MMP-9, and then only in the healthy controls. There were no major differences from cardiac or peripheral sites. HO-1 was present in HUVECs and 24-hour HUVEC supernatants but release was abolished by TNF. Platelets had no HO-1. In conclusion, HO-1 is raised in stable CAD and ACS and may arise from the endothelium but not the platelet. This may have implications for our understanding of the pathophysiology of CAD and its acute presentation as ACS.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Konstantinos Mourouzis ◽  
Gerasimos Siasos ◽  
Evangelos Oikonomou ◽  
Marina Zaromitidou ◽  
Vicky Tsigkou ◽  
...  

Abstract Background Lipoprotein-associated Phospholipase A2 (Lp-PLA2), can exert proinflammatory as well as proatherogenic properties on the vascular wall. The current study sought to evaluate the influence of high Lp-PLA2 levels on indices of arterial wall properties in patients with stable coronary artery disease (CAD). Methods Three hundred seventy-four consecutive patients with stable CAD (mean age 61 ± 11 years, 89% males) were enrolled in this single-center cross-sectional study. Flow-mediated dilation (FMD) was used to assess endothelial function and augmentation index (AIx) of the central aortic pressure was used to assess reflected waves. ELISA was used to determine Lp-PLA2 serum levels. Results After dividing the participants in 3 equal groups based on the tertiles of circulating Lp-PLA2 values, no significant differences were demonstrated between those in the 3rd tertile with Lp-PLA2 values > 138 μg/L, in the 2nd tertile with Lp-PLA2 values between 101 and 138 μg/L and in the 1st tertile (Lp-PLA2 values < 101 μg/L) regarding age, male gender, smoking habits, family history of CAD or history of a previous myocardial infarction, diabetes mellitus, arterial hypertension, hyperlipidemia, duration of CAD and treatment with relevant medication. Importantly, subjects with Lp-PLA2 values in the highest tertile, had significantly reduced FMD values compared to the middle and lower tertile (4.43 ± 2.37% vs. 4.61 ± 1.97% vs. 5.20 ± 2.52% respectively, P = 0.03). Patients in the highest tertile of Lp-PLA2 values had significantly higher AIx values (24.65 ± 8.69% vs. 23.33 ± 9.65%, P = 0.03), in comparison to the lowest tertile, with Lp-PLA2 values < 101 μg/L. A linear regression analysis showed that Lp-PLA2 values > 138 μg/L negatively correlated to FMD [b = − 0.45 (95% CI: − 0.79 – -0.11), P = 0.01] and AIx values [b = 1.81 (95% CI: 0.57–3.05), P < 0.001] independently of cofounders like gender, age, diabetes mellitus, arterial hypertension, dyslipidemia, smoking habits, family history of CAD, history of previous myocardial infarction, serum glucose, circulating lipid levels, duration of CAD, antihypertensive medication, antidiabetic drugs, statin therapy and treatment with β-blockers. Conclusions Elevated Lp-PLA2 levels relate to endothelial dysfunction and arterial stiffness in patients with stable CAD independently from classical risk factors for CAD, statin use, antihypertensive treatment, and duration of the disease.


2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Mark S Borja ◽  
Yumin He ◽  
Jacques Genest ◽  
Michael N Oda

Objective: The exchange of apolipoprotein A-I between lipid-associated and lipid-free states is a key step in reverse cholesterol transport and is representative of HDL’s functional status. Reduced HDL-apoA-I exchange (HAE) is associated with the presence of cardiovascular disease. To build on this observation, we investigated the hypothesis that HAE in a coronary artery disease-identified patient decreases with increased coronary artery disease instability. Method: HAE was measured by electron paramagnetic resonance spectroscopy (EPR), wherein nitroxide-labeled lipid-free apoA-I is introduced into apolipoprotein B-depleted plasma, incubated at 37°C and measured. When added to plasma, the nitroxide-labeled apoA-I specifically interacts with HDL and displaces resident apoA-I. The EPR spectrum reports the population of lipid-bound, spin labeled apoA-I, which is directly proportional to the amount of resident apoA-I displaced. The relative level of apoA-I displaced is representative of the plasticity of HDL and its ability to make lipid-poor apoA-I available for ABCA1-mediated cholesterol efflux. We measured HAE in the plasma of three groups: stable coronary artery disease (n=22), 3 months following acute coronary syndrome (n=19), and a control group with no history of coronary artery disease (n=15). Results: HAE was significantly lower in both the stable coronary artery disease and acute coronary syndrome groups, compared to the control group (P<0.001 and, P<0.0001, respectively). Remarkably, the ACS subjects also had significantly lower HAE compared to those with stable CAD (P<0.01). By comparing HAE to apoA-I and HDL-C levels, we observed that stable CAD and ACS subjects have lower HAE per milligram/deciliter of apoA-I, consistent with a qualitative deficiency in their apoA-I. Conclusions: HAE activity is a by-product of apoA-I qualitative status, which is inversely correlated with coronary artery disease stability.


2020 ◽  
Vol 25 (10) ◽  
pp. 3977
Author(s):  
A. V. Ponasenko ◽  
M. V. Khutornaya ◽  
I. Yu. Malyshev ◽  
O. L. Barbarash

Aim. To determine the relationship between the serum interleukin (IL) 18 level, the carriage of variant alleles IL18, IL18R1, IL18RAP and the risks of myocardial infarction (MI), hypertension, multifocal atherosclerosis in patients with stable coronary artery disease (CAD).Material and methods. Two hundred and sixty patients with stable coronary artery disease living in a large industrial region ofWestern Siberia were examined. Serum IL18 concentrations was determined by the enzyme immunoassay. Genotyping was performed by real-time polymerase chain reaction using TaqMan technology.Results. We revealed associations of rs13015714 IL18R1 and rs917997 IL18RAP sites with the MI risk (odds ratio (OR), 1,95 [95% confidence interval (CI), 1,063,58], p=0,029; OR, 2,01 [95% CI, 1,11-3,64], p=0,018, respectively). Associations of rs13015714 and rs917997 sites with high IL18 concentrations (genotypes C/T + T/T 488,0 [321,0, 687,2] pg/ml and T/G + G/G 504,2 [275,6; 655,5] pg/ml) was observed.Conclusion. The relationship between the minor alleles of rs13015714 IL18R1 and rs917997 IL18RAP sites with an increased risk of MI in patients with stable CAD was shown. Also, polymorphism at rs13015714 and rs917997 sites provides different levels of circulating IL18. In particular, the carriage of minor alleles is associated with increased IL-18 levels in patients with previous MI and multifocal atherosclerosis or hypertension, as well as with an increase in the risk of these pathologies.


2020 ◽  
Vol 16 (2) ◽  
pp. 191-198
Author(s):  
G. N. Soboleva ◽  
R. V. Gostishchev ◽  
A. N. Rogoza ◽  
T. I. Kotkina ◽  
A. N. Samko ◽  
...  

Aim. To study nicorandil prescription effects before elective percutaneous coronary intervention (PCI) to prevent myocardial injury and 4a type acute myocardial infarction (MI, primary endpoint) and cardiovascular events (CVE) in the first year after PCI (secondary endpoint) in patients with stable coronary artery disease.Material and methods. 182 patients with stable coronary artery disease were included into the study and were randomized into two groups: nicorandil treatment group (n=90) and a control group with a standard medical treatment (n=92). Nicorandil was prescribed orally: 2 days before PCI – 30 mg/day; on the day of PCI – 20 mg 2 hours before intervention and 10 mg 6-12 hours after PCI; over the next 30 days – 30 mg/day. High sensitivity troponin I (hs-Tr) and creatine kinase-MB tests were carried out before PCI, 24 and 72 hours after the intervention; the 4a type MI was diagnosed according to the 4th Universal Definition. Non-fatal myocardial infarction, nonfatal stroke, death from cardiovascular diseases, repeat revascularization (PCI, coronary artery bypass surgery due to aggravation), hospital admissions for angina pectoris recurrence (without interventions) and death from any causes were considered as cardiovascular events. Data on adverse outcomes were collected over the hospital stay, and then 30, 180 and 365 days after the hospital discharge.Results. 4a type MI was diagnosed in 14 patients (8%), in women – 12% and in men – 6%. There was a significant decrease in the incidence of type 4a MI in the nicorandil group (n=3; 3%) compared with the control group (n=11; 12%; p=0.05). Secondary endpoint was recorded in 21% of patients. The relationship was found between 4a type MI and the incidence of CVE the next year after the PCI (p=0.01). In patients with type 4a MI CVE odd ratio increases 5.8 times with confidence interval from 1.5426 to 21.6024. According to the logistic regression analysis the significant relationship between hs-Tr growth 24 hours after the PCI and CVE incidence next year after the PCI was found with cutting value 389.8 pg/ml, AUC=0.641 (p=0.04).Сonclusion. Peroral nicorandil 30 mg/day 2 days before PCI, 20 mg 2 hours before surgery and 10 mg 6-12 hours after PCI, and 30 mg/day next 30 days after PCI decreases the risk of intraoperative myocardial injury and CVE in the next year after PCI.


2021 ◽  
Vol 49 (6) ◽  
pp. 030006052110196
Author(s):  
Heyu Meng ◽  
Jianjun Ruan ◽  
Xiaomin Tian ◽  
Lihong Li ◽  
Weiwei Chen ◽  
...  

Objective This study aimed to investigate whether differential expression of the retinoic acid receptor-related orphan receptor A ( RORA) gene is related to occurrence of acute myocardial infarction (AMI). Methods This was a retrospective study. White blood cells of 93 patients with acute myocardial infarction and 74 patients with stable coronary artery disease were collected. Reverse transcription quantitative polymerase chain reaction and western blotting were used to measure RORA mRNA and protein expression, respectively. Results RORA mRNA expression levels in peripheral blood leukocytes in patients with AMI were 1.57 times higher than those in patients with stable coronary artery disease. Protein RORA levels in peripheral blood of patients with AMI were increased. Binary logistic regression analysis showed that high expression of RORA was an independent risk factor for AMI, and it increased the risk of AMI by 2.990 times. Conclusion RORA expression levels in patients with AMI is significantly higher than that in patients with stable coronary artery disease. High expression of RORA is related to AMI and it may be an independent risk factor for AMI.


Author(s):  
Tomonori Itoh ◽  
◽  
Hiromasa Otake ◽  
Takumi Kimura ◽  
Yoshiro Tsukiyama ◽  
...  

AbstractThe purpose of this study was to assess early and late vascular healing in response to bioresorbable-polymer sirolimus-eluting stents (BP-SESs) for the treatment of patients with ST-elevation myocardial infarction (STEMI) and stable coronary artery disease (CAD). A total of 106 patients with STEMI and 101 patients with stable-CAD were enrolled. Optical frequency-domain images were acquired at baseline, at 1- or 3-month follow-up, and at 12-month follow-up. In the STEMI and CAD cohorts, the percentage of uncovered struts (%US) was significantly and remarkably decreased during early two points and at 12-month (the STEMI cohort: 1-month: 18.75 ± 0.78%, 3-month: 10.19 ± 0.77%, 12-month: 1.80 ± 0.72%; p < 0.001, the CAD cohort: 1-month: 9.44 ± 0.78%, 3-month: 7.78 ± 0.78%, 12-month: 1.07 ± 0.73%; p < 0.001 respectively). The average peri-strut low-intensity area (PLIA) score in the STEMI cohort was significantly decreased during follow-up period (1.90 ± 1.14, 1.18 ± 1.25, and 1.01 ± 0.72; p ≤ 0.001), whereas the one in the CAD cohort was not significantly changed (0.89 ± 1.24, 0.67 ± 1.07, and 0.64 ± 0.72; p = 0.59). In comparison with both groups, differences of %US and PLIA score at early two points were almost disappeared or close at 12 months. The strut-coverage and healing processes in the early phase after BP-SES implantation were significantly improved in both cohorts, especially markedly in STEMI patients. At 1 year, qualitatively and quantitatively consistent neointimal coverage was achieved in both pathogenetic groups.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hack-Lyoung Kim ◽  
Jung Pyo Lee ◽  
Nathan Wong ◽  
Woo-Hyun Lim ◽  
Jae-Bin Seo ◽  
...  

AbstractThe role of ST2 in stable coronary artery disease (CAD) has not yet been well defined. This study was performed to investigate baseline serum soluble ST2 (sST2) level can predict clinical outcomes in patients with stable CAD. A total of 388 consecutive patients with suspected CAD (65 years and 63.7% male) in stable condition referred for elective invasive coronary angiography (ICA) was prospectively recruited. Major adverse cardiovascular event (MACE), including cardiac death, non-fatal myocardial infarction, coronary revascularization (90 days after ICA), and ischemic stroke during clinical follow-up was assessed. Most of the patients (88.0%) had significant CAD (stenosis ≥ 50%). During median follow-up of 834 days, there was 29 case of MACE (7.5%). The serum sST2 level was significantly higher in patients with MACE than those without (47.3 versus 30.6 ng/ml, P < 0.001). In multiple Cox regression model, higher sST2 level (≥ 26.8 ng/ml) was an independent predictor of MACE even after controlling potential confounders (hazard ratio, 13.7; 95% confidence interval 1.80–104.60; P = 0.011). The elevated level of baseline sST2 is associated with an increased risk of adverse clinical events in stable CAD patients. Studies with larger sample size are needed to confirm our findings.


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