scholarly journals The Prognostic Utility of Plasma NGAL Levels in ST Segment Elevation in Myocardial Infarction Patients

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Ahmet Avci ◽  
Bahadir Ozturk ◽  
Kenan Demir ◽  
Fikret Akyürek ◽  
Bulent Behlul Altunkeser
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Mortality ◽  
Troponin I ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Roc Curve Analysis ◽  
Ventricular Ejection Fraction ◽  
St Segment Elevation ◽  
Plasma Ngal ◽  
Creatine Kinase Mb

Introduction. Plasma neutrophil gelatinase-associated lipocalin (NGAL) levels in acute myocardial infarction (AMI) patients are markedly higher. In addition, plasma NGAL levels were increased in patients with acute and chronic heart failure as a complication of myocardial infarction. In this study, we investigated whether there is a difference between the prognostic use of plasma NGAL levels in ST-elevation myocardial infarction (STEMI) patients with preserved and reduced left ventricular ejection fraction (LVEF). Methods. 235 consecutive STEMI patients were enrolled in the study. Patients were divided into groups according to LVEF. Plasma NGAL, troponin I, creatine kinase MB (CKMB), and C-reactive protein (CRP) were measured. Finally, the study population examined with 34 reduced LVEF and 34 preserved LVEF consisted of a total of 68 patients (12 females; mean age, 61.5 ± 14.7). All patients were followed up prospectively for 6 months. This study group was divided into two subgroups as the patients who died (n = 14) and survived (n = 34), and plasma NGAL levels of the groups were compared. Results. The median of NGAL was 190.08 ng/ml. Age, troponin I, CKMB, CRP, glomerular filtration rate, and creatinine were higher in reduced LVEF groups. Plasma NGAL levels were also higher in reduced LVEF than in preserved LVEF, but statistically not significant (p=0.07). Plasma NGAL levels were significantly higher in death patients than in survived patients (p<0.001). In ROC curve analysis, the level to detect isolated cardiovascular mortality with a sensitivity of 86% and a specificity of 77% was 190 ng/mL for NGAL. Conclusion. Plasma NGAL levels can be used to predict cardiovascular mortality in STEMI patients.

Circulating MicroRNA-146a and MicroRNA-21 Predict Left Ventricular Remodeling after ST-Elevation Myocardial Infarction

Cardiology ◽  
2015 ◽  
Vol 132 (4) ◽  
pp. 233-241 ◽  
Author(s):  
Xiaoxia Liu ◽  
Yumei Dong ◽  
Song Chen ◽  
Guangde Zhang ◽  
Mingyu Zhang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Troponin I ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Circulating Microrna ◽  
Ventricular Ejection Fraction ◽  
Creatine Kinase Mb ◽  
Acute Mi

Objectives: MicroRNA (miR)-146a and miR-21 have been reported to participate in inflammatory reactions and fibrosis. Excessive inflammation and cardiac fibrosis may play important roles in the development of left ventricular remodeling (LVR). This study assessed whether miR-146a, miR-21 and other biomarkers could predict LVR after myocardial infarction (MI). Methods: Circulating miR-146a, miR-21 and other biomarker levels were measured in 198 patients with acute MI 5 days after primary percutaneous coronary intervention (PCI). All patients were assessed by transthoracic echocardiography on day 5 and 1 year after primary PCI. Results: Concentrations of circulating miR-146a, miR-21, C-reactive protein, creatine kinase MB type and troponin I, as well as estimated glomerular filtration rate (eGFR) and left ventricular ejection fraction (LVEF), were significantly higher in patients with than in those without LVR (p < 0.05). Multivariate logistic regression analysis showed that circulating miR-146a (odds ratio, OR = 2.127, p < 0.0001), miR-21 (OR = 1.119, p < 0.0001), eGFR (OR = 0.939, p = 0.0137) and LVEF (OR = 0.802, p = 0.0048) were independent predictors of LVR development. The area under the curve for the combination of miR-146a and miR-21 was significantly higher than for either alone. Conclusion: Circulating miR-146a and miR-21 may be novel biomarkers predictive of LVR after acute MI. Their combination may better predict LVR than either alone.

scholarly journals Elevated Plasma IL-38 Concentrations in Patients with Acute ST-Segment Elevation Myocardial Infarction and Their Dynamics after Reperfusion Treatment

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Yucheng Zhong ◽  
Kunwu Yu ◽  
Xiang Wang ◽  
Xiaoya Wang ◽  
Qingwei Ji ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Troponin I ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Atheromatous Plaque ◽  
Ventricular Ejection Fraction ◽  
St Segment Elevation ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment

Objective.Recent studies suggest that IL-38 is associated with autoimmune diseases. Furthermore, IL-38 is expressed in human atheromatous plaque. However, the plasma levels of IL-38 in patients with ST-segment elevation myocardial infarction (STEMI) have not yet to be investigated.Methods.On admission, at 24 h, at 48 h, and at 7 days, plasma IL-38, C-reactive protein (CRP), cardiac troponin I (cTNI), and N-terminal of the prohormone brain natriuretic peptide (NT-proBNP) levels were measured and IL-38 gene in peripheral blood mononuclear cells (PBMCs) was detected in STEMI patients.Results.The results showed that plasma IL-38 levels and IL-38 gene expression in PBMCs were significantly increased in STEMI patients compared with control group and were time dependent, peaked at 24 h. In addition, plasma IL-38 levels were dramatically reduced in patients with reperfusion treatment compared with control group. Similar results were also demonstrated with CRP, cTNI, and NT-proBNP levels. Furthermore, IL-38 levels were found to be positively correlated with CRP, cTNI, and NT-proBNP and be weakly negatively correlated with left ventricular ejection fraction (LVEF) in STEMI patients.Conclusions.The results indicate that circulating IL-38 is a potentially novel biomarker for patients with STEMI and IL-38 might be a new target for MI study.

MethotrexaTE THerapy in ST-Segment Elevation MYocardial InfarctionS

2017 ◽  
Vol 22 (6) ◽  
pp. 538-545 ◽  
Author(s):  
Daniel Medeiros Moreira ◽  
Maria Emilia Lueneberg ◽  
Roberto Leo da Silva ◽  
Tammuz Fattah ◽  
Carlos Antonio Mascia Gottschall
Keyword(s):  
Myocardial Infarction ◽  
Infarct Size ◽  
Troponin I ◽  
Area Under The Curve ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
St Segment Elevation ◽  
Timi Frame Count ◽  
St Segment

Purpose: Methotrexate is an anti-inflammatory drug that has been shown to have anti-ischemic effects. Our aim was to evaluate if methotrexate could reduce infarct size in patients with ST-segment elevation myocardial infarction (STEMI). Methods: We randomly assigned patients with STEMI to receive either methotrexate or placebo. Primary outcome was infarct size determined by calculating the area under the curve (AUC) for creatine kinase (CK) release. Secondary outcomes were AUC of CK MB (CK-MB) and AUC of troponin I; peak CK, peak CK-MB, and troponin I; B-type natriuretic peptide (BNP) level, high-sensitivity C-reactive protein (hsCRP) result, and erythrocyte sedimentation rate (ESR); left ventricular ejection fraction (LVEF); thrombolysis in myocardial infarction (TIMI) frame count; Killip score; mortality and reinfarction incidence; and incidence of adverse reactions. Results: We included 84 patients. Median AUC of CK was 78 861.0 in the methotrexate group and 68 088.0 in the placebo group ( P = .10). Patients given methotrexate and placebo exhibited, respectively, median AUC for CK-MB of 9803.4 and 8037.0 ( P = .42); median AUC for troponin of 3691.1 and 2132.6 ( P = .09); peak CK of 2806.0 and 2147.0 ( P = .05); peak CK-MB of 516.0 and 462.3 ( P = .25); and peak troponin of 121.0 and 85.1 ( P = .06). At 3 months, LVEF was lower in patients who received methotrexate (49.0% ± 14.1%) than in patients given placebo (56.4% ± 10.0%; P = .01). There were no differences in hsCRP, ESR, BNP, Killip scores, TIMI frame count, reinfarction, and mortality rates. There was a higher median serum glutamic–pyruvic transaminase levels in the methotrexate group. Conclusion: Methotrexate did not reduce infarction size and worsened LVEF at 3 months ( Clinicaltrials.gov identifier NCT01741558).

Admission Endocan Level may be a Useful Predictor for In-Hospital Mortality and Coronary Severity Index in Patients With ST-Segment Elevation Myocardial Infarction

Angiology ◽  
2016 ◽  
Vol 68 (1) ◽  
pp. 46-51 ◽  
Author(s):  
Harun Kundi ◽  
Ahmet Balun ◽  
Hulya Cicekcioglu ◽  
Orhan Karayigit ◽  
Canan Topcuoglu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Troponin I ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Syntax Score ◽  
Operating Characteristics ◽  
Ventricular Ejection Fraction ◽  
St Segment Elevation ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment

We assessed the prognostic role of serum endocan level in patients with ST-segment elevation myocardial infarction (STEMI) and compared the results with a normal coronary angiography group. A total of 133 patients were included in the study (88 patients with STEMI and 45 patients with normal coronary arteries). The SYNTAX score was determined based on the baseline coronary angiogram. Multivariate logistic regression analysis indicated that endocan independently correlated with the presence of STEMI. Moreover, high-sensitivity C-reactive protein (hsCRP), peak troponin I, and left ventricular ejection fraction (LVEF) were found to be independently associated with STEMI. Endocan level correlated significantly with hsCRP and SYNTAX score. We analyzed the discriminatory capability of endocan level for the presence of STEMI using a receiver–operating characteristics curve. A cutoff endocan level of 1.7 (ng/mL) predicted the presence of STEMI with a sensitivity of 76.1% and specificity of 73.6%. In conclusion, a high endocan level on hospital admission is an independent predictor of a worse cardiovascular outcome and a high SYNTAX score in patients with STEMI.

Abstract 13194: The Effects of Methotrexate Therapy on Myocardial Infarction With ST-Segment Elevation (TETHYS Trial)

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Daniel M Moreira ◽  
Roberto L da Silva ◽  
Maria E Lueneberg ◽  
Tammuz Fattah ◽  
Carlos A Gottschall
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Troponin I ◽  
Experimental Studies ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
St Segment Elevation ◽  
Timi Frame Count ◽  
St Segment

Introduction: Acute myocardial infarction provokes inflammatory activation. Methotrexate is one drug that has been shown to have anti-ischemic effects in experimental studies. Hypothesis: Methotrexate could reduce inflammation and the ischemia area in acute myocardial infarction Methods: We randomly assigned patients with myocardial infarction with ST-segment elevation to receive either methotrexate (0.05 mg/kg bolus followed by 0.05 mg/kg/h for 6 h) or matching placebo (riboflavin sodium phosphate 0.1%, in order to preserve double-blinding) at a ratio of 1:1. Patients in both groups were given a 5mg single dose of folic acid. The primary endpoint was infarct size, determined by the area under the curve (AUC) for creatine kinase (CK) release. Secondary endpoints were AUC of CK-MB and AUC of troponin I; peak CK, peak CK-MB and troponin I; B-type natriuretic peptide (BNP) level, high-sensitivity C-reactive protein (hsCRP) result and erythrocyte sedimentation rate (ESR); left ventricular ejection fraction (LVEF); TIMI frame count; Killip score; mortality and reinfarction incidence. The safety endpoint was the incidence of adverse reactions. Results: We included 84 patients. The AUC of CK was 78,861.00 in the methotrexate group and 68,088.00 in the placebo group (P=0.10). Patients given methotrexate and placebo exhibited, respectively, AUC for CK-MB of 9,803.40 and 8,037.00 (P=0.42); AUC for troponin I of 3,691.11 and 2,132.63 (P=0.09); peak CK of 2,806.00 and 2,147.00 (P=0.05), peak CK-MB of 516.00 and 462.25 (P=0.25) and peak troponin I of 121.00 and 85.05 (P=0,06). At 3 months, LVEF was lower in patients who received methotrexate (48.97±14.09%) than in patients given placebo (56.37±9.97%) (P=0.01). There were no differences in hsCRP, ESR, BNP, Killip scores or TIMI frame count. There were also no differences in reinfarction or mortality rates or in incidence of side effects, with the exception of higher median serum glutamic-pyruvic transaminase (SGPT) levels in the methotrexate group. Conclusions: Methotrexate did not reduce infarction size and worsened LVEF at 3 months.

scholarly journals Circulating miR-181a as a Potential Novel Biomarker for Diagnosis of Acute Myocardial Infarction

2016 ◽  
Vol 40 (6) ◽  
pp. 1591-1602 ◽  
Author(s):  
Jianbing Zhu ◽  
Kang Yao ◽  
Qian Wang ◽  
Junjie Guo ◽  
Hongtao Shi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Troponin I ◽  
Characteristic Curve ◽  
Diagnostic Value ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Dependent Manner ◽  
Ventricular Ejection Fraction ◽  
Creatine Kinase Mb

Background: In this study, we tested the hypothesis that miR-181a levels increase during acute myocardial infarction. We investigated circulating miR-181a as a potential novel biomarker for early diagnosis of acute myocardial infarction (AMI). Methods: From June 2014 to June 2016, 120 consecutive eligible patients with AMI (n = 60) or unstable angina (UA; n = 60) and 60 control subjects were enrolled. Plasma miR-181a levels were determined by quantitative reverse transcriptase-polymerase chain reaction. Results: Circulating miR-181a expression levels detected immediately after admission were higher in the AMI group than in the UA and control groups. Relative miR-181a levels in AMI patients were positively correlated with the concentrations of the creatine kinase-MB fraction and cardiac troponin I. Correlation analysis showed that plasma miR-181a was positively correlated with coronary Gensini score (r = 0.573, P < 0.05) and negatively correlated with left ventricular ejection fraction (r = -0.489, P < 0.05). Receiver operating characteristic curve analyses showed that plasma miR-181a was of significant diagnostic value for AMI (AUC, 0.834; 95% CI, 0.756-0.912, P < 0.05). Conclusion: Circulating miR-181a levels in patients with AMI were significantly changed in a time-dependent manner, indicating the value of plasma miR-181a as a novel biomarker for diagnosing AMI.

scholarly journals The stress hyperglycaemia ratio is associated with left ventricular remodelling after first acute ST-segment elevation myocardial infarction

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Shuai Meng ◽  
Yong Zhu ◽  
Kesen Liu ◽  
Ruofei Jia ◽  
Jing Nan ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
St Segment Elevation ◽  
Segment Elevation Myocardial Infarction ◽  
Stress Hyperglycaemia ◽  
St Segment ◽  
Significant Difference ◽  
First Time

Abstract Background Left ventricular negative remodelling after ST-segment elevation myocardial infarction (STEMI) is considered as the major cause for the poor prognosis. But the predisposing factors and potential mechanisms of left ventricular negative remodelling after STEMI remain not fully understood. The present research mainly assessed the association between the stress hyperglycaemia ratio (SHR) and left ventricular negative remodelling. Methods We recruited 127 first-time, anterior, and acute STEMI patients in the present study. All enrolled patients were divided into 2 subgroups equally according to the median value of SHR level (1.191). Echocardiography was conducted within 24 h after admission and 6 months post-STEMI to measure left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD), and left ventricular end-systolic diameter (LVESD). Changes in echocardiography parameters (δLVEF, δLVEDD, δLVESD) were calculated as LVEF, LVEDD, and LVESD at 6 months after infarction minus baseline LVEF, LVEDD and LVESD, respectively. Results In the present study, the mean SHR was 1.22 ± 0.25 and there was significant difference in SHR between the 2 subgroups (1.05 (0.95, 1.11) vs 1.39 (1.28, 1.50), p < 0.0001). The global LVEF at 6 months post-STEMI was significantly higher in the low SHR group than the high SHR group (59.37 ± 7.33 vs 54.03 ± 9.64, p  = 0.001). Additionally, the global LVEDD (49.84 ± 5.10 vs 51.81 ± 5.60, p  = 0.040) and LVESD (33.27 ± 5.03 vs 35.38 ± 6.05, p  = 0.035) at 6 months after STEMI were lower in the low SHR group. Most importantly, after adjusting through multivariable linear regression analysis, SHR remained associated with δLVEF (beta = −9.825, 95% CI −15.168 to −4.481, p  < 0.0001), δLVEDD (beta = 4.879, 95% CI 1.725 to 8.069, p  = 0.003), and δLVESD (beta = 5.079, 95% CI 1.421 to 8.738, p  = 0.007). Conclusions In the present research, we demonstrated for the first time that SHR is significantly correlated with left ventricular negative remodelling after STEMI.

Correlation between procollagen propeptides end echocardiography indices in patients with ST segment elevation myocardial infarction (STEMI)

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Osokina ◽  
V.N Karetnikova ◽  
O.M Polikutina ◽  
Y.S Slepynina ◽  
T.P Artemova ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Contractility ◽  
Imaging System ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Enzyme Linked Immunosorbent Assay ◽  
Ventricular Ejection Fraction ◽  
St Segment Elevation ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment

Abstract Objective To investigate the correlation between Procollagen I C-Terminal Propeptide (PICP), Procollagen III N-Terminal Propeptide (PIIINP), indices of echocardiography and anamnestic data in patients with ST segment elevation myocardial infarction (STEMI) and preserved myocardial contractility. Materials and methods 60 men and 23 women diagnosed with STEMI were examined. Echocardiographic studies were performed using SONOS 2500 Cardiac – Vascular Ultrasound (Hewlett Packard, USA). Myocardial contractility was considered to be preserved with left ventricular ejection fraction (LVEF) ≥50%. In addition to standard indices of echocardiography, mitral flow propagation velocity (FPV) was evaluated to diagnose diastolic dysfunction. Coronary angiography was performed using INNOVA 3100 Cardiovascular Imaging System (USA). All patients, during the first twelve hours of the disease, underwent percutaneous coronary intervention (PCI) with stenting of the occluded culprit infarct-related artery. On the 1st and 12th days of hospitalization, the concentrations of PICP and PIIINP were determined for all patients by enzyme-linked immunosorbent assay (ELISA) using laboratory BCM Diagnostics kits (USA). All patients at the hospital received standard therapy. Results The following marker values were obtained: 1st day: PICP 609 (583; 635) ng/ml, PIIINP 26 (18.9; 34.9) ng/ml; 12th day: PICP 588 (580; 561) ng/ml, PIIINP 24.2 (18.6; 30.3) ng/ml. The following significant correlations were revealed: PICP 1st day / isovolumic contraction time – IVCT (m/s) 12th day, r=−0.68, p=0.042; PICP 1st day / Tei Index 12th day, r=−0.72, p=0.028; PICP 1st day / diastolic rigidity 12th day, r=−0.74, p=0.021; PIIINP 1st day/age, r=0.55, p=0.016; PIIINP 1st day/ body mass index (BMI), r=−0.59, p=0.009; PIIINP 1st day / E (cm/s) 1st day, r=0.72, p=0.018; PIIINP 1st day / Em /FPV 1st day, r=0.78, p=0.007; PIIINP 12th day / Em / FPV 1st day, r=0.65, p=0.041; PIIINP 12th day / E (cm/s) 1st day, r=0.67, p=0.033; PIIINP 12th day / E / Em) 12th day, r=0.70, p=0.023; PIIINP 12th day / Em/FPV 12th day, r=0.73, p=0.014. Conclusions The data obtained indicates the correlation between serum markers of myocardial fibrosis and the indices of echocardiography, as well as age. We conclude that, all the markers listed above, are able to represent myocardial remodeling in patients with STEMI. Funding Acknowledgement Type of funding source: None

scholarly journals Is Troponin really a reliable marker in patients with acute ischemic stroke?

2018 ◽  
Vol 56 (4) ◽  
pp. 250-256 ◽  
Author(s):  
Zeynep Yildiz ◽  
Abdulkadir Koçer ◽  
Şahin Avşar ◽  
Göksel Cinier
Keyword(s):  
Myocardial Infarction ◽  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Troponin I ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Anterior Circulation ◽  
Ventricular Ejection Fraction ◽  
Coronary Syndrome ◽  
Reliable Marker

Abstract Background and purpose. Cardiac troponin I (cTnI) is a reliable marker to diagnose acute myocardial infarction, but the pathophysiological explanation for the increase in cTnI levels in patients with acute ischemic stroke (IS) remains unknown. To overcome this question, we aimed to compare serum cTnI levels in acute coronary syndrome (ACS) concomitant with and without stroke. By doing like this, we thought that we could demonstrate the effect of stroke on TrpI level. Methods. Serum cTnI levels of 41 patients having ACS with acute IS during hospitalization were compared with 97 control patients having only ACS. Cranial CT was performed to evaluate the lesions. The severity of IS was evaluated objectively by national institutes of health stroke scale. Results. cTnI levels were found to be similar in both groups. Presence of diabetes mellitus, coronary artery disease and previous myocardial infarction were more frequent in patients with acute IS. The cTnI levels in the patients with the cranial lesion in the anterior circulation was higher (p = 0.039). Presence of acute IS, cTnI level higher than 20 ng/mL and left ventricular ejection fraction < 40% were found to be independent risk factors for mortality (p < 0.05). Conclusions. We found that abnormal troponin levels were more likely to be due to cardiac causes than cerebral ones in this first study evaluating the cTnI levels in patients with ACS concomitant with acute IS. The severity of IS, lesion location in the anterior circulation and higher troponin levels were associated with mortality.

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