621 Detection of left ventricular neurohormonal activation and myocardial damage as a result of coronary angioplasty: a NT-proBNP and cardiac troponin-I correlation

2005 ◽  
Vol 4 (1) ◽  
pp. 143-143
Keyword(s):  
Coronary Angioplasty ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Cardiac Troponin I ◽  
Neurohormonal Activation

Abstract 177: Overexpression of Cardiac Troponin I-Interacting Kinase, a Cardiac-Specific MAPKKK, Promotes Cardiac Dysfunction

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Hao Tang ◽  
Kunhong Xiao ◽  
Lan Mao ◽  
Howard A Rockman ◽  
Douglas A Marchuk
Keyword(s):  
Disease Progression ◽  
Cardiac Dysfunction ◽  
Cardiac Troponin ◽  
Kinase Activity ◽  
Troponin I ◽  
Left Ventricular ◽  
Cardiac Troponin I ◽  
Cardiac Response ◽  
Kinase Assay ◽  
Idiopathic Dilated Cardiomyopathy

Cardiac Troponin I-interacting kinase (TNNI3K) is a cardiac specific kinase whose biological function remains largely unknown. We have recently shown that TNNI3K expression greatly accelerates cardiac dysfunction in mouse models of cardiomyopathy, indicating an important role in modulating disease progression. To further investigate TNNI3K kinase activity in vivo, we have generated transgenic mice expressing both wild-type and kinase-dead versions of the human TNNI3K protein. Importantly, we show that the increased TNNI3K kinase activity induces mouse cardiac hypertrophy, and the kinase activity is required to accelerate disease progression in a left-ventricular pressure overload model of mouse cardiomyopathy. We demonstrate the clinical relevance of these observations by identifying two potential missense mutations near the kinase activation loop of TNNI3K in idiopathic dilated cardiomyopathy (DCM) human patients. Using an in vitro kinase assay and proteomics analysis, we show that TNNI3K is a dual-function kinase with Tyr and Ser/Thr kinase activity. Using antisera to TNNI3K, we show that TNNI3K protein is located at the sarcomere Z disc. These combined data suggest that TNNI3K mediates cell signaling to modulate cardiac response to stress. The essential role of the kinase activity makes TNNI3K a strong potential pharmaceutical target of kinase inhibitors for heart disease.

Assessment of left ventricular function using serum cardiac troponin I measurements following myocardial infarction

1998 ◽  
Vol 272 (1) ◽  
pp. 59-67 ◽  
Author(s):  
Fred S. Apple ◽  
Scott W. Sharkey ◽  
Alireza Falahati ◽  
Maryann Murakami ◽  
Naheed Mitha ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Left Ventricular ◽  
Cardiac Troponin I ◽  
Serum Cardiac Troponin

scholarly journals Frontal QRS-T angle as a predictive marker for myocardial damage in acute carbon monoxide poisoning

2021 ◽  
pp. 096032712110434
Author(s):  
Yusuf K Tekin ◽  
Gülaçan Tekin ◽  
Naim Nur ◽  
İlhan Korkmaz ◽  
Sefa Yurtbay
Keyword(s):  
Carbon Monoxide ◽  
Creatine Kinase ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Myocardial Damage ◽  
Cardiac Troponin I ◽  
Arterial Oxygen ◽  
Co Poisoning ◽  
Arterial Blood ◽  
Creatine Kinase Mb

Introduction The present study was undertaken to investigate the prognostic value of the frontal QRS-T angle associated with adverse cardiac outcomes in patients with carbon monoxide (CO) poisoning in early stages in the emergency department. Materials and methods The data of 212 patients with CO poisoning who were admitted to the ED between January 2010 and May 2020 were retrospectively analyzed. The frontal QRS-T angle was obtained from the automatic reports of the EKG device. Results Compared to patients without myocardial damage, among patients with myocardial damage, statistically high creatinine, creatine kinase MB, cardiac troponin I, and frontal QRS-T angle values were found ( p < 0.001 for all parameters), while the saturation of arterial blood pH and arterial oxygen values were found to be lower ( p = 0.002 and p < 0.001, respectively). The frontal QRS-T angle values were correlated with creatine kinase, creatine kinase-MB, cardiac troponin I, and oxygen saturation (SpO2) in arterial blood (r = 0. 232, p = 0.001; r = 0. 253, p = < 0.001; r = 0. 389, p = < 0.001; r = −0. 198, p = 0.004, respectively). The optimum cut-off value of the frontal QRS-T angle was found to be 44.5 (area under the curve: 0.901, 95% confidence interval: 0.814–0.988, sensitivity: 87%, specificity: 84%). Conclusions The frontal QRS-T angle, a simple and inexpensive parameter that can be easily obtained from 12-lead surface electrocardiography, can be used as an early indicator in the detection of myocardial damage in patients with CO poisoning.

scholarly journals Study of Cardiac Troponin I level in Acute Coronary Syndrome and its correlation with Left Ventricular Systolic Function

2019 ◽  
Vol 12 (1) ◽  
pp. 24-29
Author(s):  
Mohammad Jakir Hossain ◽  
Khondoker Asaduzzaman ◽  
Solaiman Hossain ◽  
Muhammad Badrul Alam ◽  
Nur Hossain
Keyword(s):  
Acute Coronary Syndrome ◽  
Chest Pain ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Systolic Function ◽  
Left Ventricular ◽  
Cardiac Troponin I ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Coronary Syndrome

Background: In the diagnosis of acute coronary syndrome, cardiac troponin I is highly reliable and widely available biomarker. Serum level of cardiac troponin I is related to amount of myocardial damage and also closely relates to infarct size. Our aim of the study is to find out the relationship between cardiac troponin I and left ventricular systolic function after acute coronary syndrome. Methods: Total of 132 acute coronary syndrome patients were included in this study after admission in coronary care unit of Sir Salimullah Medical College, Mitford Hospital. Troponin I level was measured at admission and left ventricular ejection fraction (LVEF) was measured by echocardiography between 12-48 hours of onset of chest pain. Results: There was negative correlation between Troponin I at 12 to 48 hours of chest pain with LVEF in these study patients. With a cutoff value of troponin I e”6.8 ng/ml in STEMI patients there is a significant negative relation between 12 to 48 hrs troponin I and LVEF (p<0.001). Sensitivity of troponin I e” 6.8 ng/ml between 12 to 48 hours of chest pain in predicting LVEF <50% in STEMI was 93.75% and specificity was 77.78%. In NSTEMI sensitivity of troponin I e” 4.5 ng/ml between 12 to 48 hours of chest pain in predicting LVEF <50% was 65% and specificity was 54.05%. Conclusion: Serum troponin I level had a strong negative correlation with left ventricular ejection fraction after acute coronary syndrome and hence can be used to predict the LVEF in this setting. Cardiovasc. j. 2019; 12(1): 24-29

Evaluation of Myocardial Damage After Electroconvulsive Therapy: Analyses of High-Sensitive Cardiac Troponin I and N-Terminal pro-B-type Natriuretic Peptide

2018 ◽  
Vol 52 (02) ◽  
pp. 92-93
Author(s):  
Laura Kranaster ◽  
Johanna Badstübner ◽  
Suna Aksay ◽  
Jan Bumb ◽  
Rayan Suliman ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Electroconvulsive Therapy ◽  
Cardiac Troponin ◽  
Cardiovascular Events ◽  
Troponin I ◽  
Myocardial Damage ◽  
Cardiac Troponin I ◽  
Safe Procedure ◽  
Increased Risk ◽  
Before And After

AbstractElectroconvulsive therapy (ECT) is a remarkably safe procedure. However, there might exist a subgroup of patients with an increased risk for cardiovascular events. The cardiac-specific enzymes high-sensitive cardiac troponin I (hscTnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) were measured before and after ECT in 23 patients. No relevant increase of hscTnI after ECT was found. Mean NT-proBNP levels were higher after ECT and in three patients a new NT-proBNP elevation after ECT was identified. In conclusion, our small study did not find any evidence for myocardial damage due to ECT by measuring hsTnI, but an increase of NT-proBNP, whose clinical relevance could only be speculated, yet.

scholarly journals SP286SERUM FGF-23 AS A MARKER OF ECCENTRIC LEFT VENTRICULAR HYPERTROPHY AND INCREASED CARDIAC TROPONIN I SERUM LEVELS IN NON DIALYSIS, NON DIABETIC CKD PATIENTS

2018 ◽  
Vol 33 (suppl_1) ◽  
pp. i439-i440
Author(s):  
Svetlana Milovanova ◽  
Victor Fomin ◽  
Lidia Lysenko (Kozlovskay) ◽  
Ludmila Milovanova ◽  
Vasiliy Kozlov ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Cardiac Troponin ◽  
Ventricular Hypertrophy ◽  
Troponin I ◽  
Serum Levels ◽  
Left Ventricular ◽  
Cardiac Troponin I ◽  
Fgf 23

scholarly journals Pre-cardiopulmonary bypass administration of dexmedetomidine decreases cardiac troponin I level following cardiac surgery with sevoflurane postconditioning

2019 ◽  
Vol 47 (8) ◽  
pp. 3623-3635
Author(s):  
Hong-mei Zhou ◽  
Xiao-yan Ling ◽  
Yun-jian Ni ◽  
Cheng Wu ◽  
Zhi-peng Zhu
Keyword(s):  
New York ◽  
Cardiac Surgery ◽  
Cardiopulmonary Bypass ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Myocardial Damage ◽  
Heart Association ◽  
Cardiac Troponin I ◽  
Sevoflurane Postconditioning ◽  
Ctni Level

Objective This study was performed to determine the effect of dexmedetomidine (DEX) administration on myocardial damage in cardiac surgery with sevoflurane postconditioning. Methods We retrospectively examined all cardiac valve replacement surgeries from 1 April 2016 to 30 April 2017. Eligible patients were divided into two groups based on whether DEX was infused. DEX infusion was permitted only between intubation and the beginning of cardiopulmonary bypass (CPB). Sevoflurane was inhaled via the standard postconditioning procedure starting at aortic declamping. The cardiac troponin I (cTnI) level was measured at different time points. The postoperative outcomes and complications were also analyzed. Results One hundred patients were included in the study (DEX group, n = 53; non-DEX group, n = 47). Increased cTnI levels were significantly correlated with the New York Heart Association classification, CPB time, and DEX use. DEX use and the CPB time were potential independent factors contributing to changes in the cTnI level. The cTnI level at 6, 12, and 24 hours postoperatively was remarkably lower in the DEX than non-DEX group by 1.14, 7.83, and 5.86 ng/mL, respectively. Conclusions DEX decreased the cTnI level after CPB when sevoflurane postconditioning was used, especially at 6, 12, and 24 hours postoperatively.

scholarly journals NILAI DIAGNOSTIK UJI TROPONIN I KUANTITATIF METODE IMMUNOKROMATOGRAFI

2018 ◽  
Vol 14 (1) ◽  
pp. 20
Author(s):  
Siti Fatonah ◽  
Anik Widijanti ◽  
Tinny Endang Hernowati
Keyword(s):  
Cardiac Troponin ◽  
Biochemical Markers ◽  
Acute Coronary Syndromes ◽  
Troponin I ◽  
Myocardial Damage ◽  
Diagnostic Value ◽  
Cardiac Troponin I ◽  
Coronary Syndromes ◽  
Sensitivity Specificity ◽  
Cardiac Troponins

Cardiac troponins are the most sensitive and specific biochemical markers of myocardial damage but there is no standardization of WHO for cardiac troponin I, resulting in a variability for diagnostic value. It is necessary to determine diagnostic value for a new kitof troponin I. To evaluate a new quantitative immunochromatography assay for troponin I at a various cut off level. A cross sectionalstudy was conducted in 64 patients with acute myocardial infarction (AMI) and 55 non-AMI as control from February to September2007. The level of cardiac troponin I (cTnI) was measured and determined it diagnostic value at a various cut off level. The sensitivity,specificity, PPV and NPV of this assay were 91%, 91%, 92% and 89% at cut off level of 1,0 ng/ml (according to the kit), respectively.The cut off of cTnI were divided into five levels: 0.8, 1.0, 1.2, 1.5, and 2.0 with the area under curve were 0.923, 0.908, 0.912, and0.897, respectively. The sensitivity were 94%, 91%, 86%, 81% and 72%, respectively, the specificity were 91%, 91%, 96%, 98% and98%, respectively. This rapid diagnostic test is sensitive and specific to diagnose an acute coronary syndromes.

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