Degradation of rat cardiac troponin I during ischemia independent of reperfusion

2004 ◽  
Vol 287 (3) ◽  
pp. H1269-H1275 ◽  
Author(s):  
Brian S. Palmer ◽  
Paul F. Klawitter ◽  
Peter J. Reiser ◽  
Mark G. Angelos
Keyword(s):  
Cardiac Troponin ◽  
Troponin I ◽  
Progressive Increase ◽  
Protective Role ◽  
Left Ventricular ◽  
Cardiac Troponin I ◽  
Global Ischemia ◽  
Stunned Myocardium ◽  
Rat Hearts ◽  
Developed Pressure

Cardiac troponin I (cTnI) degradation has been noted in the stunned myocardium of rodents after ischemia and reperfusion and is one proposed mechanism for the decreased left ventricular (LV) contractility in postischemic hearts. cTnI degradation has been best described after reperfusion of the ischemic myocardium. The effect of ischemia, independent of reperfusion, on cTnI breakdown has not been well characterized. We tested the hypothesis that progressive cTnI degradation occurs with increasing durations of ischemia and that this ischemia-based degradation is, in part, oxidant mediated. Isolated perfused rat hearts underwent global ischemia of 15, 20, or 25 min with and without reperfusion. A second series of hearts was treated with the antioxidants tiron (10 mM) and N-acetylcysteine (4 mM) before 20 min of global ischemia without reperfusion. cTnI degradation was measured using a cTnI-specific antibody and Western blot analyses. A progressive increase in cTnI degradation was seen with increasing duration of ischemia (no reperfusion), which correlated with the return of LV developed pressure during reperfusion. The extent of cTnI degradation was increased in hearts pretreated with antioxidants, although the qualitative degradation pattern was not altered. We conclude that a time-dependent cTnI breakdown occurs during global ischemia that is independent of reperfusion. cTnI breakdown during ischemia is further increased in the presence of antioxidants, suggesting ROS generated during ischemia may play a cTnI protective role.

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 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

Challenges of Management of Stunned Myocardium Associated with Acute Subarachnoid Hemorrhage: A Case Report

2018 ◽  
Vol 4 (2) ◽  
pp. 150-153
Author(s):  
Sirajee Shafiqul Islam ◽  
Kazi Mohibur Rahman ◽  
Sharif Uddin Khan ◽  
Dewan Md Elyas ◽  
Md Aminul Hasanat ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Troponin I ◽  
Past History ◽  
Cardiac Troponin I ◽  
Stunned Myocardium ◽  
Anterior Communicating Artery ◽  
Acute Subarachnoid Hemorrhage ◽  
History Of ◽  
Digital Subtraction Angiogram ◽  
Small Aneurysm

A 40 year old lady presented with headache and vomiting having no past history of hyper-tension, diabetes, smoking, alcohol or drug abuse. Computed Tomography (CT) scan of brain revealed sub-arachnoid haemorrhage in parasaggital frontal and lt. Sylvian fissure. Digital Subtraction Angiogram (DSA) was performed and revealed a small aneurysm (4x 2.5 x 2) mm in anterior communicating artery. After 12 hours of DSA patient complaints of sudden severe headache followed by unconsciousness. Repeat CT performed and revealed new onset rt. fronto-basal intra-cranial hematoma consistent with rebleed. On admission the patient was with normal Glasgow Coma Scale (GCS-15), Blood pressure (BP125/80mm/Hg), ECG & Echocardiogram. After rebleed patient developed low BP (50/35mmHg), GCS down gread (05), ECG showed sinus tachycardia with poor progression of R(V1-V3) wave, elevated cardiac Troponin –I(-4919.6 Pg). Then patient was given a regimen of ionotropic agent noradrenalin at dose 5mcg/kg/h. From day 3th of rebleed the patient was clinically improving, BP(120/84mmHg), GCS( 8), ECG normal, Cardiac Troponin-I- (790.8 Pg/dl). Then emergency endovascular ACOM coil embolization was done.Journal of National Institute of Neurosciences Bangladesh, 2018;4(2): 150-153

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
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