Cardiac Troponin I Level in STEMI and Clinical Correlation with Left Ventricular Dysfunction in Indian Population

Background Patients with cardiac contusion have a high risk of cardiac complications during emergency anesthesia. Despite the progress in cardiac imaging, a biologic marker of myocardial damage such as cardiac troponin I remains useful and has been proposed in clinical practice. The relationship among histologic injury, left-ventricular function, and release of cardiac enzymes and cardiac troponin I has been investigated after a controlled myocardial contusion in a rabbit model. Methods A global trauma (two levels of energy: 250 and 350 mJ) was produced on an isolated preparation of rabbit's heart, of which the temperature, perfusion flow, beating rate, and left-ventricular volume were kept constant. Left-ventricular pressure and its first derivative as a function of time were measured during a 60-min period after the blow; a timed collection of the effluent was made to assess creatine kinase, lactate dehydrogenase, and cardiac troponin I. At the end of the period, an anatomic score of the contusion was calculated by histologic examination of the hearts. Results Compared with a control group, the two levels of cardiac trauma resulted in a proportional anatomic injury significantly correlated with left-ventricular dysfunction (Delta%dP/dtmax = -16 +/- 12 and -36 +/- 20% at 3 min, mean +/- SD). Transient releases in cardiac markers after the lesser amount of trauma contrasted with a prolonged and biphasic release of cardiac troponin I after the greater amount. Peak cardiac troponin I level was correlated with anatomic injury (rho = 0.596, P= 0.001) and negatively correlated with left-ventricular dysfunction (r = -0.375, P= 0.04). Conclusion Cardiac troponin I is a marker of anatomic and functional consequences of experimental cardiac trauma and may be a predictive indicator of early posttraumatic cardiac complications during the postoperative period.

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Cardiac Troponin I Is Associated With Impaired Hemodynamics, Progressive Left Ventricular Dysfunction, and Increased Mortality Rates in Advanced Heart Failure

Circulation ◽

10.1161/01.cir.0000084543.79097.34 ◽

2003 ◽

Vol 108 (7) ◽

pp. 833-838 ◽

Cited By ~ 421

Author(s):

Tamara B. Horwich ◽

Jignesh Patel ◽

W. Robb MacLellan ◽

Gregg C. Fonarow

Keyword(s):

Heart Failure ◽

Left Ventricular Dysfunction ◽

Cardiac Troponin ◽

Ventricular Dysfunction ◽

Troponin I ◽

Mortality Rates ◽

Left Ventricular ◽

Advanced Heart Failure ◽

Cardiac Troponin I

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

Circulation Research ◽

10.1161/res.111.suppl_1.a177 ◽

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.

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

Clinica Chimica Acta ◽

10.1016/s0009-8981(97)00252-0 ◽

1998 ◽

Vol 272 (1) ◽

pp. 59-67 ◽

Cited By ~ 23

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

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Heart-type fatty-acid-binding protein is a prognostic biomarker for sepsis outcome and sepsis-related left-ventricular dysfunction: a comparison with troponin I

Research and Opinion in Anesthesia and Intensive Care ◽

10.4103/roaic.roaic_8_17 ◽

2018 ◽

Vol 5 (1) ◽

pp. 42

Author(s):

HossamM Sherif ◽

Mohamed Abul Wafa ◽

Ayman Gaber ◽

Wael Sami

Keyword(s):

Fatty Acid ◽

Left Ventricular Dysfunction ◽

Fatty Acid Binding Protein ◽

Ventricular Dysfunction ◽

Troponin I ◽

Prognostic Biomarker ◽

Binding Protein ◽

Left Ventricular ◽

Fatty Acid Binding ◽

Acid Binding Protein

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

Cardiovascular Journal ◽

10.3329/cardio.v12i1.43415 ◽

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

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