scholarly journals Comparison of the Levels of Cardiac Troponin I in Patients with Duchenne and Becker Muscular Dystrophies to Assess Cardiac Dysfunction

2021 ◽  
Author(s):  
Hiroshi Yamaguchi ◽  
Hiroyuki Awano ◽  
Tetsushi Yamamoto ◽  
Masafumi Matsuo ◽  
Kazumoto Iijima
Keyword(s):  
Cardiac Dysfunction ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Troponin I ◽  
Genetic Modifier ◽  
Becker Muscular Dystrophy ◽  
Left Ventricular ◽  
Cardiac Troponin I ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction

Abstract Background: Cardiac troponin I (cTnI), uniquely expressed in the myocardium, is a marker for acute myocardial injury. Its clinical significance in Duchenne and Becker muscular dystrophy (DMD and BMD) and its relation to alpha-actinin-3 (ACTN3) genotype as a genetic modifier of cardiomyopathy are still unknown.Methods and Results: Overall, 529 and 131 serum cTnI values of 127 DMD and 47 BMD patients, respectively, were reviewed. cTnI elevation was generally observed in the second decade of life. Both cTnI levels and the proportion of abnormal cTnI levels were significantly higher in DMD patients than in BMD patients (age range: 1< years ≤10 and 10< years ≤18 and 10< years ≤18, respectively). Decreased left ventricular ejection fraction was observed after cTnI elevation in both populations. cTnI levels by age in DMD patients with ACTN3 null genotype tended to increase highly and early.Conclusions: Myocardial injury indicated by cTnI was more common and severe in DMD patients than in BMD patients. cTnI elevation preceding cardiac dysfunction may represent an early phase of cardiomyopathy progression and may be a biomarker for early detection of cardiomyopathy in DMD and BMD patients. The ACTN3 null genotype may be a risk factor for early myocardial injury.

Evidence for lack of myocardial injury in children with acute rheumatic carditis

2002 ◽  
Vol 12 (6) ◽  
pp. 519-523 ◽  
Author(s):  
Richard V. Williams ◽  
L. LuAnn Minich ◽  
Robert E. Shaddy ◽  
L. George Veasy ◽  
Lloyd Y. Tani
Keyword(s):  
Mitral Regurgitation ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Troponin I ◽  
Left Ventricular ◽  
Cardiac Troponin I ◽  
Left Ventricular Ejection ◽  
Myocardial Inflammation ◽  
Rheumatic Carditis ◽  
Ventricular Ejection Fraction

Despite pathologic evidence of myocardial inflammation, the significance of myocarditis in children with acute rheumatic carditis remains controversial. Elevations in cardiac troponin I have been demonstrated in other forms of myocarditis. The purpose of our study was to determine if levels of cardiac troponin I are elevated, suggesting myocardial injury, in patients with acute rheumatic carditis. We identified all those patients with acute rheumatic fever, presenting between July 1998 and December 2000, who had clinical evidence of carditis, such as a new murmur of mitral or aortic regurgitation, and who had an echocardiogram, measurements of levels of cardiac troponin I, erythrocyte sedimentation rate, and/or C-reactive protein performed at the time of presentation. Their charts were reviewed for demographic and clinical data. Echocardiograms were reviewed for severity of aortic and mitral regurgitation, and measurements made of left ventricular ejection fraction, fractional shortening, and end-diastolic dimension. We found 16 patients with acute rheumatic carditis, ranging in age from 2.0 to 16.1 years, with just over one-third having symptoms of congestive heart failure. All patients had evidence of acute inflammation. There was a significant relationship between symptoms and severity of mitral regurgitation. No patient had elevated levels of cardiac troponin I level. The fact that levels of cardiac troponin I are not elevated in the serum of children with acute rheumatic carditis suggests that there is minimal myocytic necrosis in this setting. This supports the concept that acute valvar regurgitation is the major hemodynamic abnormality in these patients.

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

scholarly journals Correlation of Cardiac Troponin I with Left Ventricular Systolic Function in Patients with Acute ST-segment Elevated Myocardial Infarction

2021 ◽  
Vol 16 (1) ◽  
pp. 34-38
Author(s):  
Kamal Uddin Ahmed ◽  
Mst Rabeya Bilkis ◽  
AKM Monwarul Islam ◽  
Gias Uddin Ahmed ◽  
Syed Md Romel ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Left Ventricular ◽  
Cardiac Troponin I ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Serum Cardiac Troponin

Myocardial infarction is one of the leading cause of death globally and following acute myocardial infarction prognosis depends on extent of myocardial damage. This study was aimed to correlate cardiac troponin I level with the left ventricular systolic function in patients with acute ST-elevated myocardial infarction. A total of 104 patients of acute ST-segment elevated myocardial infarction receiving streptokinase therapy within 12 hours of onset of chest pain were studied. Cardiac troponin I concentration was measured by immunometric assay and echocardiographic left ventricular ejection fraction was calculated by modified biplane Simpson's method. Left ventricular ejection fraction (LVEF) was compared with serum cardiac troponin I concentration. Study subjects were divided into two groups on the basis of LVEF. In group I, there were 54 patients with LVEF < 50% and in group II, there were 50 patients with LVEF >_ 50%. The mean cTnI within 12 hours of onset was 129 ± 8.7 ng/ml in group I and11 ± 2.1 ng/ml group II and the difference was statistically significant (p<0.001). Serum cardiac troponin I concentration has a strong negative correlation with left ventricular ejection fraction after first acute myocardial infarction. A level of serum cardiac troponin I >_ 6.6 ng/ml provided a good indication for LVEF <50% and this can be used to detect patients with higher risk. Faridpur Med. Coll. J. 2021;16(1):34-38

scholarly journals The role of neurohormonal blockers in the primary prevention of acute-, early-, and late-onset anthracycline-induced cardiotoxicity

2020 ◽  
Vol 72 (1) ◽  
Author(s):  
Ahmed Ayuna ◽  
Nik Abidin
Keyword(s):  
Primary Prevention ◽  
Myocardial Injury ◽  
Troponin I ◽  
Late Onset ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Main Body ◽  
Converting Enzyme Inhibitors ◽  
Ventricular Ejection Fraction

Abstract Background Anthracycline-induced cardiotoxicity has been classified based on its onset into acute, early, and late. It may have a significant burden on the quality and quantity of life of those exposed to this class of medication. Currently, there are several ongoing debates on the role of different measures in the primary prevention of cardiotoxicity in cancer survivors. Our article aims to focus on the role of neurohormonal blockers in the primary prevention of anthracycline-induced cardiotoxicity, whether it is acute, early, or late onset. Main body of the abstract PubMed and Google Scholar database were searched for the relevant articles; we reviewed and appraised 15 RCTs, and we found that angiotensin-converting enzyme inhibitors (ACEI) and B-blockers were the most commonly used agents. Angiotensin II receptor blockers (ARBs) and mineralocorticoid receptor antagonists (MRAs) were used in a few other trials. The follow-up period was on the range of 1–156 weeks (mode 26 weeks). Left ventricular ejection fraction (LVEF), left ventricular diameters, and diastolic function were assessed by either echocardiogram or occasionally by cardiac magnetic resonance imaging (MRI). The occurrence of myocardial injury was assessed by troponin I. It was obvious that neurohormonal blockers reduced the occurrence of LVEF and myocardial injury in 14/15 RCTs. Short conclusion Beta-blockers, especially carvedilol and ACEI, especially enalapril, should be considered for the primary prevention of acute- and early-onset cardiotoxicity. ARB and MRA are suitable alternatives when patients are intolerant to ACE-I and B-blockers. We recommend further studies to explore and establish the role of neurohormonal blockers in the primary prevention of the acute-, early-, and late-onset cardiotoxicity.

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.

Abstract P234: Hypertensive Disorders Of Pregnancy And Increased Levels Of Cardiac Troponin I After Delivery

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Takao Kato ◽  
Eri Muta ◽  
Moriaki Inoko
Keyword(s):  
Pregnant Women ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Normal Population ◽  
Laboratory Data ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Hypertensive Disorders Of Pregnancy ◽  
Ventricular Ejection Fraction ◽  
Hypertensive Disorders

Background: Cardiovascular functions and hemodynamics dramatically change during pregnancy such as cardiac output, expanded blood volume, reduced systematic vascular resistance, and heart chamber enlargement. Hypertensive disorders of pregnancy (HDP) may affect the cardiac load during pregnancy; however, the data about plasma concentration of cardiac troponin in pregnant women with HDP is very limited. Methods: We prospectively collected data of 751 pregnant women between 2012 and 2013 in Japanese general hospital. We analyzed laboratory data and echocardiographic findings after delivery. The elevated cTnI was defined as >0.015 ng/mL because the normal population have serum cTnI of less than 0.015 ng/mL in this assay. Results: The HDP were observed in 32 patients; the elevated cTnI was observed 40 patients. The age of patients with HDP (33.7 ±4.3 years) was not different from that of those without HDP (33.3 ± 5.0 years). The brain natriuretic peptides levels were not different between those with and without HDP. The proportion of elevated cTnI was higher in those with HDP (21.8%) than those without (3.6%, P<0.0001). After adjusting for confounders, the risk of elevated cTnI in those with HDP relative to those without HDP remained significant (odds ratio 4.52, 95% confidence interval 1.45-14.5). There were no women with reduced left ventricular ejection fraction. Conclusions: HDP was associated with elevated cTni, suggesting myocardial microinjury might occur more frequently in those with HDP.

Trastuzumab-Induced Cardiotoxicity: Clinical and Prognostic Implications of Troponin I Evaluation

2010 ◽  
Vol 28 (25) ◽  
pp. 3910-3916 ◽  
Author(s):  
Daniela Cardinale ◽  
Alessandro Colombo ◽  
Rosalba Torrisi ◽  
Maria T. Sandri ◽  
Maurizio Civelli ◽  
...  
Keyword(s):  
At Risk ◽  
Cardiac Dysfunction ◽  
Troponin I ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Trastuzumab Therapy ◽  
Before And After ◽  
Patients At Risk ◽  
Prognostic Implications

Purpose Treatment of breast cancer with trastuzumab is complicated by cardiotoxicity in up to 34% of the patients. In most patients, trastuzumab-induced cardiotoxicity (TIC) is reversible: left ventricular ejection fraction (LVEF) improves after trastuzumab withdrawal and with, or sometimes without, initiation of heart failure (HF) therapy. The reversibility of TIC, however, is not foreseeable, and identification of patients at risk and of those who will not recover from cardiac dysfunction is crucial. The usefulness of troponin I (TNI) in the identification of patients at risk for TIC and in the prediction of LVEF recovery has never been investigated. Patients and Methods In total, 251 women were enrolled. TNI was measured before and after each trastuzumab cycle. LVEF was evaluated at baseline, every 3 months during trastuzumab therapy, and every 6 months afterward. In case of TIC, trastuzumab was discontinued, and HF treatment with enalapril and carvedilol was initiated. TIC was defined as LVEF decrease of > 10 units and below 50%. Recovery from TIC was defined as LVEF increase above 50%. Results TIC occurred in 42 patients (17%) and was more frequent in patients with TNI elevation (TNI+; 62% v 5%; P < .001). Twenty-five patients (60%) recovered from TIC. LVEF recovery occurred less frequently in TNI+ patients (35% v 100%; P < .001). At multivariate analysis, TNI+ was the only independent predictor of TIC (hazard ratio [HR], 22.9; 95% CI, 11.6 to 45.5; P < .001) and of lack of LVEF recovery (HR, 2.88; 95% CI,1.78 to 4.65; P < .001). Conclusion TNI+ identifies trastuzumab-treated patients who are at risk for cardiotoxicity and are unlikely to recover from cardiac dysfunction despite HF therapy.

Abstract 13441: D-dimmer is a Predictor of Cancer Therapeutics-related Cardiac Dysfunction in Patients Treated With Cardiotoxic Chemotherapy

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Masayoshi Oikawa ◽  
Daiki Yaegashi ◽  
Tetsuro Yokokawa ◽  
Tomofumi Misaka ◽  
Takamasa Sato ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Troponin I ◽  
Uterine Cancer ◽  
Cancer Therapeutics ◽  
Left Ventricular ◽  
Time Dependent ◽  
Volume Index ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
D Dimer

Background: D-dimer is a sensitive biomarker for cancer-associated thrombosis, but little is known about its significance on cancer therapeutics-related cardiac dysfunction (CTRCD). Methods and Results: Consequtive 202 patients planned for cardiotoxic chemotherapy (anthracyclines, monoclonal antibodies, tyrosine kinase inhibitors, and proteasome inhibitors) were enrolled and followed up for 12 months. Cancer types were as follows: breast cancer (n=112), lymphoma (n=37), ovarian or uterine cancer (n=18), leukemia (n=13), multiple myeloma (n=6), bone cancer (n=4), and others (n=12). All patients underwent echocardiography and blood test at baseline, 3-month, 6-month, and 12-month. The patients were divided into 2 groups based on the value of D-dimer (>1.5 μg/ml or ≦1.5 μg/ml) at baseline before chemotherapy: High D-dimer group (n=52) and Low D-dimer group (n=150). At baseline, left ventricular ejection fraction (LVEF), left ventricular end-systolic volume index, and B-type natriuretic peptide levels were similar between two groups. Time-dependent decrease in LVEF was observed after chemotherapy in high D-dimer group (baseline, 66±5%; 3-month, 63±7%; 6-month, 62±7%; 12-month 62±6%; P=0.005, figure), but not in low D-dimer group. Time-dependent increase in troponin I was similarly observed after chemotherapy in both groups. The occurrence of CTRCD was higher in high D-dimer group than in low D-dimer group (11.5% vs. 4.0%, P=0.048). When we set the cut-off value of baseline D-dimer at 1.65 μg/ml from ROC analysis, sensitivity, specificity, and area under the curve to predict CTRCD were 50%, 77%, and 0.679, respectively. Multivariable logistic analysis revealed that baseline D-dimer was an independent factor to predict the decrease in LVEF more than 10% after cardiotoxic chemotherapy (odds ratio 1.210, 95% confidence interval [1.020-1.440], P=0.025). Conclusion: Baseline D-dimer is a pivotal parameter to predict CTRCD.

scholarly journals Detecting early onset of anthracyclines-induced cardiotoxicity using a novel panel of biomarkers in West-Virginian population with breast cancer

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hari Vishal Lakhani ◽  
Sneha S. Pillai ◽  
Mishghan Zehra ◽  
Benjamin Dao ◽  
Maria Tria Tirona ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Cardiac Dysfunction ◽  
Early Onset ◽  
Troponin I ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Circulating Mirnas ◽  
Ventricular Ejection Fraction

AbstractCardiotoxic manifestation associated with breast cancer treatment by anthracycline regimen increases patients’ susceptibility to myocardial injury, reduction in left ventricular ejection fraction and complications associated with heart failure. There is currently no standardized, minimally invasive, cost effective and clinically verified procedure to monitor cardiotoxicity post-anthracycline therapy initiation, and to detect early onset of irreversible cardiovascular complications. This study aims to create a panel of novel biomarkers and circulating miRNAs associated with cardiotoxicity, further assessing their correlation with cardiac injury specific markers, troponin I and T, and demonstrate the development of cardiac dysfunction in breast cancer patients. Blood obtained from West Virginian females clinically diagnosed with breast cancer and receiving anthracyclines showed upregulated level of biomarkers and circulating miRNAs after 3 and 6 months of chemotherapy initiation with increased levels of cardiac troponin I and T. These biomarkers and miRNAs significantly correlated with elevated troponins. Following 6 months of anthracycline-regimens, 23% of the patient population showed cardiotoxicity with reduced left ventricular ejection fraction. Our results support the clinical application of plasma biomarkers and circulating miRNAs to develop a panel for early diagnosis of chemotherapy related cardiac dysfunction which will enable early detection of disease progression and management of irreversible cardiac damage.

scholarly journals Cardiotoxic effects and myocardial injury: the search for a more precise definition of drug cardiotoxicity

2021 ◽  
Vol 59 (1) ◽  
pp. 51-57
Author(s):  
Daniela Maria Cardinale ◽  
Martina Zaninotto ◽  
Carlo Maria Cipolla ◽  
Claudio Passino ◽  
Mario Plebani ◽  
...  
Keyword(s):  
Early Detection ◽  
Myocardial Injury ◽  
Randomized Clinical Trials ◽  
Imaging Techniques ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Cardiac Imaging Techniques ◽  
Ventricular Ejection Fraction ◽  
Early Evaluation ◽  
Definition Of

AbstractDrug-induced cardiotoxicity is a major clinical problem; cardiotoxic drugs may induce both cardiac dysfunction and myocardial injury. Several recent studies reported that cardiac troponins measured with high-sensitivity methods (hs-cTn) can enable the early detection of myocardial injury related to chemotherapy or abuse of drugs that are potentially cardiotoxic. Several authors have some concerns about the standard definition of cardiotoxicity, in particular, regarding the early evaluation of chemotherapy cardiotoxicity in cancer patients. Several recent studies using the hs-cTn assay indicate that myocardial injury may precede by some months or years the diagnosis of heart failure (HF) based on the evaluation of left ventricular ejection fraction (LVEF). Accordingly, hs-cTn assay should considered to be a reliable laboratory test for the early detection of asymptomatic or subclinical cardiotoxic damage in patients undergoing cancer chemotherapy. In accordance with the Fourth Universal Definition of Myocardial Infarction and also taking into account the recent experimental and clinical evidences, the definition of drug-cardiotoxicity should be updated considering the early evaluation of myocardial injury by means of hs-cTn assay. It is conceivable that the combined use of hs-cTn assay and cardiac imaging techniques for the evaluation of cardiotoxicity will significantly increase both diagnostic sensitivity and specificity, and also better prevent chemotherapy-related left ventricular (LV) dysfunction and other adverse cardiac events. However, large randomized clinical trials are needed to evaluate the cost/benefit ratio of standardized protocols for the early detection of cardiotoxicity using hs-cTn assay in patients receiving chemotherapy for malignant diseases.

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