scholarly journals Main Aspects of Biochemistry, Physiology of Cardiac Troponins

2020 ◽  
Vol 6 (5) ◽  
pp. 105-112 ◽  
Author(s):  
A. Chaulin ◽  
Yu. Grigoryeva

Cardiac troponins (troponin I, T, and C) play an important role in the regulation of contractile function of the heart muscle. Mutations in cardiac troponins are associated with the development of various types of cardiomyopathies, which lead to heart failure and death. The determination of the concentration of cardiac troponins in the blood is used in the diagnosis of some cardiovascular diseases, including acute myocardial infarction, myocarditis, heart failure. This review summarizes the available data on the structure and functions of cardiac troponins, their role in the regulation of myocardial contractions and clinical application.

2021 ◽  
Vol 100 (1) ◽  
pp. 119-124
Author(s):  
D.V. Zamaraeva ◽  
◽  
I.I. Trunina ◽  
A.S. Sharykin ◽  
I.M. Osmanov ◽  
...  

Troponin I has been successfully used in the diagnosis of acute myocardial infarction in adults. According to recent studies the field of cardiac troponins was widely developed. Troponin I elevated in patients with heart failure, tachyarrhythmias, myocarditis, pulmonary hypertension, intoxications of cardiotoxic drugs, sepsis and other similar conditions. Most literature reviews represent information of using cardiac troponins only among adults. Pediatric publications contain much less information. There are no reference values and practical recommendations for troponin I in children. The aim of this article is to cover all available data of use and interpretation of troponin I in children with different cardiac pathology.


2020 ◽  
Vol 126 (9) ◽  
pp. 1260-1280 ◽  
Author(s):  
Antonio Abbate ◽  
Stefano Toldo ◽  
Carlo Marchetti ◽  
Jordana Kron ◽  
Benjamin W. Van Tassell ◽  
...  

The intracellular sensing protein termed NLRP3 (for NACHT, LRR, and PYD domains-containing protein 3) forms a macromolecular structure called the NLRP3 inflammasome. The NLRP3 inflammasome plays a major role in inflammation, particularly in the production of IL (interleukin)-1β. IL-1β is the most studied of the IL-1 family of cytokines, including 11 members, among which are IL-1α and IL-18. Here, we summarize preclinical and clinical findings supporting the key pathogenetic role of the NLRP3 inflammasome and IL-1 cytokines in the formation, progression, and complications of atherosclerosis, in ischemic (acute myocardial infarction), and nonischemic injury to the myocardium (myocarditis) and the progression to heart failure. We also review the clinically available IL-1 inhibitors, although not currently approved for cardiovascular indications, and discuss other IL-1 inhibitors, not currently approved, as well as oral NLRP3 inflammasome inhibitors currently in clinical development. Canakinumab, IL-1β antibody, prevented the recurrence of ischemic events in patients with prior acute myocardial infarction in a large phase III clinical trial, including 10 061 patients world-wide. Phase II clinical trials show promising data with anakinra, recombinant IL-1 receptor antagonist, in patients with ST-segment–elevation acute myocardial infarction or heart failure with reduced ejection fraction. Anakinra also improved outcomes in patients with pericarditis, and it is now considered standard of care as second-line treatment for patients with recurrent/refractory pericarditis. Rilonacept, a soluble IL-1 receptor chimeric fusion protein neutralizing IL-1α and IL-1β, has also shown promising results in a phase II study in recurrent/refractory pericarditis. In conclusion, there is overwhelming evidence linking the NLRP3 inflammasome and the IL-1 cytokines with the pathogenesis of cardiovascular diseases. The future will likely include targeted inhibitors to block the IL-1 isoforms, and possibly oral NLRP3 inflammasome inhibitors, across a wide spectrum of cardiovascular diseases.


2020 ◽  
Author(s):  
Marta R Moksnes ◽  
Helge Røsjø ◽  
Anne Richmond ◽  
Magnus N Lyngbakken ◽  
Sarah E Graham ◽  
...  

AbstractCirculating cardiac troponin proteins are associated with structural heart disease and predict incident cardiovascular disease in the general population. However, the genetic contribution to cardiac troponin I (cTnI) concentrations and its causal effect on cardiovascular phenotypes is unclear. We combine data from two large population-based studies, the Trøndelag Health Study and the Generation Scotland Scottish Family Health Study and perform a genome-wide association study of high-sensitivity cTnI concentrations with 48 115 individuals. We further used two-sample Mendelian randomization to investigate the causal effects of circulating cTnI on acute myocardial infarction and heart failure.We identified 12 genetic loci (8 novel) associated with cTnI concentrations. Associated protein-altering variants highlighted putative functional genes: CAND2, HABP2, ANO5, APOH, FHOD3, TNFAIP2, KLKB1 and LMAN1. Phenome-wide association tests in 1283 phecodes and 274 continuous traits in UK Biobank showed associations between a polygenic risk score for cTnI and cardiac arrhythmias, aspartate aminotransferase 1 and anthropometric measures. Excluding individuals with a known history of comorbidities did not materially change associations with cTnI. Using two-sample Mendelian randomization we confirmed the non-causal role of cTnI in acute myocardial infarction (5 948 cases, 355 246 controls). We found some indications for a causal role of cTnI in heart failure (47 309 cases and 930 014 controls), but this was not supported by secondary analyses using left ventricular mass as outcome (18 257 individuals).Our findings clarify the biology underlying the heritable contribution to circulating cTnI and support cTnI as a non-causal biomarker for acute myocardial infarction and heart failure development in the general population. Using genetically informed methods for causal inference of cTnI helps inform the role and value of measuring cTnI in the general population.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Beatrice von Jeinsen ◽  
Stergios Tzikas ◽  
Lars Palapies ◽  
Tanja Zeller ◽  
Christoph Bickel ◽  
...  

Introduction: Cardiac troponins are the gold standard to diagnose acute myocardial infarction (AMI). Troponin I (TnI) levels are known to be increased in patients with chronic kidney disease (CKD) irrespective of an AMI. The established diagnostic TnI cut-off to detect AMI is calculated based on a healthy reference population and might not be representative for CKD patients. Hypothesis: The aim of this study was to investigate TnI levels in patients with and without CKD with suspected AMI and to calculate CKD- optimized diagnostic TnI thresholds. Methods: Of 1572 patients enrolled with suspected AMI, 266 patients showed an impaired renal function with estimated glomerular filtration rate (eGFR) of less then 60ml/min and were classified as patients with CKD. N=77 (34%) of patients with CKD and n=278 (24%) without CKD had the final diagnosis AMI. TnI was measured on admission and after 3h. Based on receiver operator characterics curve analyses (AUROC) of the baseline levels CKD optimized TnI threshold were derived. Sensitivity and specifity were calculated for the 99th percentile cut-off (30.0 pg/mL), the optimized cut-off (58.0 pg/mL) and the change in TnI concentration within 3h after admission. Results: Patients with CKD had higher TnI levels then patients without CKD (6.0pg/mL vs. 20.9pg/ml; p<0.001). This difference was more pronounced in patients without AMI (median 9.1 vs. 4.4; p<0.001), whereas the difference diminished in AMI patients (median 337.4 vs. 238.6; p=0.83). In CKD patients TnI remained a strong marker to detect AMI with AUROC of 0.933 compared to 0.969 in patients without CKD. Applying the 99th percentile threshold it was associated with a relevant loss of specificity in CKD patients with 80% compared to 96% in patients without CKD. This poor specificity could be regained by use of a higher CKD-optimized threshold or use of the change in TnI concentration within 3h leading to specificities of 90% and 96%, respectively. Conclusions: Patients presenting with suspected AMI and CKD have higher TnI levels on admission compared to patients without CKD leading to a low specificity detecting AMI in CKD patients. Using an CKD-optimized TnI cut-off level on admission or using the change in TnI concentration within 3h is able to regain this lost specificity.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Masako Matsunaga ◽  
John J. Chen ◽  
Mayumi Jijiwa ◽  
Eunjung Lim

Abstract Background To date, little is known about cardiovascular disease risks among older adults with non-valvular atrial fibrillation by their association with diabetes and osteoarthritis status, based on longitudinal data with substantial amounts of non-white individuals. The objective of this study was to examine the risks for three cardiovascular diseases: stroke, acute myocardial infarction (AMI), and heart failure (HF), by diabetes and osteoarthritis status among older adults with non-valvular atrial fibrillation in Hawaii. Methods We conducted a retrospective observational cohort study for older adults (65 years and older) with non-valvular atrial fibrillation using the Hawaii Medicare data 2009–2017. Their risks for the three cardiovascular diseases by diabetes and osteoarthritis status (diabetes, osteoarthritis, diabetes and osteoarthritis, and without diabetes and osteoarthritis) were examined by multivariable Cox proportional hazard regression models. Results The analysis included 19,588 beneficiaries followed up for a maximum of 3288 days (diabetes: n = 4659, osteoarthritis: n = 1978, diabetes and osteoarthritis: n = 1230, without diabetes and osteoarthritis: n = 11,721).  Among them, those diagnosed with the cardiovascular diseases were identified (stroke: diabetes n = 837, osteoarthritis n = 315, diabetes and osteoarthritis n = 184, without diabetes and osteoarthritis n = 1630)(AMI: diabetes n = 438, osteoarthritis n = 128, diabetes and osteoarthritis n = 118, without diabetes and osteoarthritis n = 603)(HF: diabetes n = 2254, osteoarthritis n = 764, diabetes and osteoarthritis n = 581, without diabetes and osteoarthritis n = 4272). After adjusting for age, sex, race/ethnicity, and other potential confounders, those with diabetes and osteoarthritis had higher risks for HF (hazard ratio: 1.21 95% confidence interval: 1.10–1.33) than those without diabetes and osteoarthritis. They also had higher risks than those with osteoarthritis for HF. Those with diabetes had higher risks for all three cardiovascular diseases than the other three groups. Conclusions Variation in cardiovascular disease risks for older adults with non-valvular atrial fibrillation in Hawaii exists with diabetes and osteoarthritis status.


2021 ◽  
Vol 8 (30) ◽  
pp. 2724-2730
Author(s):  
Nikhila Suresh Kumar ◽  
Sivaa Rajendran ◽  
Sunil Kumar Nanda ◽  
Mark Christopher ◽  
Ravichandran Kandasamy

BACKGROUND Cardiovascular diseases (CVDs) are one of the major health problems and leading cause of death worldwide. Acute myocardial infarction (AMI) is one of the cardiovascular diseases which has high mortality in early hours of presentation and hence early and accurate diagnosis is important to reduce the morbidity and mortality. Troponin I and CKMB (Creatine Kinase-Myocardial Band) activity are the routine biomarkers used for early diagnosis of AMI. Since there is a high degree of instability in the measurement of CKMB activity and also there are frequent noncorrelation with the Troponin I levels, we aimed to estimate and compare the levels of CKMB mass and CKMB activity in patients with and without AMI. METHODS This comparative study included 40 cases and 40 controls. Cases were adult patients between the age group of 30 -70 years diagnosed with AMI by electrocardiogram (ECG) and positive troponin I, and controls were who presented with non myocardial infection (MI) chest pain. Blood samples were collected to estimate CKMB activity and CKMB mass. RESULTS The median value of CKMB activity in controls was 21 IU/L (IQR 13.25-27.75) and that in cases was 40 IU/L (IQR 30.25-94.25) and this difference is statistically significant. The median value of CKMB mass in controls was 5 ngmL (IQ 4-6) and that in cases was 19.50 ng/mL (IQR 6-61.50) which is also statistically significant in differentiating both. In Spearman correlation test, both showed a better statistical significance and correlation in cases (r = 0.787). It was evident that the median value of CKMB activity in controls was higher than that of the normal range for CKMB activity which is 8-16 IU/L, but the median value of CKMB mass in controls was well within the normal range of 5- 10 ng/mL, considering it to be a better marker for eliminating false positive results. CONCLUSIONS CKMB mass can be considered as a better marker than CKMB activity for accurate diagnosis of AMI along with troponin I. KEYWORDS Cardiovascular Diseases, Biomarker, Acute Myocardial Infarction, CKMB Mass, CKMB Activity


RSC Advances ◽  
2020 ◽  
Vol 10 (60) ◽  
pp. 36396-36403
Author(s):  
Mingjian Lang ◽  
Dan Luo ◽  
Guangyi Yang ◽  
Quanxi Mei ◽  
Guangjun Feng ◽  
...  

We have developed an ultrasensitive and highly specific electrochemical sensing platform for the detection of cardiac troponin I (cTnI), a recognized biomarker for the diagnosis of acute myocardial infarction (AMI) and related cardiovascular diseases (CVDs).


2021 ◽  

Methods for the determination of cardiac troponins have been significantly improved, facilitating further advancement of the therapeutic and diagnostic process of the cardiovascular diseases case management. In particular, acceleration of the acute myocardial infarction testing (early diagnostic algorithms: 0-1 h, 0-3 h) enabled earlier detection and choice of the optimal treatment tactics. At the same time, with the increased sensitivity in the laboratory test results interpretation, there emerged a necessity to take into account some additional factors that may affect the concentration of cardiac troponins in blood serum. Several recent studies have reported the existence of circadian rhythms in cardiac troponins. This article aims to discuss the possible mechanisms of how circadian rhythms of cardiac troponins develop and their influence on the diagnosis of acute myocardial infarction.


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