scholarly journals PENINGKATAN HIGH-SENSITIVE CARDIAC TROPONIN (HS-CTN) SETELAH LATIHAN INTENSITAS TINGGI YANG INTENSIF

2019 ◽  
Author(s):  
Indira Vidiari J ◽  
Nila Wahyuni ◽  
I Putu Adiartha Griadhi
Keyword(s):  
High Intensity ◽  
Cardiac Troponin ◽  
Meta Analysis ◽  
Cardiac Injury ◽  
High Sensitivity ◽  
Cardiac Damage ◽  
Intensive Exercise ◽  
Different Types ◽  
Underlying Pathophysiology

ABSTRACTThe role of exercise as a strategy for prevention, management and therapy in cardiovascular disease has been well described, but in some studies, it has been suggested that there is an increase in biomarkers in cardiac damage or cardiac troponin (cTn) after intensive, high-intensity exercise in healthy individuals. Several studies have shown significant increases in cardiac troponins after different types of exercise. The latest meta-analysis, showing that high-sensitivity cardiac troponin (hs-cTn) increases in about 83% of individuals after long and intensive exercise. The current pathophysiology of hs-cTn is not well understood. Several hypotheses have been proposed, such as transmembrane leakage from cytoplasmic free cTnT and cTnI or decreased troponin clearance from plasma, both caused by overloading of free radicals, myocardial stretching, elevated core temperature, or alteration of pH. Further research is needed with a full prospective study to evaluate the underlying pathophysiology of enhancing high sentivity cardiac troponin (hs-cTn) is an effective strategy for preventing or limiting cardiac injury and sport exercise safe for heart.Keywords: cardiac Troponin (cTn), high sensitivity cardiac troponin (hs-cTn), high intensity intensive exercise

scholarly journals ASSOCIATION BETWEEN ELEVATED HIGH SENSITIVITY CARDIAC-TROPONIN I LEVELS AND INCREASE IN LEVELS OF C-REACTIVE PROTEIN, INTERLEUKIN-6, D-DIMER, AND CONSEQUENT CARDIAC INJURY AND MORTALITY FOR PATIENTS WITH CORONAVIRUS DISEASE 2019: A META-ANALYSIS

2021 ◽  
pp. 160-166
Author(s):  
DHEAA SHAMIH ZAGEER ◽  
SUNDUS FADHIL HANTOOSH ◽  
WATHIQ Q SH. ALI
Keyword(s):  
Interleukin 6 ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Meta Analysis ◽  
Cardiac Injury ◽  
High Sensitivity ◽  
Cardiac Troponin I ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
D Dimer

Objectives: This meta-analysis aims to investigate the role of high sensitivity-cardiac troponin I (hs-cTnI) as a prognostic factor for cardiac injury and as a risk factor of death for patients with coronavirus disease 2019 (COVID-19). This meta-analysis studies the impact of hs-cTnI elevated levels on C-reactive protein (C-RP) protein, interleukin-6 (IL-6), and D-dimer (DD) levels in COVID-19 affected individuals. Methods: Of 557 downloaded articles according to chosen criteria for this meta-analysis, 11 were finally chosen as they met the criteria. Results: Male and elderly individuals were noticeably prone to COVID-19 infection and considerably underwent death in comparison with female and young individuals. Levels of hs-cTn I, C-RP, IL-6, and DD were significantly higher among dead compare to survivors for COVID-19 affected individuals. Conclusions: Levels of C-RP, IL-6, and DD were considerably high and in linear relation with elevated hs-cTn I levels. Hs-cTn I can be considered a reliable marker for COVID-19 infection prognosis and potent predictor of decease.

Involvement of monocytes/macrophages as key factors in the development and progression of cardiovascular diseases

2014 ◽  
Vol 458 (2) ◽  
pp. 187-193 ◽  
Author(s):  
María Fernández-Velasco ◽  
Silvia González-Ramos ◽  
Lisardo Boscá
Keyword(s):  
Myocardial Infarction ◽  
Immune System ◽  
Cardiovascular Diseases ◽  
Cardiac Tissue ◽  
Initial Period ◽  
Cardiac Injury ◽  
Key Factors ◽  
Cardiac Damage ◽  
Inflammatory Profile

Emerging evidence points to the involvement of specialized cells of the immune system as key drivers in the pathophysiology of cardiovascular diseases. Monocytes are an essential cell component of the innate immune system that rapidly mobilize from the bone marrow to wounded tissues where they differentiate into macrophages or dendritic cells and trigger an immune response. In the healthy heart a limited, but near-constant, number of resident macrophages have been detected; however, this number significantly increases during cardiac damage. Shortly after initial cardiac injury, e.g. myocardial infarction, a large number of macrophages harbouring a pro-inflammatory profile (M1) are rapidly recruited to the cardiac tissue, where they contribute to cardiac remodelling. After this initial period, resolution takes place in the wound, and the infiltrated macrophages display a predominant deactivation/pro-resolution profile (M2), promoting cardiac repair by mediating pro-fibrotic responses. In the present review we focus on the role of the immune cells, particularly in the monocyte/macrophage population, in the progression of the major cardiac pathologies myocardial infarction and atherosclerosis.

scholarly journals High-sensitive cardiac troponin-I facilitates timely detection of subclinical anthracycline-mediated cardiac injury

2016 ◽  
Vol 54 (1) ◽  
pp. 149-157 ◽  
Author(s):  
Melissa Jones ◽  
Peter O’Gorman ◽  
Catherine Kelly ◽  
Niall Mahon ◽  
Maria C Fitzgibbon
Keyword(s):  
Anticancer Agents ◽  
Cardiac Troponin ◽  
Dose Group ◽  
Troponin I ◽  
Cardiac Injury ◽  
Cardiac Troponin I ◽  
Chemotherapeutic Regimen ◽  
Continuous Dose ◽  
And Gender

Background Anthracycline drugs are effective anticancer agents, but their optimal use is limited in many patients by the associated cardiotoxicity, even at designated safe doses. As conventionally sensitive cardiac troponin-I assays fail to reliably quantify concentrations of cardiac troponin-I below 30 ng/L, we investigated the potential role of high-sensitive cardiac troponin-I in the detection of subclinical cardiomyocyte injury in patients treated with anthracycline agents. Methods Serial high-sensitive cardiac troponin-I concentrations were assessed in 84 patients, receiving anthracycline-containing ( n = 38) and non-anthracycline-containing ( n = 46) regimens. Results were assessed for change from pretreatment levels and evaluated according to unisex and gender-specific 99th percentiles (25 ng/L and M: 34 ng/L, F: 16 ng/L, respectively). Results A significant increase in high-sensitive cardiac troponin-I was observed in the anthracycline cohort following five cycles of treatment, with the greatest change correlating to an absolute δ increase of 30.7 ng/L in the early-dose group (early-dose group: P < 0.0001, late-dose group: P < 0.01 and continuous-dose group: P < 0.0001). Doxorubicin dose did not correlate directly with high-sensitive cardiac troponin-I concentrations (Spearman r < −0.22). No significant changes in high-sensitive cardiac troponin-I were reported among the non-anthracycline cohort with all measurements below the 99th percentiles. Conclusions Treatment with anthracycline-based chemotherapeutic regimen demonstrated significant elevations of high-sensitive cardiac troponin-I, indicative of subclinical cardiomyocyte damage. This study demonstrates a role for high-sensitive cardiac troponin-I in evaluating those patients where cardiotoxicity is a concern and a potential future role as a biomarker in optimizing cardioprotective treatments in patients receiving anthracycline therapy.

Kinetics of high-sensitivity cardiac troponin T or troponin I compared to creatine kinase in patients with revascularized acute myocardial infarction

2015 ◽  
Vol 53 (5) ◽  
Author(s):  
Kamila Solecki ◽  
Anne Marie Dupuy ◽  
Nils Kuster ◽  
Florence Leclercq ◽  
Richard Gervasoni ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
High Sensitivity ◽  
Cardiac Troponin T ◽  
Significant Difference ◽  
Kinetics Of

AbstractCardiac biomarkers are the cornerstone of the biological definition of acute myocardial infarction (AMI). The key role of troponins in diagnosis of AMI is well established. Moreover, kinetics of troponin I (cTnI) and creatine kinase (CK) after AMI are correlated to the prognosis. New technical assessment like high-sensitivity cardiac troponin T (hs-cTnT) raises concerns because of its unclear kinetic following the peak. This study aims to compare kinetics of cTnI and hs-cTnT to CK in patients with large AMI successfully treated by percutaneous coronary intervention (PCI).We prospectively studied 62 patients with anterior AMI successfully reperfused with primary angioplasty. We evaluated two consecutive groups: the first one regularly assessed by both CK and cTnI methods and the second group by CK and hs-cTnT. Modeling of kinetics was realized using mixed effects with cubic splines.Kinetics of markers showed a peak at 7.9 h for CK, at 10.9 h (6.9–12.75) for cTnI and at 12 h for hs-cTnT. This peak was followed by a nearly log linear decrease for cTnI and CK by contrast to hs-cTnT which appeared with a biphasic shape curve marked by a second peak at 82 h. There was no significant difference between the decrease of cTnI and CK (p=0.63). CK fell by 79.5% (76.1–99.9) vs. cTnI by 86.8% (76.6–92.7). In the hs-cTnT group there was a significant difference in the decrease by 26.5% (9–42.9) when compared with CK that fell by 79.5% (64.3–90.7).Kinetic of hs-cTnT and not cTnI differs from CK. The role of hs-cTnT in prognosis has to be investigated.

scholarly journals Association Between High-Sensitivity Cardiac Troponin and Risk of Stroke in 96 702 Individuals

Stroke ◽  
2020 ◽  
Vol 51 (4) ◽  
pp. 1085-1093 ◽  
Author(s):  
Leonie H.A. Broersen ◽  
Helena Stengl ◽  
Christian H. Nolte ◽  
Dirk Westermann ◽  
Matthias Endres ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Ischemic Stroke ◽  
General Population ◽  
Cardiac Troponin ◽  
Meta Analysis ◽  
High Sensitivity ◽  
Hazard Ratio ◽  
Risk Of Bias ◽  
Adjusted Hazard Ratio ◽  
Previous Stroke

Background and Purpose— Our study aim was to estimate risk of incident stroke based on levels of hs-cTn (high-sensitivity cardiac troponin), a specific biomarker indicating myocardial injury, in the general population, patients with atrial fibrillation, and patients with previous stroke. Methods— Embase, PubMed, and Web of Science were searched until March 14, 2019 to identify relevant articles. Randomized controlled trials and cohort studies assessing the risk of incident stroke based on hs-cTn were eligible. Pooled adjusted hazard ratios including 95% CI were calculated using a random-effects model due to study heterogeneity per population, coding of hs-cTn (categorical/continuous data), per hs-cTn subunit (T or I), for low risk of bias, and for all-cause and ischemic stroke separately. Results— We included 17 articles with 96 702 participants. In studies conducted in the general population (n=12; 77 780 participants), the pooled adjusted hazard ratio for incident stroke was 1.25 (CI, 1.10–1.40) for high versus low hs-cTn (as defined by included studies) during an average follow-up of 1 to 20 years (median 10). When categorical data were used, this was increased to 1.58 (CI, 1.26–1.90). The results were robust when accounting for stroke classification (all-cause stroke/ischemic stroke), hs-cTn subunit, risk of bias, and coding of hs-cTn. In patients with atrial fibrillation (4 studies; 18 725 participants), the pooled adjusted hazard ratio for incident stroke was 1.95 (CI, 1.29–2.62) for high versus low hs-cTn. Due to lack of data (one study, 197 participants), no meta-analysis could be performed in patients with previous stroke. Conclusions— This meta-analysis suggests that hs-cTn can be regarded as a risk marker for incident stroke, with different effect size in different subgroups. More research about the association between hs-cTn and incident stroke in high-risk populations is needed, especially in patients with history of ischemic stroke.

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