scholarly journals Cardiac Troponin Elevation After Long-Distance Cycling is Associated with Oxidative Stress and Exercise Intensity: An Observational Study

2020 ◽  
Vol 11 (4) ◽  
Author(s):  
Mahalul Azam ◽  
Sri Ratna Rahayu ◽  
Arulita Ika Fibriana ◽  
Hardhono Susanto ◽  
Martha Irene Kartasurya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Exercise Intensity ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Density Lipoprotein ◽  
Long Distance ◽  
Troponin Elevation ◽  
Post Exercise ◽  
Artery Disease ◽  
Blood Specimens

Background: To date, the mechanisms of post-exercise cardiac troponin elevation are debatable. Previous studies have reported that oxidative stress happens after extended exercise. Objectives: This study purposed to establish the association between the elevation of malondialdehyde (MDA), which is a marker of oxidative stress, and cardiac troponin-I (cTn-I) after prolonged cycling. Methods: Ninety-two males in Indonesian cycling tours participated in the present study. Baseline and post-exercise blood specimens were obtained to define MDA and cTn-I levels. The elevations of MDA and cTn-I were determined as positive differences of post-cycling MDA and cTn-I levels to the baseline, respectively. Results: Eighty-eight participants (age, mean = 45.3 years old, [SD]:11.47; body mass index (BMI), mean=24.2 kg/m2, [SD]: 3.03) finished the cycling tours. Subjects’ characteristics were comparable based on the touring category, except for the family history of coronary artery disease, high-density lipoprotein cholesterol level, neutrophil count, resting heart rate, exercise intensity, and cTn-I elevation. MDA significantly escalated at the level of 210.90 µmol/mL at post-exercise, from 190.18 µmol/mL at baseline. cTn-I also increased at the level of 13.65 ng/dL from 5.16 ng/dL. The elevation of MDA was related to the elevation of cTn-I. Elevation of cTn-I after prolonged cycling was contributed by elevation of MDA and exercise intensity. Conclusions: The present findings support existing confirmation that cTn-I elevation after prolonged exercise is related to oxidative stress and exercise intensity.

P1513Exercise-induced cardiac troponin I release and incident cardiovascular morbidity and mortality

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
V Aengevaeren ◽  
M T E Hopman ◽  
P D Thompson ◽  
E A Bakker ◽  
K P George ◽  
...  
Keyword(s):  
Risk Factors ◽  
Myocardial Infarction ◽  
Primary Endpoint ◽  
Cardiac Troponin ◽  
Cardiovascular Events ◽  
Troponin I ◽  
Long Distance ◽  
Post Exercise ◽  
All Cause Mortality ◽  
Exercise Induced

Abstract Background Blood concentrations of cardiac troponin I (cTnI) above the 99th percentile (upper reference limit, URL) are a key criterion for the diagnosis of acute myocardial injury and infarction. cTnI concentrations, even below the URL, also predict adverse outcomes in general and patient populations. cTnI increases after exercise, but the clinical significance of this exercise-induced cTnI increase is unknown. We examined the association between exercise-induced cTnI elevations and clinical outcomes in long-distance walkers. Methods cTnI was measured in 726 participants (median 61 [54–69] yrs) before and immediately after 30–55 km of walking. The primary endpoint was a composite of all-cause mortality and major adverse cardiovascular events (MACE, i.e. myocardial infarction, stroke, heart failure, revascularization or sudden cardiac arrest). Results Participants walked 498 [440–555] min at 68±10% of their maximum heart rate. Baseline cTnI concentrations were 2 [0–8] ng/L, with 9 participants (1%) demonstrating a baseline cTnI value above the URL (>40 ng/L). cTnI increased after walking (8 [1–18] ng/L, p<0.001) and 63 participants (9%) had a post-exercise cTnI value >URL. During 43 [23–77] months of follow-up, 62 participants (9%) experienced a primary endpoint; 29 died and 33 had MACE. 27% of participants with post-exercise cTnI >URL experienced a primary endpoint compared to only 7% with cTnI below the URL (log-rank p<0.001). The hazard ratio was 2.35 (95% CI: 1.21–4.53) after adjusting for age, sex, cardiovascular risk factors (hypertension, hypercholesterolemia or diabetes mellitus), cardiovascular diseases (myocardial infarction, stroke or heart failure) and baseline cTnI. Kaplan-Meier of Mortality and MACE Conclusion Post-exercise cTnI concentrations >URL were associated with higher all-cause mortality and MACE, independent of age, sex, presence of cardiovascular risk factors or cardiovascular diseases and baseline cTnI concentrations in a large cohort of older long-distance walkers. Exercise-induced increases in cTnI may not be a benign physiological response to exercise in all, but an early marker of future mortality and cardiovascular events. Acknowledgement/Funding V.L.A was supported by a grant from the Radboud Institute for Health Sciences, T.M.H.E by a Horizon 2020 grant from the European Commission

Cardiac troponin I in patients with acute upper and lower limb ischemia

VASA ◽  
2008 ◽  
Vol 37 (4) ◽  
pp. 327-332 ◽  
Author(s):  
Koutouzis ◽  
Sfyroeras ◽  
Moulakakis ◽  
Kontaras ◽  
Nikolaou ◽  
...  
Keyword(s):  
Upper Limb ◽  
Lower Limb ◽  
Cardiac Troponin ◽  
Cardiac Involvement ◽  
Troponin I ◽  
Limb Ischemia ◽  
Elevated Troponin ◽  
Troponin Elevation ◽  
Lower Limb Ischemia ◽  
Ischemia Group

Background: The aim of this study was to investigate the presence, etiology and clinical significance of elevated troponin I in patients with acute upper or lower limb ischemia. The high sensitivity and specificity of cardiac troponin for the diagnosis of myocardial cell damage suggested a significant role for troponin in the patients investigated for this condition. The initial enthusiasm for the diagnostic potential of troponin was limited by the discovery that elevated cardiac troponin levels are also observed in conditions other than acute myocardial infarction, even conditions without obvious cardiac involvement. Patients and Methods: 71 consecutive patients participated in this study. 31 (44%) of them were men and mean age was 75.4 ± 10.3 years (range 44–92 years). 60 (85%) patients had acute lower limb ischemia and the remaining (11; 15%) had acute upper limb ischemia. Serial creatine kinase (CK), isoenzyme MB (CK-MB) and troponin I measurements were performed in all patients. Results: 33 (46%) patients had elevated peak troponin I (> 0.2 ng/ml) levels, all from the lower limb ischemia group (33/60 vs. 0/11 from the acute upper limb ischemia group; p = 0.04). Patients with lower limb ischemia had higher peak troponin I values than patients with upper limb ischemia (0.97 ± 2.3 [range 0.01–12.1] ng/ml vs. 0.04 ± 0.04 [0.01–0.14] ng/ml respectively; p = 0.003), higher peak CK values (2504 ± 7409 [range 42–45 940] U/ml vs. 340 ± 775 [range 34–2403] U/ml, p = 0.002, respectively, in the two groups) and peak CK-MB values (59.4 ± 84.5 [range 12–480] U/ml vs. 21.2 ± 9.1 [range 12–39] U/ml, respectively, in the two groups; p = 0.04). Peak cardiac troponin I levels were correlated with peak CK and CK-MB values. Conclusions: Patients with lower limb ischemia often have elevated troponin I without a primary cardiac source; this was not observed in patients presenting with acute upper limb ischemia. It is very important for these critically ill patients to focus on the main problem of acute limb ischemia and to attempt to treat the patient rather than the troponin elevation per se. Cardiac troponin elevation should not prevent physicians from providing immediate treatment for limb ischaemia to these patients, espescially when signs, symptoms and electrocardiographic findings preclude acute cardiac involvement.

scholarly journals Value of Cardiac Troponin I Cutoff Concentrations below the 99th Percentile for Clinical Decision-Making

2009 ◽  
Vol 55 (1) ◽  
pp. 85-92 ◽  
Author(s):  
Kai M Eggers ◽  
Allan S Jaffe ◽  
Lars Lind ◽  
Per Venge ◽  
Bertil Lindahl
Keyword(s):  
Coronary Artery Disease ◽  
Acute Coronary Syndrome ◽  
Coronary Artery ◽  
Risk Stratification ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Reference Population ◽  
Cardiac Troponin I ◽  
Coronary Syndrome ◽  
Artery Disease

Abstract Background: The aim of this study was to evaluate factors influencing the 99th percentile for cardiac troponin I (cTnI) when this cutoff value is established on a highly sensitive assay, and to compare the value of this cutoff to that of lower cutoffs in the prognostic assessment of patients with coronary artery disease. Methods: We used the recently refined Access AccuTnI assay (Beckman-Coulter) to assess the distribution of cTnI results in a community population of elderly individuals [PIVUS (Prospective Study of the Vasculature in Uppsala Seniors) study; n = 1005]. The utility of predefined cTnI cutoffs for risk stratification was then evaluated in 952 patients from the FRISC II (FRagmin and Fast Revascularization during InStability in Coronary artery disease) study at 6 months after these patients had suffered acute coronary syndrome. Results: Selection of assay results from a subcohort of PIVUS participants without cardiovascular disease resulted in a decrease of the 99th percentile from 0.044 μg/L to 0.028 μg/L. Men had higher rates of cTnI elevation with respect to the tested thresholds. Whereas the 99th percentile cutoff was not found to be a useful prognostic indicator for 5-year mortality, both the 90th percentile (hazard ratio 3.1; 95% CI 1.9–5.1) and the 75th percentile (hazard ratio 2.8; 95% CI 1.7–4.7) provided useful prognostic information. Sex-specific cutoffs did not improve risk prediction. Conclusions: The 99th percentile of cTnI depends highly on the characteristics of the reference population from which it is determined. This dependence on the reference population may affect the appropriateness of clinical conclusions based on this threshold. However, cTnI cutoffs below the 99th percentile seem to provide better prognostic discrimination in stabilized acute coronary syndrome patients and therefore may be preferable for risk stratification.

Post-exercise cardiac troponin I release and clearance in normal Standardbred racehorses

2018 ◽  
Vol 51 (1) ◽  
pp. 97-101 ◽  
Author(s):  
T. M. Rossi ◽  
P. A. Kavsak ◽  
M. G. Maxie ◽  
D. L. Pearl ◽  
W. G. Pyle ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Troponin I ◽  
Cardiac Troponin I ◽  
Post Exercise ◽  
Standardbred Racehorses

scholarly journals Markers of Myocardial Stress, Myocardial Injury, and Subclinical Inflammation and the Risk of Sudden Death

Circulation ◽  
2020 ◽  
Vol 142 (12) ◽  
pp. 1148-1158
Author(s):  
Brendan M. Everett ◽  
M.V. Moorthy ◽  
Jani T. Tikkanen ◽  
Nancy R. Cook ◽  
Christine M. Albert
Keyword(s):  
Cardiovascular Disease ◽  
High Density Lipoprotein ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Troponin I ◽  
Density Lipoprotein ◽  
High Sensitivity ◽  
C Reactive Protein ◽  
Cholesterol Ratio ◽  
Reactive Protein

Background: The majority of sudden cardiac deaths (SCDs) occur in low-risk populations often as the first manifestation of cardiovascular disease (CVD). Biomarkers are screening tools that may identify subclinical cardiovascular disease and those at elevated risk for SCD. We aimed to determine whether the total to high-density lipoprotein cholesterol ratio, high-sensitivity cardiac troponin I, NT-proBNP (N-terminal pro-B-type natriuretic peptide), or high-sensitivity C-reactive protein individually or in combination could identify individuals at higher SCD risk in large, free-living populations with and without cardiovascular disease. Methods: We performed a nested case-control study within 6 prospective cohort studies using 565 SCD cases matched to 1090 controls (1:2) by age, sex, ethnicity, smoking status, and presence of cardiovascular disease. Results: The median study follow-up time until SCD was 11.3 years. When examined as quartiles or continuous variables in conditional logistic regression models, each of the biomarkers was significantly and independently associated with SCD risk after mutually controlling for cardiac risk factors and other biomarkers. The mutually adjusted odds ratios for the top compared with the bottom quartile were 1.90 (95% CI, 1.30–2.76) for total to high-density lipoprotein cholesterol ratio, 2.59 (95% CI, 1.76–3.83) for high-sensitivity cardiac troponin I, 1.65 (95% CI, 1.12–2.44) for NT-proBNP, and 1.65 (95% CI, 1.13–2.41) for high-sensitivity C-reactive protein. A biomarker score that awarded 1 point when the concentration of any of those 4 biomarkers was in the top quartile (score range, 0–4) was strongly associated with SCD, with an adjusted odds ratio of 1.56 (95% CI, 1.37–1.77) per 1-unit increase in the score. Conclusions: Widely available measures of lipids, subclinical myocardial injury, myocardial strain, and vascular inflammation show significant independent associations with SCD risk in apparently low-risk populations. In combination, these measures may have utility to identify individuals at risk for SCD.

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