scholarly journals HEMODYNAMIC CARDIAC STRESS INDUCED MYOCARDIAL ISCHEMIA AS DETECTED BY THE RELEASE OF CARDIAC BIOMARKERS: CARDIAC TROPONIN T AND I, CK-MB AND MYOGLOBIN

2013 ◽  
Vol 61 (10) ◽  
pp. E192
Author(s):  
Affan Irfan ◽  
Tobias Reichlin ◽  
Rapahel Twerenbold ◽  
Karin Wildi ◽  
Christian Mueller
Author(s):  
Natthapon Traiperm ◽  
Rungchai Chaunchaiyakul ◽  
Martin Burtscher ◽  
Hannes Gatterer

Purpose: Plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) and cardiac troponin T levels show a transient increase after marathon running. The aim of this study was to investigate whether running duration influences the patterns of changes in cardiac biomarkers. Methods: Twenty participants with fast and slow finishing times were included in the study. Blood samples were taken before the marathon race, immediately after, and 24 hours after the race. Samples were analyzed for NT-proBNP and cardiac troponin T concentration. Furthermore, a complete blood cell count was performed. Results: After the marathon race, the fast and slow runners showed similar changes of NT-proBNP and cardiac troponin T (ie, a transient increase). Curve estimation regression analysis showed a curvilinear relationship (quadratic model) between running times and NT-proBNP increments immediately after the race, with less of an increase in the very fast and the very slow runners (r2 = .359, P = .023). NT-proBNP increments immediately after the race were correlated to the decline 24 hours after the marathon (r = −.612, P = .004). Conclusions: This study indicates that NT-proBNP release immediately after marathon running varies in a curvilinear fashion with running time. It is speculated that low NT-proBNP release is associated with training adaptation in most elite runners and the relatively low cardiac stress in the slowest (but experienced) runners. The combination of less adaptation and relatively large cardiac wall and metabolic stress may explain the highest NT-proBNP values in runners with average running times. In addition, NT-proBNP decrements 24 hours after the race depend primarily on the values reached after the marathon and not on running time.


Cor et Vasa ◽  
2018 ◽  
Vol 60 (6) ◽  
pp. e645-e648
Author(s):  
Johannes Mierke ◽  
Stefanie Jellinghaus ◽  
Anna Selle ◽  
Hagen Schroetter ◽  
David M. Poitz ◽  
...  

2019 ◽  
Vol 188 (8) ◽  
pp. 1444-1455 ◽  
Author(s):  
Annemarie Wentzel ◽  
Leoné Malan ◽  
Roland von Känel ◽  
Nicolaas T Malan

Abstract Acute mental stressor–induced cardiac stress responses might contribute to excessive myocardial strain and resultant cardiovascular episode risk. We assessed ethnicity-specific acute cardiac stress (by measuring cardiac troponin T (cTnT) and N-terminal prohormone of brain natriuretic peptide) related to hemodynamic activity. The prospective Sympathetic Activity and Ambulatory Blood Pressure in Africans (SABPA) study was conducted during 2007–2008 in South Africa. In the cross-sectional phase of the SABPA study, 388 black and white participants underwent a 1-minute acute mental stressor, during which blood pressure was continuously measured. Fasting blood samples for cardiac stress markers were obtained before and 10 minutes after stress (% change). Resting 10-lead electrocardiogram measured the R wave of the aVL lead (RaVL). Black participants exhibited greater cardiac stress responses (P < 0.001), diastolic blood pressure, total peripheral resistance, and stroke volume compared with white participants, who displayed decreases in cardiac stress and increases in cardiac output. Prestress and stressor cTnT cutpoints of 4.2 pg/mL predicted 24-hour, daytime, and nighttime diastolic hypertension in black participants (P < 0.001). These cTnT cutpoints were associated with an ethnicity-specific RaVL cutpoint of 0.28 mV (odds ratio = 3.49, 95% confidence interval: 2.18, 5.83; P = 0.021). Acute mental stress elicited an α-adrenergic activation pattern and cardiac stress hyperreactivity only in black participants. Mental stress might increase the black population’s risk for ischemic episodes and heart disease.


2016 ◽  
Vol 49 (6) ◽  
pp. 421-432 ◽  
Author(s):  
Seoung Mann Sou ◽  
Christian Puelacher ◽  
Raphael Twerenbold ◽  
Max Wagener ◽  
Ursina Honegger ◽  
...  

2009 ◽  
Vol 36 (12) ◽  
pp. 2711-2714 ◽  
Author(s):  
ROHIT AGGARWAL ◽  
DOROTA LEBIEDZ-ODROBINA ◽  
ALPANA SINHA ◽  
AUGUSTINE MANADAN ◽  
JOHN P. CASE

Objective.To study the association of serum cardiac troponin T (cTnT) and cardiac troponin I (cTnI) with creatine kinase (CK) in patients with idiopathic inflammatory myopathies (IIM).Methods.We performed a retrospective study on patients with IIM followed by the rheumatology service of a county hospital from 2004 to 2008. Patients with myocardial ischemia and/or with renal failure were excluded. Clinical data including electromyogram, muscle biopsy, and CK, cTnT and cTnI were recorded. Patients who had simultaneous analysis of CK and cardiac troponin (cTnT or cTnI) levels were studied. CK levels were correlated with cTnT and cTnI by chi-square test and Spearman correlation.Results.We identified 49 patients with IIM (69 observations) who satisfied our inclusion criteria. The primary diagnosis was polymyositis in 23, dermatomyositis in 16, and myositis associated with connective tissue disease in 10 patients. There were 33/49 women with average age 45.8 years. Twenty-eight patients with IIM had simultaneous CK and cTnT values assayed. Of those patients, 18/23 with elevated CK also had elevated cTnT, and 5/5 patients with normal CK levels had normal cTnT levels (p = 0.005). In 41 patients with IIM who had simultaneous CK and cTnI levels assayed, only 1/29 with elevated CK had elevated cTnI, and 12/12 patients with normal CK had normal cTnI (p = 0.5). CK correlated strongly with the cTnT (r = 0.62, p = 0.001) but did not correlate with cTnI.Conclusion.Elevated cTnT, but not cTnI, was highly associated with CK in patients with IIM despite the absence of myocardial ischemia.


2012 ◽  
Vol 58 (6) ◽  
pp. 1049-1054 ◽  
Author(s):  
Christoph Liebetrau ◽  
Helge Möllmann ◽  
Holger Nef ◽  
Sebastian Szardien ◽  
Johannes Rixe ◽  
...  

Abstract BACKGROUND The release kinetics of cardiac troponin T measured with conventional vs high-sensitivity cardiac troponin T (hs-cTnT) assays in patients with acute myocardial infarction (AMI) is difficult to establish. METHODS We analyzed the release kinetics of cTnT measured by fourth generation and high-sensitivity assays, creatine kinase-MB (CK-MB), and myoglobin in patients with hypertrophic obstructive cardiomyopathy undergoing transcoronary ablation of septal hypertrophy (TASH), a model of AMI. Consecutive patients (n = 21) undergoing TASH were included. Serum and EDTA-plasma samples were collected before and at 15, 30, 45, 60, 75, 90, and 105 min, and 2, 4, 8, and 24 h after TASH. RESULTS cTnT concentrations measured by the hs assay were significantly increased at 15 min [21.4 ng/L, interquartile range (IQR) 13.3–39.7 ng/L vs 11.3 ng/L, IQR 6.0–18.8 ng/L at baseline; P = 0.031]. In comparison, cTnT concentrations measured by the conventional fourth generation assay increased significantly at 60 min (30.0 ng/L, IQR 20.0–30.0 ng/L vs <10.0 ng/L, IQR <10.0–10.0 ng/L; P < 0.01), CK-MB at 90 min (8.4 μg/L, IQR 6.9–14.4 μg/L vs 0.9 μg/L, IQR 0.4–1.1 μg/L; P < 0.01), and myoglobin at 30 min (188.0 μg/L, IQR 154.0–233.0 μg/L vs 38.0 μg/L, IQR 28.0–56.0; P < 0.01). CONCLUSIONS cTnT concentrations measured by the hs assay were significantly increased after TASH at all of the time points, with a doubling at 15 min after induction of AMI, confirming earlier evidence of myocardial injury compared to the fourth generation cTnT assay and CK-MB and myoglobin.


2011 ◽  
Vol 7 (1) ◽  
pp. 14 ◽  
Author(s):  

On 31 August 2010 Roche Diagnostics hosted a satellite symposium at the European Society of Cardiology Congress in Stockholm entitled ‘Clinical Benefits of the Cardiac Troponin T-high Sensitive Test in Acute Coronary Syndrome.’ The symposium was chaired by Hugo Katus, Medical Director of Cardiology at the Angiology and Pneumology Medical Clinic in Heidelberg and Allan Jaffe, Chair of the Division of Core Clinical Laboratory Services at the Department of Laboratory Medicine and Pathology at the Mayo Clinic in Rochester. The symposium consisted of three talks by leaders in the field of cardiac biomarkers addressing the latest improvements in the diagnosis of acute coronary syndrome.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
N Kozhuharov ◽  
D Wussler ◽  
R Twerenbold ◽  
J Walter ◽  
J Du Fay De Lavallaz ◽  
...  

Abstract Background Better characterization of the different pathophysiological mechanisms involved in normotensive and hypertensive acute heart failure (AHF) might help to develop novel individualized treatment strategies. Methods The extent of hemodynamic cardiac stress and cardiomyocyte injury was quantified by measuring B-type natriuretic peptide (BNP) as well as high-sensitive cardiac troponin T (hs-cTnT) in 1,152 unselected patients presenting with AHF to the emergency department (derivation cohort). Systolic blood pressure (SBP) of 90 - 140 mmHg at presentation was used to define normotensive AHF. Findings regarding hemodynamic cardiac stress and cardiomyocyte injury were validated in a second independent AHF cohort (validation cohort; n=324). Results In the derivation cohort 667 (58%) patients had hypertensive AHF. Hemodynamic cardiac stress, as quantified by BNP levels, was significantly higher in normotensive AHF as compared to hypertensive AHF (1,105 pg/mL versus 827 pg/mL, p<0.001). In addition, the extent of cardiomyocyte injury, as quantified by hs-cTnT, was significantly higher in normotensive AHF as compared to hypertensive AHF (41 ng/L versus 33 ng/L, p<0.001). These findings were confirmed in the validation cohort. Table 1. Cardiac stress and myocardial necrosis as quantified by BNP and hs-cTnT plasma concentrations Overall Hypertensive AHF Normotensive AHF p-value BNP in pg/ml, median (IQR) 974 (536–1,712) 827 (448–1,419) 1,105 (611–1,956) <0.001 hs-cTnT in ng/L, median (IQR) 37 (22–67) 33 (19–59) 41 (24–71) <0.001 BNP = B-type natriuretic peptide; hs-cTnT = high-sensitivity cardiac Troponin T; IQR = inter-quartile range. Figure 1 Conclusion Biomarker profiling revealed that the extent of hemodynamic stress and cardiomyocyte injury is different in patients with normotensive and hypertensive AHF. This characterization could help to understand AHF phenotypes better, which in turn may lead to more specific management in future, thus improving the dismal prognosis in these patients. Acknowledgement/Funding European Union, Swiss National Science Foundation, Swiss Heart Foundation, Cardiovascular Research Foundation Basel, University of Basel


1996 ◽  
Vol 335 (18) ◽  
pp. 1333-1342 ◽  
Author(s):  
E. Magnus Ohman ◽  
Paul W. Armstrong ◽  
Robert H. Christenson ◽  
Christopher B. Granger ◽  
Hugo A. Katus ◽  
...  

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