Background: It is unclear if isolated postoperative cardiac-troponin elevation, often referred to as myocardial injury, represents a pathological event, as control studies in otherwise healthy adults are lacking.
Methods: In this single-centre prospective observational cohort study, serial high-sensitivity cardiac troponin T (hscTnT) plasma concentrations were obtained from young, healthy adults undergoing elective orthopaedic surgery at three time points: before operation, 2-6 h, and 18-30 h after surgery. End points were hscTnT increases after surgery: ≥20% (exceeding analytical variability), ≥50% (exceeding short-term biological variability), and ≥85% (exceeding long-term biological variability). The secondary end point was myocardial injury, defined as new postoperative hscTnT elevation >99th % upper reference limit (URL) (women >10 ng litre; men >15 ng litre).
Results: Amongst the study population (n=95), no hscTnT increase ≥20% was detected in 68 patients (73%). A hscTnT increase between 20% and 49% was observed in 17 patients (18%), 50-84% in seven patients (7%), and ≥85% in three patients (3%). Twenty patients (21%) had an absolute ΔhscTnT between 0 and 2 ng litre, 12 patients (13%) between 2 and 4 ng litre, three patients between 4 and 6 ng litre, and one patient (1%) between 6 and 8 ng litre. Myocardial injury (new hscTnT elevation >99th%) was diagnosed in one patient (1%). The median hscTnT concentrations did not increase after operation, and were 4 (3.9-5, inter-quartile range) ng litre at baseline, 4 (3.9-5) ng litre at 2-6 h after surgery, and 4 (3.9-5) ng litre on postoperative day 1.
Conclusions: One in four young adult patients without known cardiovascular disease developed a postoperative hscTnT increase, but without exceeding the 99th% URL and without evidence of myocardial ischaemia. These results may have important ramifications for the concept of postoperative myocardial injury, as they suggest that, in some patients, postoperative cardiac-troponin increases may be the result of a normal physiological process in the surgical setting.
Clinical Trial Registration: NCT 02394288.
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http://dx.doi.org/10.1016/j.bja.2017.09.001 | DOI Listing |
Clin Chem Lab Med
January 2025
Deparment of Laboratory Medicine, 16268 La Paz University Hospital, Madrid, Spain.
Objectives: Cardiac biomarkers are useful for the diagnostic and prognostic assessment of myocardial injury (MI) and heart failure. By measuring specific proteins released into the bloodstream during heart stress or damage, these biomarkers help clinicians detect the presence and extent of heart injury and tailor appropriate treatment plans. This study aims to provide robust biological variation (BV) data for cardiac biomarkers in athletes, specifically focusing on those applied to detect or exclude MI, such as myoglobin, creatine kinase-myocardial band (CK-MB) and cardiac troponins (cTn), and those related to heart failure and cardiac dysfunction, brain natriuretic peptide (BNP) and N-terminal brain natriuretic pro-peptide (NT-proBNP).
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January 2025
Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, and the Department of Physiology, School of Basic Medicine, Shanxi Medical University, Taiyuan, China.
Programmed necrosis/necroptosis greatly contributes to the pathogenesis of cardiac disorders including myocardial infarction, ischemia/reperfusion (I/R) injury and heart failure. However, the fundamental mechanism underlying myocardial necroptosis, especially the mitochondria-dependent death pathway, is poorly understood. Synaptotagmin-1 (Syt1), a Ca sensor, is originally identified in nervous system and mediates synchronous neurotransmitter release.
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January 2025
TaiKang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan, China; Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan, China. Electronic address:
Aims: Vertebrates vary greatly in their abilities to regenerate injured hearts. Zebrafish possess a remarkable capacity for cardiac regeneration, making them an excellent model for regeneration research. Recent studies have reported the activation and underlying regulatory mechanisms of leptin b (lepb) and the leptin b-linked enhancer (LEN) in injured hearts.
View Article and Find Full Text PDFEur J Pharmacol
January 2025
Department of Basic Medicine, Institute of Respiratory Diseases Xiamen Medical College, Xiamen Medical College, Xiamen, Fujian 361023, P. R. China; State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), Harbin Medical University, Harbin, Heilongjiang 150081, P. R. China. Electronic address:
ITFG2 is an intracellular protein known to modulate the immune response of T-cells. Our previous investigation revealed that ITFG2 specifically targets ATP5b to regulate ATP energy metabolism and maintain mitochondrial function, thereby protecting the heart from ischemic injury. However, the role of ITFG2 in ischemic ventricular arrhythmias and its underlying mechanisms have not been previously reported.
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January 2025
The Second Department of Cardiovascular Medicine, Baoji People's Hospital, Baoji, China.
Dihydromyricetin (Dih), a naturally occurring flavonoid, has been identified to exert a protective effect against ischemia/reperfusion injury. However, the detailed mechanisms remain unclear. Here we investigated the biological role of Dih in preventing hypoxia/reoxygenation (H/R) injury in cardiomyocytes.
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