Objective: To investigate the effect of aprotinin on the myocardial injury during the off-pump coronary artery bypass grafting (OPCAB).
Methods: Twenty-four patients undergoing OPCAB randomly were of 12 patients divided into two groups: aprotinin group and Control group (n = 12). In the aprotinin group a loading dose (2 x 10(6) KIU) was administered within the first 30 minutes after the induction followed by continuous infusion of 0.5 x 10(6) KIU/h throughout the operation. The plasma myocardial injury markers CK-MB and cTnI were measured at the four points: (1) After induction; (2) 1 hour after coronary anastomosis; (3) 6 hours and (4) 24 hours after the operation. The blood loss was recorded by autotransfusion in the operation, and the drainage immediately, 6 hours, and 24 hours after the operation.
Result: Myocardial injury markers CK-MB and cTnI increased significantly after the anastomosis in each group; cTnI was lower in the aprotinin group than in the control group at the third and forth points (P < 0.05). The post-operative drainage after 6 hours and 24 hours were lower in the aprotinin group than in control group (P < 0.05).
Conclusions: There is the myocardial injury during OPCAB. Aprotinin can reduce the myocardial injury during OPCAB.
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Cureus
December 2024
Cardiology, King Khalid University Hospital, Riyadh, SAU.
Troponin is a highly specific biomarker for myocardial injury. It plays a critical role in the diagnosis of acute coronary syndrome (ACS). However, elevated troponin levels are not exclusively due to cardiac ischemia and may be observed in many non-cardiac conditions, including inflammatory myopathies.
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State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing 100191, China.
Macrophage-mediated inflammation plays a pivotal role in cardiovascular disease pathogenesis. However, current cell-based models lack a comprehensive understanding of crosstalk between macrophages and cardiomyocytes, hindering the discovery of effective therapeutic interventions. Here, a microfluidic model has been developed to facilitate the coculture of macrophages and cardiomyocytes, allowing for mapping key signaling pathways and screening potential therapeutic agents against inflammation-induced dynamic myocardial injury.
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View Article and Find Full Text PDFZhongguo Zhong Yao Za Zhi
December 2024
School of Traditional Chinese Medicine, Binzhou Medical College Yantai 264003, China Institute of Basic Medicine, Xiyuan Hospital, China Academy of Chinese Medical Sciences Beijing 100091, China.
This article explored the specific mechanism by which ginsenoside Rg_1 regulates cellular autophagy to attenuate hypoxia/reoxygenation(H/R) injury in HL-1 cardiomyocytes through the microRNA155(miR-155)/neurogenic gene Notch homologous protein 1(Notch1)/hairy and enhancer of split 1(Hes1) pathway. An HL-1 cell model with H/R injury was constructed, and ginsenoside Rg_1 and/or Notch1 inhibitor DAPT and miR-155 mimics were used to treat cells. Cell counting kit(CCK)-8 was used to detect the relative viability of HL-1 cells with H/R injury.
View Article and Find Full Text PDFBiochim Biophys Acta Mol Basis Dis
January 2025
College of Life Sciences, Institute of Life Science and Green Development, Hebei University, Baoding 071002, China; The Key Laboratory of Zoological Systematics and Application, College of Life Sciences, Hebei University, Baoding 071002, China. Electronic address:
Excessive alcohol consumption is a major cause of alcoholic cardiomyopathy (ACM) and myocardial injury. This study aims to investigate the role of transcription factor EB (TFEB) in ethanol-induced cardiac anomalies using a murine model, AC16 human cardiomyocytes, and human plasma. Wild-type mice treated with a TFEB activator (Compound 1) or vehicle (25 mg/kg/d) were challenged with or without ethanol (3 g/kg/d, i.
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