scholarly journals eComment: Is early assessment of cardiac troponin I a valuable predictor of mortality after cardiac surgery?

2010 ◽  
Vol 10 (3) ◽  
pp. 416-417 ◽  
Author(s):  
Petros Tzimas ◽  
Nikolaos G. Baikoussis ◽  
Kallirroi Kalantzi ◽  
Georgios Papadopoulos
2019 ◽  
Vol 47 (8) ◽  
pp. 3623-3635
Author(s):  
Hong-mei Zhou ◽  
Xiao-yan Ling ◽  
Yun-jian Ni ◽  
Cheng Wu ◽  
Zhi-peng Zhu

Objective This study was performed to determine the effect of dexmedetomidine (DEX) administration on myocardial damage in cardiac surgery with sevoflurane postconditioning. Methods We retrospectively examined all cardiac valve replacement surgeries from 1 April 2016 to 30 April 2017. Eligible patients were divided into two groups based on whether DEX was infused. DEX infusion was permitted only between intubation and the beginning of cardiopulmonary bypass (CPB). Sevoflurane was inhaled via the standard postconditioning procedure starting at aortic declamping. The cardiac troponin I (cTnI) level was measured at different time points. The postoperative outcomes and complications were also analyzed. Results One hundred patients were included in the study (DEX group, n = 53; non-DEX group, n = 47). Increased cTnI levels were significantly correlated with the New York Heart Association classification, CPB time, and DEX use. DEX use and the CPB time were potential independent factors contributing to changes in the cTnI level. The cTnI level at 6, 12, and 24 hours postoperatively was remarkably lower in the DEX than non-DEX group by 1.14, 7.83, and 5.86 ng/mL, respectively. Conclusions DEX decreased the cTnI level after CPB when sevoflurane postconditioning was used, especially at 6, 12, and 24 hours postoperatively.


Circulation ◽  
2006 ◽  
Vol 114 (14) ◽  
pp. 1468-1475 ◽  
Author(s):  
Bernard L. Croal ◽  
Graham S. Hillis ◽  
Patrick H. Gibson ◽  
Mohammed T. Fazal ◽  
Hussein El-Shafei ◽  
...  

2002 ◽  
Vol 19 (Supplement 27) ◽  
pp. 31
Author(s):  
M. Filipovic ◽  
C. Probst ◽  
R. Arsenic ◽  
C. Werner ◽  
E. Seeberger ◽  
...  

1998 ◽  
Vol 12 (3) ◽  
pp. 288-294 ◽  
Author(s):  
Marie-Alexandra Alyanakian ◽  
Monique Dehoux ◽  
Didier Chatel ◽  
Christophe Seguret ◽  
Jean-Marie Desmonts ◽  
...  

2005 ◽  
Vol 230 (6) ◽  
pp. 413-420 ◽  
Author(s):  
Kelvin H. H. Lim ◽  
Andrew P. Halestrap ◽  
Gianni D. Angelini ◽  
M.-Saadeh Suleiman

The general anesthetic propofol has been shown to be cardioprotective. However, its benefits when used in cardioplegia during cardiac surgery have not been demonstrated. In this study, we investigated the effects of propofol on metabolic stress, cardiac function, and injury in a clinically relevant model of normothermic cardioplegic arrest and cardiopulmonary bypass. Twenty anesthetized pigs, randomized to propofol treatment ( n = 8) and control ( n =12) groups, were surgically prepared for cardiopulmonary bypass (CPB) and cardioplegic arrest. Doses of warm blood cardioplegia were delivered at 15-min intervals during a 60-min aortic cross-clamped period. Propofol was continuously infused for the duration of CPB and was therefore present in blood cardioplegia. Myocardial biopsies were collected before, at the end of cardioplegic arrest, and 20 mins after the release of the aortic cross-clamp. Hemodynamic parameters were monitored and blood samples collected for cardiac troponin I measurements. Propofol infusion during CPB and before ischemia did not alter cardiac function or myocardial metabolism. Propofol treatment attenuated the changes in myocardial tissue levels of adenine nucleotides, lactate, and amino acids during ischemia and reduced cardiac troponin I release on reperfusion. Propofol treatment reduced measurable hemodynamic dysfunction after cardioplegic arrest when compared to untreated controls. In conclusion, propofol protects the heart from ischemia-reperfusion injury in a clinically relevant experimental model. Propofol may therefore be a useful adjunct to cardioplegic solutions as well as being an appropriate anesthetic for cardiac surgery.


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