Relationship between cardiac troponin I (cTnI) release during cardiac operations and myocardial cell death

JF Vazquez-Jimenez¹, Ma Qing², B Klosterhalfen³, O Liakopoulos¹, G von Bernuth², BJ Messmer¹ and M-C Seghaye²

¹Department. of Cardiac Surgery, Aachen University of Technology, Pauwelsstrasse. 30, D-52057, Aachen, Germany

²Pediatric Cardiology, Aachen University of Technology, Pauwelsstrasse. 30, D-52057, Aachen, Germany

³Pathology, Aachen University of Technology, Pauwelsstrasse. 30, D-52057, Aachen, Germany

from 20th International Symposium on Intensive Care and Emergency Medicine
Brussels, Belgium. 21–24 March 2000

Critical Care 2000, 4(Suppl 1):P2doi:10.1186/cc722

Published:

21 March 2000

Full text

Aims

To study the relationship between myocardial release of cTnI and myocardial cell death as assessed by the amount of apoptosis and necrosis after cardiac surgery.

Methods

Eighteen young pigs were operated on with standardized cardiopulmonary bypass (CPB). Release of cTnI in the cardiac lymph (CL), coronary sinus (CS), and arterial blood (A) was related to postoperative myocardial cell death by both necrosis and apoptosis. Apoptotic cells were detected by a TUNEL detection kit. Necrotic cells were counted by light microscopy.

Results

In all animals, cTnI was significantly released and reached peak values observed simultaneously in A (cTnI, 20.1 ± 2.6 ng/ml) (mean ± SEM), CS (19.5 ± 3.2 ng/ml) and CL (5202 ± 2500 ng/ml). Percentage of total myocardial cell death was 3.1 ± 0.5%, including 1.2 ± 0.35% necrosis and 1.9 ± 0.5% apoptosis. cTnI release during and after CPB did not correlate with the degree of myocardial apoptosis or necrosis.

Conclusion

Cardiac operations with CPB are related to myocardial cell damage including myocardial cell death due to both necrosis and apoptosis. As the loss of cTnI is not related to the amount of cell death, our results suggest that increased cardiac myocyte membrane permeability more than cell death is responsible for intraoperative and postoperative cTnI release.

This article is part of the supplement: 20th International Symposium on Intensive Care and Emergency Medicine