Release of cardiac troponin I in antegrade crystalloid versus cold blood cardioplegia.
OBJECTIVE
The purpose of this study was to assess the efficacy of myocardial protection, comparing antegrade crystalloid cardioplegia with cold blood cardioplegia, in patients with preserved left ventricular function who were undergoing elective first coronary artery bypass grafting. Release of cardiac troponin I was used as a marker for the effectiveness of myocardial protection.


METHODS
A consecutive series of 62 patients were randomly assigned to receive crystalloid or blood cardioplegia. Cardiac troponin I concentrations were determined in venous blood samples before the operation, immediately after unclamping, at 6, 9, 12, and 24 hours, and daily thereafter for 5 days.


RESULTS
Rising levels of troponin I were found in all patients. The time course and peak release were similar in the crystalloid cardioplegia and the blood cardioplegia groups. No patients in either group had electrocardiographic evidence of perioperative myocardial infarction. Cardiac troponin I was able to detect small areas of myocardial damage, not revealed by electrocardiography or creatine kinase MB release. Aprotinin administration was associated with lower cardiac troponin I release in both groups. Cardiac troponin I was lower in patients whose conditions did not require electrical defibrillation after aortic unclamping, irrespective of cardioplegia type. The presence of a main stem lesion was associated with higher cardiac troponin I release only in the crystalloid cardioplegia group.


CONCLUSIONS
Antegrade cold blood cardioplegia is equally effective as antegrade crystalloid cardioplegia in a randomized group of patients with preserved left ventricular function who were undergoing elective first coronary artery bypass grafting. Aprotinin administration resulted in lower cardiac troponin I release, whereas electrical defibrillation was related to a higher release irrespective of cardioplegia type. The presence of a main stem lesion resulted in higher cardiac troponin I release in the crystalloid cardioplegia group.
Hendrikx
M
M
Faculty of Medicine, Limburgs Universitair Centrum, Diepenbeek, Belgium.
Jiang
H
H
Gutermann
H
H
Toelsie
J
J
Renard
D
D
Briers
A
A
Pauwels
J L
JL
Mees
U
U
D000368:Aged; D007611:Aprotinin / Q000008:administration & dosage; D015415:Biomarkers / Q000097:blood; D002314:Cardioplegic Solutions / Q000008:administration & dosage*; D001026:Coronary Artery Bypass / Q000379:methods; D003402:Creatine Kinase / Q000097:blood; D000077324:Crystalloid Solutions; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006324:Heart Arrest, Induced / Q000379:methods*; D006801:Humans; D007036:Hypothermia, Induced / Q000379:methods; D007124:Immunoenzyme Techniques; D007527:Isoenzymes; D007552:Isotonic Solutions; D008297:Male; D017202:Myocardial Ischemia / Q000097:blood / Q000503:physiopathology / Q000601:surgery*; D009206:Myocardium / Q000378:metabolism*; D010952:Plasma Substitutes / Q000008:administration & dosage*; D011446:Prospective Studies; D015532:Rehydration Solutions / Q000008:administration & dosage; D015842:Serine Proteinase Inhibitors / Q000008:administration & dosage; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood*; D016277:Ventricular Function, Left / Q000187:drug effects
D015415:Biomarkers; D002314:Cardioplegic Solutions; D000077324:Crystalloid Solutions; D007527:Isoenzymes; D007552:Isotonic Solutions; D010952:Plasma Substitutes; D015532:Rehydration Solutions; D015842:Serine Proteinase Inhibitors; D019210:Troponin I; D007611:Aprotinin; D003402:Creatine Kinase