| Background and Objective: Myocardial protection is the issue frequently involved in operation of cardiac surgery and also is the one of the primary questions for study in cardiac surgery. It is a important factor determining patients smoothly recovering and living or dying after operation. It has go through for more than 40 years from opening-heart surgery. Applying of CBP make it rapidly progress, following it techniques of myocardial protection also constantly improve. 1950,Bigelow WC and associates started a epoch of cardiac surgery for referring advantages of profound hypothermia in intracardiac procedures. Later combining with high-potassium cardioplegia, cold high-potassium Crystalloid cardioplegia occurred, and it got a good effect in clinic.But it has some blemishes. For example, during cross-clampping of aorta, cardiac muscle obtains energy almost all by no-oxygen metabolization, therefore acidosis come into being; Utilizing of glucose and reserving of ATP sharply depress, synthesis of ATP is blocks, activity of Na~+-K~+-ATP enzyme descends; Stability of cell membrane declines, cells appear edema, cardiac muscle come to harm or turn up necrosis, endothelium cells are injured, blood vessel's diastole is handicapped, endothelium cells of blood vessel and mesenchymal tissue of cardiac muscle turn up edema, therefore blood flow of coronal vessels is handicapped and phenomenon of "no-reflow" occurs during re-perfusion of cardiac muscle. Along with more progress of techniques of myocardialprotection, "aerobic myocardial protection " occurred. Among these techniques discontinous perfusion of cold blood cardioplegia is universally utilized. And this technique is relatively mature. And relatively more studies about this have been done. Cardiac troponin(cTn) is a more sensitive more specific indicator of myocardial cell jnjury than other .biochemical cardiac markers. It has important value in passing judgement on ischemic myocardial injury and reperfusion. This "golden marker" was frequently utilized in studies of myocardial protection of cold blood cardioplegia.Usually, the history of rheumatoid heart disease is long, reconstruction and dysfunction of myocardium is severe. Myocardium's tolerance is weak to ischemia , hypoxia and CPB. So myocardial protection is very important during peri-operation, especially peri-CPB.Through the measurement of the several moment concentration of myocardial enzymes and cardiac troponin I during peri-CPB of rheumatic heart disease with mitral valvular replacement. This study attempt to determine the influence of cold blood cardioplegia on the level of cTnl and observe the effect of myocardial protection comparing with cold crystalloid cardioplegia.Methods: Consecutive twenty-two patients with rheumatoid heart diseaseand without liver and renal dysfunction were randomly divided into cold blood cardioplegia group (group CBC) and cold crystalloid cardioplegia group (group CCC). Blood samples were taken from center vein before operation (Ti), at the end of CPB (T2), lh(T3),12h(T4) ,24h(T5), 72h(T6), and 144h(T7) after CPB to measure activity of aspartate transaminase (AST), lactic dehydrogenase (LDH), creatine kinase (CK), creatine kinase isoenzyme (CK-MB), hydroxybutyric dehydrogenase (HBDH) and level of cardiac troponin I(cTnl).Results: (1) All patients survived the surgery and were discharged in good condition. No complication was observed. There were no statistical significance in patients characteristics between cold blood cardioplegia group and cold crystalloid cardioplegia group. (2)Ratio of auto-beat is 81.2% (9/11) in group CBC and support time of dopamine is 26.54±6.83h after beat; Ratio of auto-beat is 63.6% (7/11) ingroup CCC(P>0.05,compared with group CBQand support time of dopamine is 48.73 + 10.50h(P<0.05,compared with group CBC) after beat. (3)A11 the biochemical markers rise significantly. Among these markers, cTnl and CK-MB are more remarkablely rise. The mean of peak-level of cTnl is 45-68 times compared with reference value; The mean of peak-level of CK-MB is 17-22 times compared with reference value. The concentration of cTnl rise rapidly and reach peak-level at 12h after CPB and sustained for 3-6d. The concentration of CK-MB reach peak-level at 12h after CPB accordant to the concentration of cTnl and sustained for 2-3d. The concentration of AST,LDH,HBDH and CK rises slowly and sustained for a long time and range of raiseing is short. (4) There was no difference in the levels of AST baseline value between group CBC and group CCC before operation (P>0.05). The levels of AST increased significantly from the end of CPB to 144h after CPB (P<0.05), and reach peak levels 24h after CPB (P<0.01). The levels of AST decreased at 72h after CPB (P<0.05) and the level of 144h after CPB is significantly higher than that of baseline value yet. The levels of AST in group CBC lower than in group CCC significantly from the end of CPB to 144h after CPB (P<0.05). There was no difference in the levels of LDH baseline value between group CBC and group CCC before operation (P>0.05). The levels of LDH increased significantly from the end of CPB to 144h after CPB (P<0.05), and reach peak levels 24h after CPB (P<0.01). The levels of LDH decreased at 72h after CPB (P<0.05) and the level of 144h after CPB is significantly higher than that of baseline value yet. The levels of LDH in group CBC lower than in group CCC significantly from the end of CPB to 144h after CPB (P<0.05). There was no difference in the levels of HBDH baseline value between group CBC and group CCC before operation (P>0.05). The levels of HBDH increased significantly from the end of CPB to 144h after CPB (P<0.05), and reach peak levels 24h after CPB (P<0.01). The levels of HBDH decreased at 72h after CPB (P<0.01) and the level of 144h after CPB is significantly higher than that of baseline value yet. The levels of HBDH in group CBC lower than in group CCC significantly from the end of CPB to 144h after CPB (P<0.05). There was no difference in the levels of CK baseline value between group CBC and group CCC before operation (P>0.05). Thelevels of CK increased significantly from the end of CPB to 72h after CPB (P<0.01), and reach peak levels 24h after CPB (P<0.01). The levels of CK decreased at 72h after CPB (P<0.01). The levels of CK in group CBC lower than in group CCC significantly from the end of CPB(i><0.05), lh^O.05), 12 h(P<0.01), 24h(iM).Ol) after CPB to 72h after CPB (P<0.05). There was no difference in the levels of CKMB baseline value between group CBC and group CCC before operation (P>0.05). The levels of CK-MB increased significantly from the end of CPB to 24h after CPB (P<0.01), and reach peak levels 12h after CPB (P<0.01). The levels of CK-MB decreased from 24h after CPB (P<0.01), and to the baseline 72h after CPB (P>0.05). The levels of CK-MB in group CBC lower than in group CCC significantly from the end of CPB, lh(P<0.01), 12 h(P<0.01) after CPB to 24h after CPB (P<0.05). There was no difference in the levels of cTnl baseline value between group CBC and group CCC before operation (P>0.05). The levels of cTnl increased significantly after CPB(P<0.01), and reach peak levels 12h after CPB (P<0.01) and then decrease. The levels of cTnl decreased to the baseline at 72h after CPB (P>0.05) in group CBC and at 144h after CPB (P>0.05) in group CCC. The levels of cTnl in group CBC is lower than in group CCC significantly from the end of CPB, lh(P<0.01), 12 h(P<0.01), 24h(P<0.01) after CPB to 72h after CPB (P<0.05).Concllltion: (1) The sensitivity of cTnl in judging myocardial injury is morethan that of CK and CKMB peri-operation in open heart surgery. The cTnl has more value in clinic in diagnosing myocardial ischemic injury and in evaluating prognosis and effect of myocardial protection. (2) The sensitivity of CK-MB in judging myocardial injury is more than that of ASTn LDH> HBDH and CK peri-operation in open heart surgery. (3)Activity of myocardial enzymes and level of cTnl are high in group CCC vs group CBC peri-CPB. (4) Cold blood cardioplegia is better than cold crystalloid cardioplegia in enhanceing myocardial protection and in lingtening myocardial injury peri-operation of cardiac surgery. |
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