الفهرس 
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Abstract
IschaemiaReperfusion injury remains the most uncontrolled phenomenon during cardiac operations as it damages the myocardium through several mechanisms. Laboratory testing for prediction of these events is a major task for clinical pathologists, aiming to reduce suffering and reduce the incidence of these complications. The current study is a trial to assess the myocardial function after open heart surgery the using cardiac TnI, CK, CKMB and LDH as markers of postoperative myocardial infarction. The present study is conducted on 23 patients subjected to open heart surgery. They were selected randomly from the inpatients of the cardiothoracic surgery department of Mansoura University Hospital. The patients were grouped according to the type of operation required. Eight patients were subjected to ventricular septal defect repair with an age range of 116 years (6.1 (R+ (B5.8 years) and 15 patients were subjected to valve replacement with an age range of 2063 years (31.4 (R+ (B19.6 years). Each patient was subjected to full history taking, clinical examination, ECG, ECHO, routine laboratory investigations and measurement of serum levels of cardiac Troponin I, CK, CKMB and LDH both before operation, and at 2, 6 and 20 hrs postoperatively. The present study reports the following results: LDH: The baseline LDH activity is higher than the upper reference limit in group 1 and higher in group 1 than group 2 at all timings; 2hrs, 6 hrs and 20 hrs after aortic crossclamp release: LDH activity rises significantly in the subsequent samples; 2 hrs, 6 hrs and 20 hrs after clamp release for both groups with a peak activity at 20 hrs. Total CK: The baseline value of total CK is not significantly different between the two groups but higher than the reference value. There is a significant difference in the total CK level between both groups at 2 hrs and 6 hrs after clamp release followed by an insignificant difference between both groups at 20 hrs after clamp release: Total CK rises significantly in the subsequent samples; 2 hrs, 6 hrs and 20 hrs after clamp release for both groups with a peak activity at 20 hrs. CKMB: The baseline value of CKMB is not significantly different between the 2 groups but within the reference value. There is a significant difference in CKMB level between both groups at 2 hrs after clamp release followed by an insignificant difference between both groups at 6 and 20 hrs after clamp release. CKMB level rises significantly in the subsequent sample at 2 hrs after clamp release reaching its peak mean value for both groups then declines in the subsequent samples at 6 hrs and 20 hrs after clamp release. Troponin I: The baseline value of Troponin I is not significantly different between the two groups but within the reference value. There is a siginificant difference in Troponin I level between both groups at 2 hrs and 6 hrs after clamp release followed by an insignificant difference between both groups at 20 hrs after clamp release. Troponin I level rises significantly in the following sample at 2 hrs after clamp release to reach its peak mean value then declines in subsequent samples for group 1.It rises significantly in the following two samples at 2 and 6 hrs after clamp release to reach its peak mean value then declines in the following sample for group 2. Percent increment: The percent change in marker activity between each two consequetive samples reveals that the most marked increase is observed when comparing the baseline time value of all four markers with that 2 hrs after clamp release. ECG: 100% of the patients developed postoperative ischaemic changes in their ECG in group 1, while 13.33% developed these changes in group 2. Ischaemic time and Perfusion time: There is a positive correlation between the ischaemic time and perfusion time with the marker levels at all postoperative times for all markers. The most significant correlations are between cTnI level at all times; 2 hrs, 6 hrs and 20 hrs after clamp release and ischaemic time in group 1, total CK at 2 hrs after clamp release and ischaemic time in group 1 and LDH at 20 hrs after clamp release and perfusion time in group 1. ROC curves: Receiver operating characteristic curves show that the best markers to discriminate patients with poMI from those without poMI at 2 hrs are CKMB and Troponin I for group 1 and total CK for group 2.At 6 hrs, best markers are CKMB, cTnI and total CK for group 1 and total CK and cTnI for group 2. At 20 hrs, the best marker is LDH and total CK for group 1 and is LDH, total CK and cTnI for group 2. Conclusions: The use of laboratory panels for assessment of an organ function is advocated by many clinicians. However, the sensitivity and specificity for each individual marker should be taken into consideration, in addition to costbenefit relationship. Laboratory markers of cardiac damage are now widely used, especially when false negative ECG changes are taken into consideration. The newly introduced cardiac Troponin I has established its place as a sensitive and specific marker, replacing CK and CKMB. The pediatric heart is more vulnerable to the effects of ischaemia and reperfusion than the adult heart. Recommendations: The estimation of CKMB mass can be used instead of CKMB activity to improve the results. As the pediatric heart is more vulnerable to the effects of ischaemia and reperfusion than the adult heart, strict protocols for follow up should be adopted. If heart failure is suspected, the newly introduced laboratory marker pro BNP, should be advised. Fortunately, rapid pointofcare for this marker are now available.