J. Mair et al., USE OF CARDIAC TROPONIN-I TO DIAGNOSE PERIOPERATIVE MYOCARDIAL-INFARCTION IN CORONARY-ARTERY BYPASS-GRAFTING, Clinical chemistry, 40(11), 1994, pp. 2066-2070
Cardiac troponin I (cTnl) is a regulatory protein unique to myocardium
. We used a cardiospecific 30-min ELISA to measure cTnl in EDTA-plasma
samples serially drawn from 28 patients before and after coronary art
ery bypass grafting (CABG)-26 elective and 2 salvage cases. The cTnl i
ncrease in 22 of the elective CABG patients, who did not have perioper
ative myocardial infarction (not-PMI), reflected the inevitable myocar
dial damage caused by cannulation and cardioplegic arrest, with peak v
alues of 1.7 +/- 1.0 mu g/L (mean +2 SD = 3.7 mu g/L), the peaks occur
ring on average 8 h (range 4-24) after aortic unclamping. Two of the 2
2 not-PMI, elective CABG patients showed cTnl peaks > 3.0 mu g/L (3.9
and 3.4 mu g/L), indicating more extensive perioperative myocardial da
mage than the other 20, as confirmed by clinical and electrocardiograp
hic or echocardiographic signs, although creatine kinase isoenzyme MB
(CKMB) activity was below our PMI decision limit of 20 U/L (25 degrees
C). As classified by electrocardiography, echocardiography, and incre
ased CKMB activity, four of the 26 elective CABG patients did have a P
MI. One patient with Q-wave PMI had peak cTnl similar to 30 mu g/L, an
d three with non-Q-wave PMI had lower peak values (similar to 5 mu g/L
). The two salvage CABG cases had increased cTnl before surgery. One d
eveloped a Q-wave acute myocardial infarction with a 3-h cTnl peak of
similar to 35 mu g/L. We conclude that, after elective CABG, cTnl peak
s > 3.7 mu g/L and concentrations > 3.1 mu g/L at 12 h or > 2.5 mu g/L
at 24 h indicate PMI with high probability.