Conclusions
The present study is an attempt to provide an analytical overview of postoperative cardiac enzyme release considering various influencing factors in cardiac surgery. We deliberately did not select patients but considered different operations including additional procedure-related factors to cover a representative spectrum of everyday cardiac surgery. One problem of postoperative troponin release is its multifactorial origin. Therefore, systematic classification remains a challenge. It is a difference whether the operation and the resulting trauma is limited to epicardial regions (as in CABG) or whether opening of the heart cavities is necessary (as in MVR). Comparison of median postoperative hs-cTnT (and of CK-MB) shows an increase depending on the type and complexity of surgery. This was described for non-high-sensitive troponin by Landoni et al, who showed that “different operations were associated with a different release of … biomarkers”, with the highest troponin release after MVR, analogous to results presented here [5].
Mortality was rather low (1.8%), and little association with hs-cTnT was found, in contrast to other studies that inferred increased mortality from postoperative dose-dependent troponin release [6, 7]. However, an association between mortality and increased CK-MB release was also demonstrated here.
In what is, to our knowledge, the only analysis of postoperative (after CABG) hs-cTnT to verify type 5 MI criteria, the authors found that isolated hs-cTnT raise was not related to mortality [8]. In contrast, if ECG and/or echocardiographic criteria were present, hs-cTnT elevation above 10 times the URL (> 140 ng/l) was associated with increased 30-day and 1.8-year follow-up mortality, thus apparently confirming guidelines. Strikingly, the authors state “the level of post-operative hs-cTnT > 140 ng/l was found in 90% of all patients…” which is consistent with the present results (hs-cTnT was above 140 ng/l in 91.6% of CABG patients) [8]. This leads to the question of the usefulness of hs-cTnT determination when a possible threshold for intervention-related ischemia is exceeded in more than 90% and thus the diagnosis is essentially based on ECG and/or echocardiographic findings. Thus, a fundamental problem regarding a precise threshold definition of the type 5 MI-indicating troponin increase emerges, which should be redefined specifically for ”high-sensitive” assays (in which only the detection method has become more sensitive, whereas the measured troponin T type remains unchanged).
To complicate matters, other factors influence troponin increase. Studies in nonsurgical patients have shown that the utility of the marker for the diagnosis and management of acute coronary syndrome in the presence of renal insufficiency is limited [9, 10]. However, in the surgical patients studied here, a possible initial association in this regard could be excluded after sorting out those with preoperatively elevated hs-cTnT. Thus, the Maze procedure, emergency intervention, blood transfusion, prolonged cardiopulmonary bypass time, and, in particular, intra-pericardial defibrillation remain as independent parameters influencing hs-cTnT release. Regarding the Maze procedure, enzyme release seems to be directly measurable and dependent on the invasiveness of ablation therapy [11].
An analysis of troponin T measurements in 847 CABG patients concluded that although only 2% had new Q waves or left bundle branch block after surgery (comparable to the incidence recorded here),”… troponin T concentrations … (are) … almost universally elevated and are determined by numerous factors …”[12]. The latter included prolonged cardiopulmonary bypass time and intraoperative defibrillation, both of which were associated with increased, whereas higher postoperative glomerular filtration rate and off-pump procedures were associated with decreased troponin [12]. Januzzi noted, in one of the first reviews of troponin testing after cardiac surgery, that:”… biomarker (s)… could lead to an inordinate percentage of patients diagnosed with ’acute MI’ … (with)… a sensitivity of 100% … observed for post-CABG MI … associated with a specificity of 4.2% and an alarmingly high misclassification rate…” [13].
The use of high-sensitive troponin assays has done little to change this problem. An even higher overall postoperative rise in cardiac enzyme markers may further limit its specificity. Thus, it seems important to include not only the hs-cTnT but also the CK-MB rise and, of course in accordance with guidelines, any ECG changes and/or regional wall motion abnormalities that may occur. Pointing this out and supporting these findings with further studies is of current importance, especially in view of possible reinterpretation attempts, as occurred in a recent large therapy optimization study, in which, deviating from the existing guidelines, the isolated postoperative troponin rise with a new low-threshold definition served as the sole assessment criterion of type V MI [14].
With regard to a generally applicable hs-cTnT threshold definition, a binding statement based on the results presented in this study seems difficult. The calculated high hs-cTnT cutoff of 1075.5ng/l (>120URL) results from the patients evaluated here, including those who had clearly detectable surgery-induced myocardial ischemia as defined above. With an AUROC of more than 95%, the model has good discriminatory predictive value in the classification chosen herein for type V MI. However, only 11 patients with clearly detectable perioperative infraction events constitute the type V MI group thus defined, which certainly allows only limited generalizability.
On the other hand, the calculated concomitant CK-MB increase with its type V MI-indicating threshold seems to allow some comparability with the results of previous analyses [15, 16]. In addition, comparison of the two markers shows that CK-MB is slightly inferior to hs-cTnT in terms of sensitivity but has higher specificity, and according to regression analysis, a stronger focus on exclusively myocardial ischemic events seems possible with simultaneous consideration of CK-MB.
In conclusion, the postoperative hs-cTnT increase is multifactorial, with particular influence of intra-pericardial defibrillation, type and duration of surgery, and emergency intervention. A reevaluation of the current thresholds regarding type V MI, especially in the context of the use of high-sensitive troponin markers, should be considered, but larger prospective (multicenter) studies are needed for assessment as well as a possible redefinition.