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.