Discussion
The principal finding of this study was that a higher level of
preoperative peak troponin was associated with increased ICU time and
hospital length of stay. However, there was no association with peak
troponin level and short- and long-term MACCE or mortality. In
sub-analysis, peak troponin >10.00 ng/mL was also not
associated with increased hazards for MACCE or mortality.
Previous studies have demonstrated associations with serum troponin
elevation with size of myocardial infarction, degree of coronary artery
disease, and/or short term morbidity and mortality in patients
presenting with acute coronary syndromes5,8,9.
Furthermore, preoperative troponin elevation has been associated with
increased operative morbidity and mortality, as well as increased rates
of complications and/or hospital length of stay following
CABG11–15. In our study, patients with high and low
peak troponin levels were fairly well-matched with respect to age and
preoperative comorbidity. However, we noticed that the high serum
troponin group had a lower median preoperative left ventricular ejection
fraction. Additionally, they required bridging to CABG with intra-aortic
balloon pump counterpulsation more frequently, and also had a higher
incidence of preoperative congestive heart failure with advanced New
York Heart Association class symptoms (III or IV) in comparison to the
low troponin group. Based on these findings, it is possible that higher
peak troponin may indicate a larger infarction with higher degree of
myocardial stunning, which may account for lower preoperative ejection
fractions, higher incidence of heart failure, and need for mechanical
support. However, it may be possible that patients with history of
preexisting heart failure with decreased ejection fraction are more
prone to higher serum troponin leakage after NSTEMI, representing a
combination of infarction as well as heart failure. In this theory,
these patients with worse baseline cardiac function may require
intra-aortic balloon pump bridging more frequently after an equivalent
cardiac insult as would a patient with normal baseline function and
greater cardiopulmonary reserve.
The timing of CABG following acute coronary syndrome has remained
controversial16–19. Patients presenting with STEMI or
ongoing ischemia in NSTEMI require immediate revascularization. Often
times these patients can present with arrhythmias, hemodynamic
instability, and end-organ dysfunction. As a result, emergent immediate
revascularization in these scenarios is often met with a high likelihood
of morbidity and mortality, especially between 6 and 24 hours of symptom
onset16,19. In the setting of NSTEMI or smaller
infarctions with no ongoing active ischemia where cardiac function is
preserved or mildly depressed, surgical timing can vary between centers.
Some groups advocate for prompt
revascularization20,21, whereas other centers advocate
for a delay prior to surgery22. This delay can allow
for the stable patient to undergo preoperative testing and
risk-assessment, and also allow any high-dose antiplatelets and/or
anticoagulants the patient may have received at time of initial
presentation to be metabolized, which may allow for decreased bleeding
complications. Other advantages of delaying surgery in some surgeons’
opinion is that tissues and coronary vessels are less edematous and
easier to handle, and that there is less myocardial stunning which
allows the heart to tolerate the operation better. In our series of
NSTEMI patients, we did not observe increasing time from peak troponin
level to surgical revascularization to have any significant influence on
mortality in multivariable modeling. It is likely that timing of surgery
in this patient population can be tailored to the individual
circumstances and needs of the patient, and that revascularization does
not necessarily need to occur within a specific “surgical window”.
There is always a theoretical risk that delaying surgery too long can
lead to lethal arrhythmias, cardiac arrest, or worsening cardiac
function due to expanding infarction.
In our series, we observed a small but significant increase in intensive
care unit time (47.0 hours [IQR 26.0 to 81.6] vs 43.0 hours [IQR
24.6 to 69.0], P=0.004) and hospital length of stay in patients with
higher peak troponin levels (10 days [IQR 8 to 13] vs 9 days [IQR
8 to 12], P=0.013). However, in our sub-analysis, with patient cohorts
stratified by a troponin level of 10.00 ng/mL, we did not observe
differences in intensive care unit (47.1 hours [IQR 25.3 to 85.5] vs
45.0 hours [IQR 25.0 to 72.0], P=0.217) or hospital length of stay
(10 days [IQR 8 to 13 vs 10.0 hours [IQR 8 to 12], P=0.124)
(Supplemental Table 3 ). Though there is a possibility for
increased intensive care and/or hospital times with increased peak
troponin, the absolute difference is small and the clinical and
logistical relevance are likely limited.
Lastly, our findings support the notion that preoperative peak troponin
levels have little predictive value on long-term MACCE or mortality
following surgical revascularization. These findings are corroborated by
those of Beller and colleagues. In their analysis of 1,272 urgent or
emergent CABG procedures, they discovered that presence of preoperative
troponin elevation to be associated with higher risk of morbidity,
1-year, and long-term mortality, when compared to no troponin elevation.
However, when evaluating the actual troponin levels, increasing levels
did not have association with postoperative morbidity or survival
following CABG6. Our study did not observe a
significant difference in mortality when peak troponin levels were above
the median value across patients (> 1.95 ng/mL). Because
this median value seemed to be low from a clinical perspective, we
elected to perform a post hoc secondary analysis, and evaluate a
clinically meaningful cutoff of 10.00 ng/dL. Despite this, high and low
troponin cohorts did not have any significant differences in 5-year
MACCE or mortality. Similarly, these findings held true when troponin
was modeled as a continuous variable. Furthermore, peak troponin
>10.00 ng/ML was not associated with increased hazards for
MACCE or mortality in our multivariable models. Collectively, these data
suggest that the strategy of basing timing of CABG in NSTEMI on
normalization of troponin or having the troponin levels downtrend to a
certain level does not appear to be warranted.