Predictors of Cardiac Troponin Release After Mitral Valve Surgery
Fabrizio Monaco, MD,* Giovanni Landoni, MD,* Camilla Biselli, MD,* Monica De Luca, MD,*
Giovanna Frau, MD,* Elena Bignami, MD,* James L. Januzzi Jr, MD,† and Alberto Zangrillo, MD*
Objectives: Although cardiac troponin I (cTnI) measure-
ment is used extensively as a marker of perioperative myo-
cardial injury, limited knowledge exists in noncoronary ar-
tery bypass graft surgery.
Design: Observational study.
Setting: Single-center intensive care unit.
Intervention: None.
Participants: One hundred eighty-five consecutive adult
patients undergoing mitral valve surgery for predominant
mitral regurgitation were enrolled and underwent measure-
ment of cTnI at 24 hours after surgery.
Measurements and Main Results: CTnI release after mitral
valve surgery was significantly associated with an adverse
outcome. The optimal cTnI value for predicting adverse out-
comes was 14 ng/mL. Univariate preoperative predictors of
cTnI release were prior use of diuretics (p 0.04) or a
rheumatic (p 0.006), ischemic (p 0.004), or myxomatous
(p 0.005) etiology to mitral disease, whereas intraopera-
tive variables predictive of cTnI release were cross-clamp
time (p 0.005), cardiopulmonary bypass time (p < 0.001),
need for mitral valve replacement (p 0.024), number of
electrical cardioversions (p 0.03), patent foramen ovale
closure (p 0.03), tricuspid valve repair (p 0.04), need for
epinephrine/norepinephrine (p 0.004) or intra-aortic bal-
loon pump (p 0.03) in the operating room; and, finally, the
surgeon who performed the surgery (p 0.014). There were
no postoperative predictors of excessive cTnI release. In
multivariate analysis, the only predictors of cTnI release
were the cardiopulmonary bypass time (odds ratio, 1.42;
confidence intervals, 1.019-1.064; p 0.001) and the infusion
of epinephrine/norepinephrine in the operating room (odds
ratio, 4.002; confidence intervals, 1.238-12.929; p 0.02).
Conclusions: After mitral surgery, the need for epineph-
rine/norepinephrine perioperatively and the cardiopulmo-
nary bypass time independently predict a cTnI release sig-
nificantly related to an adverse outcome.
© 2010 Elsevier Inc. All rights reserved.
KEY WORDS: anesthesia, cardiopulmonary bypass, myocar-
dial injury, mitral valve
C
ARDIAC TROPONIN (cTn) is a contractile myocardial
protein that is released into the circulation after myocar-
dial cell injury. Unlike creatine kinase and its MB isoenzyme,
which are present in skeletal muscle, cTn is a highly sensitive
and specific marker of myocardial damage.
1,2
In the last decade,
cTn has evolved as the gold standard for the evaluation of
myocardial infarction in patients presenting with an acute cor-
onary syndrome.
1
This is based not only on the superior per-
formance of cTn for the diagnosis of myocardial infarction but
also for prognostication in this setting. For instance, among
patients with acute coronary syndromes, both cTnT and cTnI
concentrations were associated with a nearly linear risk for
death.
3,4
Similarly, in the postoperative setting, cTn concentra-
tions offer important prognostic value in those with coronary
ischemia; as an example, vascular surgery patients with a
postoperative cTn 1.5 ng/mL are 6 times more likely to die
within 6 months compared with patients with levels 1.5
ng/mL.
5
It also is worthwhile to briefly address the differences be-
tween cTnT and cTnI assays. According to a meta-analysis
performed in acute coronary syndrome patients, the 2 biomark-
ers have been shown to be sensitive and specific for predicting
myocardial infarction and cardiac death.
6
Most studies report
troponin I instead of troponin T. Historically, the cTnT assay is
produced by 1 manufacturer, whereas the more widely used
cTnI assays are produced by different companies, and the
assays generally could be implemented in hospital laboratories
using existing hardware; thus, the isoform I usually is more
affordable and widely adopted.
6
What is needed now is a
standardization of cTnI methods in order to definitively estab-
lish a useful post–mitral surgery risk cutoff. In addition, with
the advent of the high-sensitivity cTn methods, it is reasonable
to expect that most differences in sensitivity between cTnI and
cTnT will be more closely related; what will be more important
in this setting will be the understanding that the detection of
cardiac injury likely will be absolutely universal in this popu-
lation.
The picture becomes more complex when cardiac surgery is
considered, however, because among patients undergoing car-
diac surgery, a degree of myocardial injury commonly is ob-
served related to the surgery itself.
7
In fact, intraoperative
injury may occur during cardiac manipulation, inadequate myo-
cardial protection, intraoperative defibrillation, and hemody-
namic instability; whereas postoperative injury may be associ-
ated with myocardial ischemia related to numerous factors,
including the early loss of bypass grafts. In the context of
cardiac surgery, the magnitude of the cTn release is consider-
ably higher than what is seen in acute coronary syndromes,
potentially rendering cTn a less reliable predictor of myocardial
injury.
8
However, studies consistently have shown an associa-
tion between cTn values and adverse outcomes after cardiac
surgery. In this setting, different cTn thresholds may be nec-
essary to predict early and late postoperative complications.
8
In fact, recent studies have found cTn to be one of the
strongest predictors of short-, medium-, and long-term mortal-
ity after cardiac surgery
9-12
; the value of cTn also appears to be
independent of (and additive to) risk models for postoperative
outcomes such as the Society for Thoracic Surgery risk score.
Therefore, in total, the identification of patients with a higher
risk of postoperative cTn elevation is of paramount importance,
From the *Department of Anesthesia and Intensive Care, Università
Vita-Salute San Raffaele, Milan, Italy; and †Department of Medicine
and Division of Cardiology, Massachusetts General Hospital, Boston,
MA.
Address reprint requests to Giovanni Landoni, MD, Department of
Anesthesia and Intensive Care, Università Vita-Salute San Raffaele, via
Olgettina 60, 20132 Milan, Italy. E-mail: Landoni.giovanni@hsr.it
© 2010 Elsevier Inc. All rights reserved.
1053-0770/2406-0005$36.00/0
doi:10.1053/j.jvca.2010.06.029
931 Journal of Cardiothoracic and Vascular Anesthesia, Vol 24, No 6 (December), 2010: pp 931-938