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