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Is there a clinical need to measure the cardiac troponin I concentration before major abdominal surgery in high-risk patients?

Boccara, G.*; Coriat, P.; Colson, P.

European Journal of Anaesthesiology (EJA): February 2006 - Volume 23 - Issue 2 - p 173–175
doi: 10.1017/S0265021505212115

*Department of Anaesthesia and Intensive Care American Hospital of Paris, Neuilly, France

Department of Anaesthesia and Intensive Care University Hospital of Pitié-Salpétrière Paris, France

Department of Anaesthesia and Intensive Care University Hospital of Montpellier Montpellier, France

Correspondence to: Gilles Boccara, Service d'Anesthésie et Réanimation, American Hospital of Paris, 63 Boulevard Victor Hugo, 92202 Neuilly sur Seine Cedex, France. E-mail:; Tel: +33 1 46 41 25 25; Fax: +33 1 46 41 25 83

Accepted for publication 31 October 2005

First published online January 2006


Cardiac specific troponins were shown to be a powerful independent predictor of future cardiac events in patients suffering from coronary artery disease (CAD) [1]. This disease comprises a wide spectrum of conditions ranging from chronic stable angina to acute myocardial infarction. In CAD patients undergoing major non-cardiac surgery the immediate preoperative period may be associated with silent unstable angina, as suggested by the occurrence of ST segment depression, indicating the development of an ischaemic episode [2]. Consequently, we postulated that an abnormal preoperative troponin plasma level might help identifying patients at very high risk for postoperative coronary complications. This prospective study determined whether abnormal serum cardiac troponin I (cTnI) concentration is associated with an increased risk for postoperative coronary complication in CAD patients undergoing non-cardiac surgery.

After approval from the Institutional Ethics Committee, we performed a prospective study during a 1-yr period in a single hospital (CHU Montpellier). We studied 71 consecutive and informed patients suffering from documented CAD undergoing elective major abdominal surgery. The presence of CAD was defined by at least one of the following criteria: history of typical angina pectoris, past history of myocardial infarction or Q-wave electrocardiographic (ECG) evidence of myocardial infarction, positive exercise ECG or stress echocardiography, preoperative dipyridamidole thallium defect, angiographically proven coronary artery stenosis (>50%), previous coronary artery bypass surgery or percutaneous coronary angioplasty. Patients with patent unstable angina or recent myocardial infarct (less than 1 month) were excluded. Before operation, a consultant cardiologist clinically evaluated patients. Oral premedication with hydroxyzine was systematically associated with usual cardiac treatment, especially beta-adrenergic blocker, except inhibitors of the renin-angiotensin system which were withdrawn the eve of surgery. Aspirin and other antiplatelet agents were discontinued 8-10 days before surgery and patients received low molecular weight heparin injections. Anaesthesia was left at the discretion of the anaesthesiologist in charge of the patient. Perioperative ST segment analysis was continuously and automatically recorded in leads II, V4 and V5. ST segment deviations were considered as significant when there was a reversible ST segment shift from baseline of ≥1 mm depression (planar or downsloping), measured 60 ms after the J-point, or ≥1 mm increase at the J-point, and lasting for at least 1 min. Significant ST segment changes were treated either by correction of the haemodynamic variations or the haematocrit (>28%) when required, or by an anti-ischaemic therapy (diltiazem, nitroglycerin or beta-adrenergic blocker drug) when the ST segment change persisted. The preoperative coronary treatment of the patient was resumed postoperatively. Postoperative analgesia was ensured by intravenous morphine or epidural patient-controlled administration or intermittent subcutaneous morphine injections. ECG was recorded 1 day before surgery, at arrival in the post-anaesthesia care unit and daily during 3 days and at day 7. Blood samples were obtained for plasma measurement of cTnI the evening before surgery, and at postoperative days 1 and 3. Serum cTnI concentration was measured using the ACCESS® Troponin I Immunoassay of Sanofi Diagnostics Pasteur, France. The ACCESS® Troponin I Immunoassay is a double-monoclonal immunoenzymometric assay for quantitative determination of cTnI using magnetic separation and chemoluminescence detection. The analytical range of this test is 0.03-50.0 ng mL−1 and the cut-off value considered as abnormal is 0.1 ng mL−1. A value higher than 0.15 ng mL−1 indicates myocardial necrosis [3]. Cardiac complications were defined as the occurrence of myocardial infarction defined as a serum cTnI concentration ≥0.15 ng mL−1 associated with permanent new ST segment depression changes or dysrhythmic episode or an acute left ventricular failure. Data were expressed in mean ± SD or number of patients and analysed with the χ2 and Fisher's exact tests.

One patient having a preoperative value of cTnI higher than 0.15 ng mL−1, above the myocardial necrosis threshold [3] was unfit for surgery and sent to a cardiology intensive care unit (ICU). A coronary angioplasty was performed 24 h later. A preoperative serum cTnI concentration between 0.1 and 0.15 ng mL−1 was noted in five patients. All these five patients with preoperative serum cTnI concentration higher than 0.1 ng mL−1 experienced a postoperative complication: three experienced a postoperative myocardial infarction (cTnI and ECG changes) with two cardiac-related deaths (40%), one had postoperative peritonitis and one had septic shock requiring infusion of high norepinephrine doses. A postoperative myocardial infarction was noted in 11 among the 65 patients with preoperative cTnI value lower than 0.1 ng mL−1: cTnI and ECG changes (8 patients), cTnI and atrial fibrillation (2 patients), cTnI and death from left ventricular failure (1 patient). Postoperative septic shock syndrome occured in four patients having postoperative cTnI measurements greater than 0.15 ng mL−1 without evidence of myocardial ischaemia. Patients with and without elevated preoperative cTnI (>0.1 ng mL−1) value were similar with respect to patient characteristics (Table 1). However the incidence of cardiac complication was significantly higher in patients with abnormal i.e. greater than 0.1 ng mL−1 preoperative cTnI (60% vs. 17%, P = 0.001).

Table 1

Table 1

Major efforts in patients with CAD undergoing non-cardiac surgery are directed towards identifying patients at high risk of postoperative adverse outcome and subsequently to institute measures to improve the prognosis. This study shows that in patient with patent CAD scheduled for elective major abdominal surgery a preoperative abnormal troponin serum concentration before surgery is associated with a very high risk for postoperative life threatening cardiac complication. In the immediate preoperative period, several factors may provoke unstable angina in patients with chronic stable CAD, a critical phase of the disease which may be silent. These factors include the preoperative emotional stress and cessation of anti-platelet agent [4]. The superiority of cardiac specific troponins over the ECG to predict future cardiac events in patients with unstable angina has been confirmed by both prospective and retrospective analysis. Troponin may seem to be a surrogate marker for unstable atherosclerotic plaques and consequent microembolization causing myocardial damage. Myocardial cell injury before necrosis can be accurately detected by elevated values of cardiac troponin in the circulation during unstable angina [5]. Furthermore, a slight elevation of troponin plasma level is an accurate indicator for unstable coronary states, which could be silent, and represents a reliable predictor of early high-risk patients [6]. These observations lead us to add the measurement of these markers in the immediate preoperative period in patients suffering from patent CAD.

In this study, an abnormal serum troponin concentration, even a very slight increase with a serum concentration lower than 0.15 ng mL−1, which may reveal a critical phase of the ischaemic heart disease, indicated a very high incidence of postoperative complications. These observations provide additional impetus for considering the measurements of these markers in the immediate preoperative period which may help detecting patients at very high risk who certainly deserve specific managements aimed at improving the postoperative outcome.

G. Boccara

P. Coriat

P. Colson

*Department of Anaesthesia and Intensive Care American Hospital of Paris, Neuilly, France

Department of Anaesthesia and Intensive Care University Hospital of Pitié-Salpétrière Paris, France

Department of Anaesthesia and Intensive Care University Hospital of Montpellier Montpellier, France

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© 2006 European Society of Anaesthesiology