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Department of Anaesthesiology, Pitié-Salpêtrière Hospital, Paris, France Department of Anaesthesia, St.Vincent’s Hospital, Melbourne, Australia
To the Editor:
We have read with interest the article by Licker et al. (1) that aims to assess the impact of implementing the ACC/AHA guidelines (2) and postoperative use of antiadrenergic drugs in patients undergoing high-risk surgery such as abdominal aortic surgery on postoperative morbidity and mortality. They have studied a large cohort of 468 patients operated on either aortic aneurysmectomy or aortic stenosis, during an 8-year period using a retrospective analysis. We feel that several issues need to be raised regarding their article.
The set up of the "cardioprotective protocol" implemented in this center remains unclear to us. The two periods of clinical practice simply discuss the changes in clinical practice with regard to tighter screening investigations, follow-up, and an increase in the use of antiadrenergic drugs in the unit. No clear set out protocol is described in this study.
We question the biochemical follow-up of the patients included in this study. It appears that if one considers Figure 2 in the article, only 24% of patients in the control period had cardiac troponin I (cTnI) measured as a marker of myocardial damage. It is unclear whether this marker was ordered only in those patients with clinical symptoms and/or ECG changes and/or a raised CK-MB. The absence of routine surveillance of cTnI in all patients undergoing high-risk vascular surgery may mean that the authors grossly underestimate the incidence of postoperative acute myocardial infarction in their center (3–5). Consequently, we are surprised that in the control period 1993-1996, the authors report an increase of 14% in cTnI in such a selected population with an estimated incidence of coronary artery disease of 30%.
We would also like to draw attention to the diagnostic criteria of acute myocardial infarction used by the authors, specifically to the cutoff level used for cTnI. If only cTnI levels greater than 1.5 ng/mL when associated with clinical signs and/or ECG changes are considered (see Appendix 1 in the article), this excludes three patients in the 1993–1996 control period and one patient in the 1997–2000 intervention period. How do the authors explain a rise in cTnI higher than 1.5 ng/mL in these patients if they exclude a myocardial infarction as a diagnosis?
Finally, the essential point of the work presented by Licker et al. seems to be that their system of preoperative screening has been improved by the application of ACC/AHA guidelines in their unit. In the control period of 1993–1996, 35% of 247 patients had a noninvasive screening test, and 50 patients of this group underwent preoperative coronary angiography. In the intervention period 1997–2000, 64% of 221 patients had a noninvasive test and coronary angiography was performed in 52 patients. However, performing a similar number of coronary revascularizations in both periods led to greatly different intervention outcomes: 4% and 30% of patients, respectively, underwent coronary revascularization in both groups. Could this difference account for the decrease in acute myocardial infarcts (11 patients) in the intervention period?
References
Division of Anesthesiology, University Hospital, Geneva, Switzerland
In Response:
We agree that our study is mainly descriptive and presents biases and confounding variables associated with all nonrandomized controlled trials.
In this observational study, clinical outcome of vascular surgical patients was compared between two consecutive 4-yr periods, before and after implementation of a cardioprotective protocol, including: 1) application of ACC/AHA guidelines for preoperative screening of cardiovascular diseases, and 2) use of 
2-agonist intraoperatively and ß1-blockers to control heart rate (<80/bpm) postoperatively.
As reported in other studies, cardiac complications included cardiac death, congestive heart failure, arrhythmia, and myocardial infarct, the definition of myocardial infarction being based on the new consensus document formulated by the Joint Cardiology American/European Task Force, taking into account ECG abnormalities, clinical signs, and biological markers (1).
Total CPK and CK-MB were analyzed in all patients and, cardiac troponin I (cTn I) was selectively measured in 45% and 67% of patients during the two consecutive periods (when CPK, CK-MB were above reference limits, if indicated by ECG changes or unstable hemodynamics). Troponin levels below the sensitivity threshold have not been reported.
In vascular surgical patients, Landesberg et al. defined postoperative myocardial infarct as an increase in cTn I > 3.1 ng/mL (2). Similarly to Zaugg et al. (3), we used prespecified criteria to interpret cTn I levels: <0.5ng/mL, normal range for healthy individual; 0.5–1.5 ng/mL myocardial damage (micronecrosis); >1.5 ng/mL myocardial infarct (sensitivity, 93%; specificity, 99%)—this level was above the 99th percentile of a reference population in our laboratory.
Total cardiac complications decreased from 11.3% to 4.5% (control vs intervention period) and minor myocardial necrosis also occurred less frequently during the second period (1.8% vs in 7.7% patients, with cTn I between 0.5–1.5 ng/mL).
Better identification of high-risk patients (those requiring coronary revascularization: 0.8% and 7.7% of patients, for the two consecutive periods) and, more importantly, tight hemodynamic control with increasing administration of antiadrenergic treatments (15% and 79% for the two periods, respectively) lead to a 65% reduction in cardiac morbidity and improved cardiac event-free 1-yr survival (from 91.3% to 98.2%).
References
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