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Correspondence  |   March 2001
Perioperative Myocardial Infarction (PMI): A Never-ending Story
Author Affiliations & Notes
  • Juraj Sprung, M.D., Ph.D.
    *
  • *Mayo Clinic, Rochester, Minnesota. sprung.juraj@mayo.edu
Article Information
Correspondence
Correspondence   |   March 2001
Perioperative Myocardial Infarction (PMI): A Never-ending Story
Anesthesiology 3 2001, Vol.94, 541. doi:
Anesthesiology 3 2001, Vol.94, 541. doi:
In Reply:—
We thank Dr. Mollhoff et al.  for addressing our article. 1 We wish to offer clarification on their questions.
We agree that the rate of perioperative myocardial infarction (PMI) may be underestimated in our study, as we acknowledged in our study limitations section. In the article, we listed four reasons: (1) perioperative surveillance for PMI was not done prospectively; (2) not all patients were monitored for PMI; (3) monitoring sometimes was not performed in a systematic manner; and (4) troponin concentrations were not assessed in any of the patients. As we have stated, we are confident that we reported all cases of clinically significant PMI, and it is possible that a certain number of silent PMIs were not diagnosed. It should be noted that, for another variable we studied, mortality after PMI (death is an unmistakable complication), the rate we reported (17%) is similar to the one reported by Badner et al.  2 (20%).
In our study, general anesthesia carried a higher risk of PMI than did neuraxial anesthesia (odds ratio, 3.25, P  < 0.003). However, in the multivariate analysis, type of anesthesia did not play a significant role in PMI or cardiac mortality. We cannot comment about possible differences in perioperative pain management between the two groups because we did not analyze this variable.
In our discussion, we suggested some of the explanations for why we think β blockade did not reduce the PMI rate in our population. First, patients to whom β blockers are administered are not absolutely protected against perioperative myocardial ischemia, and Slogoff and Keats 3 demonstrated that patients with coronary artery disease who use β blockers may experience myocardial ischemia intraoperatively, despite better hemodynamic control. Second, β blockade in our patients was probably inadequate because we found no difference between the heart rates in the two groups. Third, β blockade may have been administered preferentially to the patients with more severe coronary artery disease, and it may be that the increased severity of disease was the reason why these particular patients had a higher incidence of PMI.
The patients who had undergone percutaneous transluminal coronary angioplasty (PTCA) and subsequently experienced PMI had lower odds of cardiac death than did patients with PMI who had not undergone PTCA (the odds ratio of 0.32, however, was not statistically significant). Because we did not know the preoperative coronary artery anatomy (sites of stenoses) of our patients, we may postulate the following: PTCA is typically used to dilate stenotic lesions in larger coronary vessels, and, therefore, occlusions on smaller coronary artery branches may persist even after successful PTCA, but PMI that results from occlusion of these areas affects less cardiac muscle mass, with consequently lower mortality. Therefore, our finding has some logical explanation but needs to be further studied. We collected data on PTCA and categorized the procedures in four intervals: less than 3 months before surgery, 3–6 months previously, 7–12 months previously, and more than 12 months previously. In the PMI group, we had 12 patients: 3 underwent PTCA within 3 months before surgery, 4 underwent it 4–6 months before surgery, and 5 underwent it more than 12 months before surgery (1 of these 5 patients died). Although we have representative subjects in three of four categories, this is a small number of patients to make a definitive conclusion about the optimal timing of surgery after PTCA. In our previous (retrospective) study, we found very low cardiac morbidity in patients undergoing vascular surgery who underwent PTCA up to 18 months preoperatively. 4 The retrospective study by Postner et al.  5 did not provide one important piece of information for the patients who had PTCA and subsequent PMI: Did PMI develop in the area that was treated with PTCA or in some other area that was not originally amenable to treatment? It is moot to discuss the value of PTCA without this information. This issue may be resolved only by analyzing coronary angiograms in patients who underwent PTCA and consequently experienced PMI, and, to the best of our knowledge, this type of study does not exist.
References
Sprung J, Abdelmalak B, Gottlieb A, Mayhew C, Hammel J, Levy PJ, O’Hara P, Hertzer NR: Analysis of risk factors for myocardial infarction and cardiac mortality after major vascular surgery. A nesthesiology 2000; 93: 129–40Sprung, J Abdelmalak, B Gottlieb, A Mayhew, C Hammel, J Levy, PJ O’Hara, P Hertzer, NR
Badner NH, Knill RL, Brown JE, Novick TV, Gelb AW: Myocardial infarction rate after noncardiac surgery. A nesthesiology 1998; 88: 572–8Badner, NH Knill, RL Brown, JE Novick, TV Gelb, AW
Slogoff S, Keats AS: Does chronic treatment with calcium entry blocking drugs reduce perioperative myocardial ischemia? A nesthesiology 1988; 68: 676–80Slogoff, S Keats, AS
Gottlieb A, Banoub M, Sprung J, Levy PJ, Beven M, Mascha EJ: Perioperative cardiovascular morbidity in patients with coronary artery disease undergoing vascular surgery after percutaneous transluminal coronary angiography. J Cardiothor Vasc Anesth 1998; 12: 501–6Gottlieb, A Banoub, M Sprung, J Levy, PJ Beven, M Mascha, EJ
Posner KL, Van Norman GA, Chan V: Adverse cardiac outcomes after noncardiac surgery in patients with prior percutaneous transluminal coronary angioplasty. Anesth Analg 1999; 89: 553–60Posner, KL Van Norman, GA Chan, V