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Anesthesiology:
doi: 10.1097/ALN.0b013e3181ce9da1
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Not All Perioperative Myocardial Infarctions Can Be Prevented with Preoperative Revascularization

Subramaniam, Balachundhar M.D., M.P.H.*; Subramaniam, Kathirvel M.D.†

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CURRENT universal definitions classify myocardial infarction (MI) into five types.1 In general, perioperative MI (PMIs) are of type I (plaque rupture) or type II (prolonged supply-demand imbalance) variety.2 Increased catecholamines, hemodynamic instability, inflammation, and coronary vasoconstriction during and after surgery can lead to rupture or erosion of a potentially unstable coronary plaque, often referred to as a “vulnerable” plaque, resulting in acute coronary thrombosis and PMI.3 However, the relative proportion of plaque rupture, demand ischemia, or their combination as the etiology of PMI is unknown. In this issue of Anesthesiology, Galal et al.4 demonstrated that although preoperative dobutamine stress echocardiography can predict patients who are at risk for PMI, it could not predict the location of those PMI in 54 consecutive patients undergoing major vascular surgery.
How can we reconcile this surprising finding? Only 10% of patients undergoing vascular surgery were shown to have pristine coronary anatomy.5 The majority of them have multivessel disease, and they can be identified as at risk for PMI by preoperative dobutamine stress echocardiography. It was previously shown that 66% of MI occur in plaques with less than a 50% luminal stenosis6 and that the MI-related coronary vascular territory is frequently not related to the territory with the most severe coronary stenosis as seen by coronary angiography.7 Moreover, statin therapy markedly reduces the risk of MI8 with minimal effect on the severity of coronary luminal stenosis.9 This disconnection between the severity of anatomic obstruction and the MI risk is one of the main pieces of evidence that plaque rupture depends on its composition rather than on its size.10 Although preoperative dobutamine stress echocardiography and other functional tests are good for the diagnosis of significant coronary artery obstruction and the identification of patients at risk for MI,11 they may fail to identify the myocardial territory at risk from rupture of a nonobstructive coronary artery plaque. If this etiology contributes significantly to PMI, preoperative revascularization approaches based on dobutamine stress echocardiography and coronary angiography will not protect against all PMI. This may in part explain why it has been difficult to show short-term benefit (up to 3 yr) of preoperative revascularization in reduction of PMI or survival12,13 but may show better long-term survival.14 These findings are consistent with the current American Heart Association/American College of Cardiology consensus recommendations that preoperative revascularization is warranted if it would benefit patients in the long-term irrespective of the planned surgery.15
Galal et al. also found that the new wall motion abnormalities (WMA) detected by intraoperative transesophageal echocardiography (TEE) had 100% positive predictive value and better agreement with the location of PMI compared with preoperative dobutamine stress echocardiography. Deterioration of regional WMA correlates better with in-hospital16 and long-term adverse cardiac outcomes17 after cardiac surgery. This led to some positive findings when monoplane TEE was used as an ischemia monitor in smaller trials in noncardiac surgery. However, a larger well-designed trial18 concluded that TEE findings were sensitive, nonspecific, and did not correlate with postoperative MI. Subsequently, the presence of sustained WMA (3 h) after aortic cross clamp was shown to predict PMI.19 Eisenberg et al.20 concluded that in 332 patients undergoing vascular and abdominal surgery, TEE offered little incremental value compared with two-lead electrocardiogram monitoring, even though the new WMA by intraoperative TEE had a 2.2 relative risk of predicting postoperative outcomes. It is to be noted that the relevant ischemic outcome in all these studies was seen in very few patients, and there was no attempt to correlate PMI location with intraoperative WMA. Thus, unlike in cardiac surgical patients, routine use of TEE as an intraoperative ischemia monitor in high-risk noncardiac surgery did not gain widespread acceptance due to the paucity of literature, the lack of studies with multiplane TEE, nonselective target population studied, and concerns about personnel availability, cost, and safety. This is reflected in the current American Society of Anesthesiologists/Society of Cardiovascular Anesthesiologists recommendation that TEE can be used in acute persistent hemodynamically unstable and life threatening situations during noncardiac surgery (Class IIa, Level C).
As TEE interpretation has improved with omniplane imaging, three-dimensional TEE, and strain rate imaging, it is now primed to be a cutting-edge technology for early intraoperative ischemia detection. The findings of Galal et al. provide a compelling argument for further exploration of intraoperative TEE in high-risk patients such as the ones with preoperative positive dobutamine stress echocardiography (a high pretest probability increases the posttest probability). Galal et al. performed protocol-based TEE ischemia and WMA monitoring and analyzed the recordings in the echo-laboratory afterward. They did not study the effect of intraoperative clinical interventions in response to TEE-detected ischemia on PMI. It will be important to study the effect of comprehensive patient management using preoperative risk stratification, early intraoperative detection of ischemia by TEE, and targeted intra- and postoperative interventions and management of PMI with multimodal therapy in an intensive/high-dependency setting.
On the basis of the findings by Galal et al., the authors suggest that preoperative revascularization will often be ineffective because preoperative myocardium “at risk” identified differs from the actual location of PMI. This is an interesting and a provocative finding; however, there are several caveats to be considered. The composite outcome was seen in just 15 patients, and the agreement of location of PMI, a major focus of this study, is based only on six patients. A detailed description of the characteristics of these six patients could give more insights. It would be interesting to see whether the disagreement in location of PMI was in major versus minor coronary arterial distribution. For example, the disagreement between inferior and anterior wall is different from the disagreement between anterior and anteroseptal walls. Whether all PMIs were seen in patients with aortic surgery with cross-clamping is unknown. It may very well be that the aortic cross-clamp is a more severe or a “better” stress test than the dobutamine stress echocardiography. It is to be noted that perioperative aspirin and statin therapy that can stabilize the plaques was achieved only in two thirds of this study population. Other limitations include lack of description of the duration and severity of new WMA, relationship to loading conditions, and correlation to intraoperative electrocardiogram evidence of ischemia. Patients with severe valvular disease, decreased ejection fraction, and female gender were not investigated in this study; therefore, the findings may not be generalized to these populations.
PMI remains a significant cause of morbidity, mortality, and increased healthcare costs. The mechanisms of PMI need to be further explored and well understood before an effective intervention strategy can be established. The current strategies of revascularization and optimal medical therapy to reduce the incidence of PMI have met with some success, but PMI is still a common occurrence. Alternative surgical approaches, such as minimally invasive techniques, is an attractive option but it is not suitable for all procedures or patients. The current challenge is to establish a comprehensive strategy with long-term β-adrenergic blockade, statin therapy, and targeted preoperative revascularization, keeping in mind the added risk of coronary stent thrombosis or dual antiplatelet therapy. The study by Galal et al. suggests that intraoperative TEE may be a sensitive method for identification of patients at risk for PMI, should these measures fail and allow for early aggressive treatment of these patients.
The authors thank Brett A. Simon, M.D., Ph.D., Professor and Chair, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, and Thomas H. Hauser, M.D., M.M.Sc., M.P.H., Director of Nuclear Cardiology, Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Assistant Professor of Medicine, Harvard Medical School, for critical revision and manuscript editing.
Balachundhar Subramaniam, M.D., M.P.H.
Kathirvel Subramaniam, M.D.
*Department of Anesthesiology, Pain Medicine and Critical Care, Beth Israel Deaconess Medical Center, Boston, Massachusetts. bsubrama@bidmc.harvard.edu. †Department of Anesthesia, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
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References

1. Thygesen K, Alpert JS, White HD: Universal definition of myocardial infarction. J Am Coll Cardiol 2007; 50:2173–95

2. Landesberg G, Beattie WS, Mosseri M, Jaffe AS, Alpert JS: Perioperative myocardial infarction. Circulation 2009; 119:2936–44

3. Naghavi M, Libby P, Falk E, Casscells SW, Litovsky S, Rumberger J, Badimon JJ, Stefanadis C, Moreno P, Pasterkamp G, Fayad Z, Stone PH, Waxman S, Raggi P, Madjid M, Zarrabi A, Burke A, Yuan C, Fitzgerald PJ, Siscovick DS, de Korte CL, Aikawa M, Juhani Airaksinen KE, Assmann G, Becker CR, Chesebro JH, Farb A, Galis ZS, Jackson C, Jang IK, Koenig W, Lodder RA, March K, Demirovic J, Navab M, Priori SG, Rekhter MD, Bahr R, Grundy SM, Mehran R, Colombo A, Boerwinkle E, Ballantyne C, Insull W Jr, Schwartz RS, Vogel R, Serruys PW, Hansson GK, Faxon DP, Kaul S, Drexler H, Greenland P, Muller JE, Virmani R, Ridker PM, Zipes DP, Shah PK, Willerson JT: From vulnerable plaque to vulnerable patient: A call for new definitions and risk assessment strategies: Part I. Circulation 2003; 108:1664–72

4. Galal W, Hoeks SE, Flu WJ, van Kuijk JP, Goei D, Galema T, den Uil C, van Gestel YRBM, Bax JJ, Verhagen HJM, Poldermans D: Relation between preoperative and intraoperative new wall motion abnormalities in vascular surgery patients: A transesophageal echocardiographic study. Anesthesiology 2010; 112:557–66

5. Hertzer NR, Beven EG, Young JR, O'Hara PJ, Ruschhaupt WF III, Graor RA, Dewolfe VG, Maljovec LC: Coronary artery disease in peripheral vascular patients. A classification of 1,000 coronary angiograms and results of surgical management. Ann Surg 1984; 199:223–33

6. Little WC, Constantinescu M, Applegate RJ, Kutcher MA, Burrows MT, Kahl FR, Santamore WP: Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild-to-moderate coronary artery disease? Circulation 1988; 78:1157–66

7. Giroud D, Li JM, Urban P, Meier B, Rutishauer W: Relation of the site of acute myocardial infarction to the most severe coronary arterial stenosis at prior angiography. Am J Cardiol 1992; 69:729–32

8. Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP): Expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel III). JAMA 2001; 285:2486–97

9. Effect of simvastatin on coronary atheroma: The Multicentre Anti-Atheroma Study (MAAS). Lancet 1994; 344:633–8

10. Mann JM, Davies MJ: Vulnerable plaque. Relation of characteristics to degree of stenosis in human coronary arteries. Circulation 1996; 94:928–31

11. Cheitlin MD, Armstrong WF, Aurigemma GP, Beller GA, Bierman FZ, Davis JL, Douglas PS, Faxon DP, Gillam LD, Kimball TR, Kussmaul WG, Pearlman AS, Philbrick JT, Rakowski H, Thys DM: ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography-summary article: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). J Am Coll Cardiol 2003; 42:954–70

12. McFalls EO, Ward HB, Moritz TE, Goldman S, Krupski WC, Littooy F, Pierpont G, Santilli S, Rapp J, Hattler B, Shunk K, Jaenicke C, Thottapurathu L, Ellis N, Reda DJ, Henderson WG: Coronary-artery revascularization before elective major vascular surgery. N Engl J Med 2004; 351:2795–804

13. Poldermans D, Schouten O, Vidakovic R, Bax JJ, Thomson IR, Hoeks SE, Feringa HH, Dunkelgrun M, de Jaegere P, Maat A, van Sambeek MR, Kertai MD, Boersma E: A clinical randomized trial to evaluate the safety of a noninvasive approach in high-risk patients undergoing major vascular surgery: The DECREASE-V Pilot Study. J Am Coll Cardiol 2007; 49:1763–9

14. Landesberg G, Berlatzky Y, Bocher M, Alcalai R, Anner H, Ganon-Rozental T, Luria MH, Akopnik I, Weissman C, Mosseri M: A clinical survival score predicts the likelihood to benefit from preoperative thallium scanning and coronary revascularization before major vascular surgery. Eur Heart J 2007; 28:533–9

15. Fleisher LA, Beckman JA, Brown KA, Calkins H, Chaikof E, Fleischmann KE, Freeman WK, Froehlich JB, Kasper EK, Kersten JR, Riegel B, Robb JF, Smith SC, Jr., Jacobs AK, Adams CD, Anderson JL, Antman EM, Buller CE, Creager MA, Ettinger SM, Faxon DP, Fuster V, Halperin JL, Hiratzka LF, Hunt SA, Lytle BW, Nishimura R, Ornato JP, Page RL, Tarkington LG, Yancy CW: ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery): Developed in collaboration with the American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Rhythm Society, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, and Society for Vascular Surgery. Circulation 2007; 116:e418–99

16. Leung JM, O'Kelly B, Browner WS, Tubau J, Hollenberg M, Mangano DT: Prognostic importance of postbypass regional wall-motion abnormalities in patients undergoing coronary artery bypass graft surgery. SPI Research Group. Anesthesiology 1989; 71:16–25

17. Swaminathan M, Morris RW, De Meyts DD, Podgoreanu MV, Jollis JG, Grocott HP, Milano CA, Newman MF, Mathew JP: Deterioration of regional wall motion immediately after coronary artery bypass graft surgery is associated with long-term major adverse cardiac events. Anesthesiology 2007; 107:739–45

18. London MJ, Tubau JF, Wong MG, Layug E, Hollenberg M, Krupski WC, Rapp JH, Browner WS, Mangano DT: The “natural history” of segmental wall motion abnormalities in patients undergoing noncardiac surgery. SPI Research Group. Anesthesiology 1990; 73:644–55

19. Koolen JJ, Visser CA, Reichert SL, Jaarsma WJ, Kromhout JG, van Wezel HB, Dunning AJ: Improved monitoring of myocardial ischaemia during major vascular surgery using transoesophageal echocardiography. Eur Heart J 1992; 13:1028–33

20. Eisenberg MJ, London MJ, Leung JM, Browner WS, Hollenberg M, Tubau JF, Tateo IM, Schiller NB, Mangano DT: Monitoring for myocardial ischemia during noncardiac surgery. A technology assessment of transesophageal echocardiography and 12-lead electrocardiography The Study of Perioperative Ischemia Research Group. JAMA 1992; 268:210–6

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