CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Kristian Thygesen, MD, DMSc*,
Joseph S. Alpert, MD,
Allan S. Jaffe, MD,
Harvey D. White, MD, DSc on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction
* Department of Medicine and Cardiology A, Aarhus University Hospital, Tage-Hansens Gade 2, DK-8000 Aarhus C, Denmark (Email: Kristian.Thygesen{at}as.aaa.dk).
We thank Dr. Gualandro and colleagues for their thoughtful letter. We have considered a number of different clinical scenarios but decided not to target every specific clinical situation, because there are too many to be contained within the framework of the European Society of Cardiology/American College of Cardiology Foundation/American Heart Association/World Heart Federation expert consensus document (1).
We agree that there is a great deal to learn about perioperative myocardial infarctions as the pathophysiology of these differs somewhat from that of myocardial infarction occurring in the usual setting. We also agree that it can be hard to tell whether these infarctions are type 1 or type 2. However, there are some data to guide us.
Studies of patients undergoing noncardiac surgery strongly support the concept that many of the infarctions diagnosed in this connection are caused by prolonged imbalance between myocardial oxygen supply and demand on the background of coronary artery disease (2,3), which together with rise and fall of cardiac markers points toward myocardial infarction type 2.
The fact that many such patients have type 2 infarctions should not obscure the likelihood that some of the infarctions are type 1 as well. Pathology of fatal peri- or post-operative myocardial infarctions shows plaque rupture and platelet aggregation leading to thrombus formation in approximately half of these events (4). Given the differences that likely exist in the therapeutic approaches to each, close clinical scrutiny to identify this group is essential.
Some patients may not have myocardial infarction at all. Careful clinical evaluation including a detailed history, examination, and evaluation of further investigations to identify and treat those with pulmonary embolism, sepsis, and/or the many other conditions associated with myocyte necrosis and troponin elevations is strongly advocated (1).
Although we cannot make criteria for all clinical judgments such as this one, the available information suggests that the use of contemporary troponin assays (5,6) and the decision levels advocated by the expert consensus document (1) maximizes the ability to identify patients with this diagnosis and then to configure the care according to the type based on that judgment.
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References
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- Thygesen K, Alpert JS, White HD. Universal definition of myocardial infarction J Am Coll Cardiol 2007;50:2173-2195.[Free Full Text]
- Fleisher LA, Nelson AH, Rosenbaum SH. Postoperative myocardial ischemia: Etiology of cardiac morbidity or manifestation of underlying disease? J Clin Anesth 1995;7:97-102.[CrossRef][ISI][Medline]
- Landesberg G, Mosseri M, Shatz V, et al. Cardiac troponin after major vascular surgery: the role of perioperative ischemia, preoperative thallium scanning, and coronary revascularization J Am Coll Cardiol 2004;44:569-575.[Abstract/Free Full Text]
- Cohen MC, Aretz TH. Histological analysis of coronary artery lesions in fatal postoperative myocardial infarction Cardiovasc Pathol 1999;8:133-139.[CrossRef][ISI][Medline]
- Landesberg G, Shatz V, Akopnik I, et al. Association of cardiac troponin, CK-MB, and postoperative myocardial ischemia with long-term survival after major vascular surgery J Am Coll Cardiol 2003;42:1547-1554.[Abstract/Free Full Text]
- Bursi F, Babuin L, Barbieri A, et al. Vascular surgery patients: perioperative and long-term risk according to the ACC/AHA guidelines, the additive role of post-operative troponin elevation Eur Heart J 2005;26:2448-2456.[Abstract/Free Full Text]
Related Article
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Perioperative Myocardial Infarction Has Been Forgotten
- Danielle Menosi Gualandro, Bruno Caramelli, Pai Ching Yu, Andre Coelho Marques, and Daniela Calderaro
J. Am. Coll. Cardiol. 2008 51: 1825-1826.
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