LETTER
Type 2 Myocardial Infarction: The Next Frontier To the Editor: For decades, physicians have fought to improve the diagnosis and management of acute coronary syndromes.1 Extensive educational efforts have been invested in generations of medical professionals to learn protocols tailored toward identifying the complexities of acute coronary syndromes.2 With implementation of high-sensitivity cardiac troponin assays, previously underestimated pathologies responsible for myocardial necrosis not due to plaque rupture are being increasingly identified.3 In The American Journal of Medicine, Saaby et al4 have presented data on outcomes among patients with type 2 myocardial infarction and report a mortality rate that approached 50% at 2.1 years, in contrast to 26% for type 1 myocardial infarction. Type 2 myocardial infarction mortality was concluded to be more likely due to the nature of the myocardial infarction rather than comorbidities, and independent of the underlying triggering conditions that led to it. Despite using a contemporary troponin assay (not high sensitivity) and defining type 2 myocardial infarction by their own strict criteria, it represented approximately 25% of all myocardial infarctions. Thus, one can only wonder about the frequency of type 2 myocardial infarction using the less strict definition if high-sensitivity troponin assays were used. Saaby et al’s4 proposed own specific criteria for type 2 myocardial infarction are intended to facilitate replication by other researchers. Nonetheless, the authors recognized that their criteria do not represent the “gold standard.” Most clinicians are not challenged by an obvious type 1 myocardial infarction or by ischemia in the presence of hemoglobin less than 5 mmol/L or ventricular tachyarrhythmias lasting 20 minutes as proposed. In practice, clinicians are troubled by the “borderline” patients, in whom distinguishing the source of ischemia is not obvious and determining myocardial infarction subtype is difficult. Advocating for these strict clinical criteria could simplify Funding: None. Conflict of Interest: FSA is a consultant to or has an advisory role for T2 Biosystems and Instrumentation Laboratory; and has received honoraria from Abbott Laboratories and research funding, without salary, from the majority of manufacturers marketing cardiac troponin assays. Authorship: All authors had access to the data and played a role in writing this manuscript.
0002-9343/$ -see front matter Ó 2014 Elsevier Inc. All rights reserved.
event adjudication for research proposes. However, a “one-size fits all” approach using these criteria is limited and should not be advised. Of note, patients who underwent noncardiac surgery were included in the study, and it was concluded that among them, type 2 myocardial infarction was less frequent than originally supposed. The data on perioperative myocardial infarction is limited. First, there were a limited number of events. Second, troponin measurements were done at physician discretion. Third, the myocardial infarction definition is limited among individuals undergoing noncardiac surgery, in whom ischemia may remain subclinical.5 Type 2 myocardial infarction has now become increasingly recognized because of the increased sensitivity of troponin assays that were originally intended for acute coronary syndromes. In contrast to type 1 myocardial infarction, type 2 myocardial infarction is poorly defined, and a new knowledge base to identify and manage it is required. Saaby et al4 have highlighted the magnitude of this problem and the need for ongoing investigation. Yader Sandoval, MDa Stephen W. Smith, MD, MDb Fred S. Apple, PhDc a
Division of Cardiology Department of Medicine b Department of Emergency Medicine Hennepin County Medical Center Minneapolis, Minn c Department of Laboratory Medicine and Pathology Hennepin County Medical Center and University of Minnesota Minneapolis
http://dx.doi.org/10.1016/j.amjmed.2014.02.027
References 1. Nabel EG, Braunwald E. A tale of coronary artery disease and myocardial infarction. N Engl J Med. 2012;366:54-63. 2. O’Connor RE, Brady W, Brooks SC, et al. Part 10: acute coronary syndromes: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 Suppl 3):S787-S817. 3. Korley FK, Jaffe AS. Preparing the United States for high-sensitivity cardiac troponin assays. J Am Coll Cardiol. 2013;61:1753-1758. 4. Saaby L, Poulsen TS, Diederichsen AC, et al. Mortality rate in type 2 myocardial infarction: observations from an unselected hospital cohort. Am J Med. 2014;127:295-302. 5. Garcia S, Marston N, Sandoval Y, et al. Prognostic value of 12-lead electrocardiogram and peak troponin I level after vascular surgery. J Vasc Surg. 2013;57:166-172.
Type 2 Myocardial Infarction: The Next Frontier To the Editor: For decades, physicians have fought to improve the diagnosis and management of acute coronary syndromes.1 Extensive educational efforts have been invested in generations of medical professionals to learn protocols tailored toward identifying the complexities of acute coronary syndromes.2 With implementation of high-sensitivity cardiac troponin assays, previously underestimated pathologies responsible for myocardial necrosis not due to plaque rupture are being increasingly identified.3 In The American Journal of Medicine, Saaby et al4 have presented data on outcomes among patients with type 2 myocardial infarction and report a mortality rate that approached 50% at 2.1 years, in contrast to 26% for type 1 myocardial infarction. Type 2 myocardial infarction mortality was concluded to be more likely due to the nature of the myocardial infarction rather than comorbidities, and independent of the underlying triggering conditions that led to it. Despite using a contemporary troponin assay (not high sensitivity) and defining type 2 myocardial infarction by their own strict criteria, it represented approximately 25% of all myocardial infarctions. Thus, one can only wonder about the frequency of type 2 myocardial infarction using the less strict definition if high-sensitivity troponin assays were used. Saaby et al’s4 proposed own specific criteria for type 2 myocardial infarction are intended to facilitate replication by other researchers. Nonetheless, the authors recognized that their criteria do not represent the “gold standard.” Most clinicians are not challenged by an obvious type 1 myocardial infarction or by ischemia in the presence of hemoglobin less than 5 mmol/L or ventricular tachyarrhythmias lasting 20 minutes as proposed. In practice, clinicians are troubled by the “borderline” patients, in whom distinguishing the source of ischemia is not obvious and determining myocardial infarction subtype is difficult. Advocating for these strict clinical criteria could simplify Funding: None. Conflict of Interest: FSA is a consultant to or has an advisory role for T2 Biosystems and Instrumentation Laboratory; and has received honoraria from Abbott Laboratories and research funding, without salary, from the majority of manufacturers marketing cardiac troponin assays. Authorship: All authors had access to the data and played a role in writing this manuscript.
0002-9343/$ -see front matter Ó 2014 Elsevier Inc. All rights reserved.
event adjudication for research proposes. However, a “one-size fits all” approach using these criteria is limited and should not be advised. Of note, patients who underwent noncardiac surgery were included in the study, and it was concluded that among them, type 2 myocardial infarction was less frequent than originally supposed. The data on perioperative myocardial infarction is limited. First, there were a limited number of events. Second, troponin measurements were done at physician discretion. Third, the myocardial infarction definition is limited among individuals undergoing noncardiac surgery, in whom ischemia may remain subclinical.5 Type 2 myocardial infarction has now become increasingly recognized because of the increased sensitivity of troponin assays that were originally intended for acute coronary syndromes. In contrast to type 1 myocardial infarction, type 2 myocardial infarction is poorly defined, and a new knowledge base to identify and manage it is required. Saaby et al4 have highlighted the magnitude of this problem and the need for ongoing investigation. Yader Sandoval, MDa Stephen W. Smith, MD, MDb Fred S. Apple, PhDc a
Division of Cardiology Department of Medicine b Department of Emergency Medicine Hennepin County Medical Center Minneapolis, Minn c Department of Laboratory Medicine and Pathology Hennepin County Medical Center and University of Minnesota Minneapolis
http://dx.doi.org/10.1016/j.amjmed.2014.02.027
References 1. Nabel EG, Braunwald E. A tale of coronary artery disease and myocardial infarction. N Engl J Med. 2012;366:54-63. 2. O’Connor RE, Brady W, Brooks SC, et al. Part 10: acute coronary syndromes: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 Suppl 3):S787-S817. 3. Korley FK, Jaffe AS. Preparing the United States for high-sensitivity cardiac troponin assays. J Am Coll Cardiol. 2013;61:1753-1758. 4. Saaby L, Poulsen TS, Diederichsen AC, et al. Mortality rate in type 2 myocardial infarction: observations from an unselected hospital cohort. Am J Med. 2014;127:295-302. 5. Garcia S, Marston N, Sandoval Y, et al. Prognostic value of 12-lead electrocardiogram and peak troponin I level after vascular surgery. J Vasc Surg. 2013;57:166-172.
