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Letter by Madias Regarding Article, "Long-Term Outcomes in Patients With Type 2 Myocardial Infarction and Myocardial Injury".

Circulation. 2018;138:1176–1177. DOI: 10.1161/CIRCULATIONAHA.118.035681 1176 John E. Madias, MD To the Editor: The interesting article by Chapman et al1 about the long-term outcomes in patients with type 2 myocardial infarction (T2MI) and myocardial injury (MIN) prompts one to contemplate the diagnostic fuzziness and probable underlying heterogeneous pathophysiological nature among a score of poorly demarcated or overlapping clinical entities, including T2MI, MIN, myocardial infarction with nonobstructive coronary artery disease, coronary spasm, coronary plaque disruption, coronary dissection, microvascular dysfunction, desolved coronary thrombus, coronary embolus, myocarditis, takotsubo syndrome, 2 noncardiac disorders (pulmonary embolism and renal impairment), and possibly other as-yet unidentified causes of a transient rise of high-sensitivity troponins. The authors found in a cohort of 2122 consecutive patients with elevated (≥0.05 μg/L) cardiac troponin I concentrations adjudicated according to the universal definition of myocardial infarction (MI)2 to 3 groups—1171 patients (55.2%) with type 1 myocardial infarction, 429 patients (20.2%) with T2MI, and 522 patients (24.6%) with MIN—that their corresponding 5 year all-cause mortality rates were 36.7%, 62.5%, and 72.4%, with the majority of excess mortality in the patients with T2MI or MIN being the result of noncardiovascular causes.1 Furthermore, the authors reported that, despite the excess in noncardiovascular mortality of patients with T2MI and MIN, their crude rate of major adverse cardiovascular events was similar to that of patients with type 1 myocardial infarction and that it is important to evaluate for underlying coronary heart disease in the patients with T2MI and MIN and treat them accordingly.1 A burgeoning literature shows the heterogeneous pathophysiological entities under the multiple diagnostic rubrics enumerated above, adopted by clinicians and researchers for communication purposes and for the preliminary characterization of patients showing transiently elevated troponins while admitted with a diverse array of clinical phenotypes.3 Thus, patients reported as having myocardial infarction with nonobstructive coronary artery disease were found to have myocarditis,3 patients diagnosed with type 1 myocardial infarction or T2MI had also clinical and imaging attributes of takotsubo syndrome, and patients with myocardial infarction with nonobstructive coronary artery disease were labeled as such on the basis of corollary arteries with <50% diameter stenosis on coronary angiography (ie, luminography), many of whose coronary anatomy and physiology would have been indicative of severe coronary heart disease had other more sophisticated diagnostic methods (ie, intravascular ultrasound, optical coherence tomography) been used. The uncertainties currently encountered when we try to diagnostically “pigeon-hole” patients admitted with a diverse clinical phenotype and a rise and fall in troponin blood concentrations indicate that we have to accomplish a lot before the diagnostic muddle we are in is elucidated. To this end, we need to embark on amplifying our current diagnostic armamentarium with certain important additions beyond the use of biomarkers (serial troponins), serial ECG, coronary angiography, © 2018 American Heart Association, Inc. LETTER TO THE EDITOR