Gautam R. Shroff, MB, BS
Disclosures: The author has disclosed no conflicts of interest. Forms can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M14-2259.
Requests for Single Reprints: Gautam R. Shroff, MB, BS, Cardiovascular Division, Hennepin County Medical Center, 701 Park Avenue, Minneapolis, MN 55415; e-mail, email@example.com.
Author Contributions: Conception and design: G.R. Shroff.
Drafting of the article: G.R. Shroff.
Critical revision of the article for important intellectual content: G.R. Shroff.
Final approval of the article: G.R. Shroff.
Shroff G.; Acute Myocardial Infarction: What's in a Name?. Ann Intern Med. 2015;162:448-449. doi: 10.7326/M14-2259
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Published: Ann Intern Med. 2015;162(6):448-449.
The development of newer-generation troponin assays has led to remarkable progress in the rapid diagnosis or exclusion of acute myocardial infarction (AMI) (1). With increasing use of higher-sensitivity assays, it has also become evident that troponin level elevations are prevalent in several clinical situations in the absence of an acute coronary syndrome (ACS) (2). Experts have developed a universal classification system to categorize AMI on the basis of differing pathophysiologic mechanisms (3).
Type 1 or spontaneous myocardial infarction (T1MI, or ACS in common parlance) is secondary to acute atherosclerotic plaque instability in the coronary bed with intraluminal thrombosis, decreased myocardial blood flow, downstream platelet embolization, and myocardial necrosis. In contrast, type 2 myocardial infarction (T2MI) occurs in the absence of ACS from an imbalance between myocardial oxygen supply and demand. However, an important but overlooked corollary to the definition of T2MI is that there is currently no separate International Classification of Diseases (ICD) diagnostic code for this important and increasingly prevalent clinical entity in the ICD-9 (currently active in the United States) and ICD-10 (implemented in several countries around the world) manuals. This situation poses important clinical, epidemiologic, and economic ramifications that deserve careful consideration.
Sukhchain Singh, MD; Amandeep Singh, MD; Snadeep Khosla, MD FACC
Ingalls Memorial Hospital, Harvey, Illinois; Sanford Medical Center, Thief River Falls, MN; Mount Sinai Hospital Medical Center, Chicago, Illinois;Rosalind Franklin University of Medicine and Science,
March 20, 2015
Misuse of high sensitivity troponins assays
High sensitivity assays are proving to be a costly problem facing internists in hospital medicine practice and payers such as Medicare (1). The high sensitivity troponin assays, when used in proper clinical context, are very useful and improve diagnostic accuracy of myocardial infarction (MI). Author correctly highlighted higher mortality and lack of evidence based treatment options for type 2 MI or elevation in troponins without treatable intracoronary lesions or obstruction. There is no sound empirical evidence to support risk stratification based on troponin assays or its routine use to rule out or rule in MI when patients present with non-cardiac symptoms to the emergency departments.However, troponin assays are routinely ordered in the emergency room without proper clinical rationale for most abdomen-thoracic and neurological symptoms. The admitting internist, while treating an unrelated non-cardiac condition, is left to deal with the aftermath of abnormal troponins. This starts an unnecessary cascade of cardiology consultation and further testing. It prolongs hospitalization and complicates management of the patient.This diagnostic quest to nowhere does not end with cardiology consultation alone. Most recent, “Third Universal Definition of Myocardial Infarction” defines diagnosis of MI as at least one value of troponins above 99th percentile and one of the following; A) symptoms of ischemia; B) ST segment changes; C) pathological Q-wave; D) Imaging evidence of loss of viable myocardium or new regional wall motion abnormality; E) identification of intracoronary thrombus on angiography or autopsy. The cardiologist who is consulted to solve the problem faces a difficult conundrum. Symptoms are unreliable to rule out or rule in MI (3). A normal or equivocal ECG does not help to narrow the differential diagnosis either. Notwithstanding the sound clinical judgement that MI is unlikely in a specific clinical setting, a cardiologist is forced to order invasive or noninvasive work because most patients admitted to hospitals usually have some cardiovascular risk factors. The internal medicine, cardiovascular and emergency medicine sections of the hospitals should develop a collaborative protocol for judiciously ordering troponins assays. Unless acute MI is in the differential diagnosis, troponin assays should be ordered in consultation with cardiologist. Since the advent of high sensitivity troponins, it has become new “D-dimer” for the heart.References1) Gautam R. Shroff, MB, BS. Acute Myocardial Infarction: What's in a Name? Ann Intern Med. 2015; 162(6):448-449. doi: 10.7326/M14-2259. 2) Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, White HD; Joint ESC/ACCF/AHA/WHF Task Force for Universal Definition of Myocardial Infarction. Third universal definition of myocardial infarction. J Am Coll Cardiol. 2012 Oct 16; 60(16):1581-98. 3) Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the Management of Patients With Non-ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014 Dec 23; 130(25):e344-426.
James R. Johnson, MD
University of Minnesota
April 7, 2015
In his editorial entitled "Acute myocardial infarction: what's in a name?" Shroff points out the possible unintended negative clinical consequences of labeling all minor troponin elevations, which now are detected by highly sensitive newer-generation assays, as "acute myocardial infarction (MI)" . Such adverse consequences could include overtreatment, over-investigation, and impaired future insurability and employability. An analogous situation, which – although less dramatic – is similarly insidious and much more common, occurs with the labeling of an abnormal urinalysis result or positive urine culture as "urinary tract infection (UTI)", even in the absence of relevant clinical manifestations [2-4]. Once a "UTI" label has been applied, antimicrobial therapy usually follows, with its potential direct and indirect harms [2-4]. Moreover, the patient may acquire a new problem list entry that can become self-perpetuating, since it may inspire future providers to test and treat. It even can train the patient to regard cloudy or foul-smelling urine as indicative of "UTI", which the patient comes to believe needs treatment because that's what previous providers have done. Unlike the troponin problem, this one stems not from the development of a new, super-sensitive test but from clinicians' ill-informed interpretation of two traditional highly sensitive but non-specific tests: urinalysis and urine culture. Shroff appropriately calls for well-designed prospective studies regarding best strategies to manage patients with type 2 MI . Similarly, we need studies of best strategies to dissuade providers and patients from labeling asymptomatic bacteriuria and pyuria as "UTI" and, because of this misapplied and misleading label, treating it as such.Respectfully,James R. Johnson, MDNo financial COIs with this submission.1. Shroff GR. Acute myocardial infarction: what's in a name? Ann Intern Med 2015;162:446-7.
Gautam R. Shroff, MB, BS
Hennepin County Medical Center
May 21, 2015
Whereas the focus of the original article (1) was on consideration of a unique diagnostic code for type 2 myocardial infarction (MI); the comment by Singh et al (1) is focused on indiscriminate use of troponin assays for non-cardiac symptoms. As pointed out by the authors, an uncritical and unscrutinized pattern of troponin checks can lead to an unintended cascade of downstream testing that can be medically unnecessary, expensive, time-consuming and potentially anxiety provoking for the patient, and therefore should therefore be discouraged and avoided. Most cardiologists would agree that the management of a patient with an elevated troponin value obtained out of the clinical context for which it is designed (i.e. detection of acute MI), is clinically exceedingly problematic. It therefore bears emphasis that the experts that proposed the Universal Definition of MI (3) recommend that the terminology “myocardial infarction” be used only in a clinical setting consistent with myocardial ischemia. By extrapolation therefore, it would be most appropriate for troponin levels to be checked only in clinical settings where myocardial ischemia is suspected. There is undoubtedly a value of cardiac troponins in determining long-term prognosis in several different clinical scenarios, but how to inculcate information regarding long-term prognosis into the immediate management of patients has not been very well defined in the literature so far. The onus is on clinicians to recognize the context in which requesting troponin levels is appropriate; certainly “protocol driven” reflexive checks should be strongly discouraged. It certainly behooves us as clinicians to ensure that indiscriminate use of troponins is discouraged in our respective settings, and as educators to ensure that we edify our trainees well in this regard. References:1) Shroff GR. Acute myocardial infarction: what's in a name? Ann Intern Med. 2015 Mar 17;162(6):448-92) Singh S, Singh A, Khosla S. Misuse of high sensitivity troponin assays. Ann Intern Med. Posted on March 20, 2015.
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Cardiology, Emergency Medicine, Acute Coronary Syndromes, Coronary Heart Disease.
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