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Acute MI: Lack of precise definition continues to lead to misdiagnoses
Members of the Task Force for the Redefinition of MI talked with Cardiology Today about the current issues that have arisen from the current definition of acute MI and how these concerns will be addressed at the upcoming committee meeting in May.
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The question of what exactly constitutes an acute MI has been debated in cardiology for many years and, to this day, has still not been adequately answered, according to members of the Task Force for the Redefinition of MI.
The task force, which is a joint committee of the European Society of Cardiology, the American College of Cardiology Foundation, the American Heart Association and the World Heart Foundation, had previously made two attempts to address this issue, which were published in 2000 and 2007. In the most recent attempt, the authors of this consensus document stated that the term acute MI should be used “when there is evidence of myocardial necrosis in a clinical setting consistent with myocardial ischemia.”
The authors then broke acute MI into five different types that are highlighted in the following:
- Detection of rise and/or fall of cardiac biomarkers — preferably troponin — with at least one value above the 99th percentile of the upper reference limit (URL) together with evidence of myocardial ischemia;
- Sudden, unexpected cardiac death involving cardiac arrest;
- Elevations of cardiac biomarkers above the 99th percentile of the URL among percutaneous coronary intervention patients with normal baseline troponin levels;
- Elevations of cardiac biomarkers above the 99th percentile of the URL among CABG patients with normal baseline troponin levels;
- Pathological findings of an acute MI.
In other words, said Joseph Alpert, MD, with the department of medicine, University of Arizona, and one of the chairpersons of this committee, acute MI is based upon use of the troponin assay as “the gold standard for evidence of myocardial injury and then a great deal of clinical information to make sure it is due to ischemic heart disease, because the heart can be injured in a variety of ways.”
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Problems abound in practice
Despite the committee’s attempt to incorporate as many appropriate variables as possible into the definition of acute MI, problems with these criteria are still evident in clinical practice.
“One of the tensions in this issue is that clinicians — particularly in the US more than other countries — are reluctant to use the [assay] cut-offs that are recommended because they are highly sensitive and identify a large number of patients that don’t have MI but have another reason to be at risk with myocardial injury,” said Allan S. Jaffe, MD, with the Mayo Clinic in Rochester, Minn., who is the chairperson of the biochemistry committee of the task force.
Other clinical syndromes that cause an elevation in troponin, Jaffe said, include pulmonary embolism, sepsis and myocarditis.
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“There has been substantial controversy over how one should classify those,” he said. “So, one has to do clinical work to figure out which elevations of troponin, even those with a rising pattern, are due to acute MI and which ones are due to something else.”
Areas of interest at upcoming meeting
One of the major issues to be addressed at the upcoming task force meeting to better define MI, which will be held in Paris in May, is how to incorporate ultra-sensitive assays into the definition of MI, according to Bernard R. Chaitman, MD, of the Saint Louis University School of Medicine, and a member of the ECG group on the 2007 document. These assays, he said, have led to a higher incidence of MI diagnoses because they can detect very small amounts of troponin leakage.
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“That is a headache for a lot of us in terms of how to use it and what the cut-off points should be,” said Chaitman, who is also on Cardiology Today’s Editorial Board. “Sometimes you can measure troponin in people who are doing some type of physical exertion, like jogging, and just by itself that doesn’t indicate that a heart attack occurred. … Imagine if you had a supersensitive assay that could detect if you knocked off one heart cell during the procedure so that 100% of people who had an angioplasty with a stent all had a leak of enzymes. So did they all have heart attacks? The definition of a heart attack requires you to have ischemia and cell death. So, if you increase the number of people who have an MI, it has all kinds of implications in terms of the health care system.”
Even with this potential for misdiagnoses with ultra-sensitive assays, Jaffe said it is important to use assays as recommended, which has particular consequence post-procedure.
“If you use the 99th percentile of the upper reference range (which is what the guidelines recommend), then the results of post-PCI studies look different than if you use higher cut off values because you capture most of the risk associated with a procedure at the baseline sample,” he said. “This is the real problem, which is that we have not gotten clinicians to use the proper cut-offs, and if we did, it would make their world tremendously easier for them in many ways. The tension is that it will unmask a larger number of elevations they don’t want to deal with because they are not sure how to deal with them. This has in part been why there are problems with application of the post-PCI criteria.
Although maybe 20% to 30% of angioplasty/stent procedures have a small elevation in troponin afterward, the reality is “if you had a 99% lesion and you already had a little heart attack and they open up that artery and it’s now patent, the fact that you paid the price of a little tiny bump in troponin is nothing,” said Alpert, who is on Cardiology Today’s CHD and Prevention Editorial Board.
Also slated for discussion at the upcoming committee meeting will be relatively new topics for the guidelines, Chaitman said, including the use of supplemental or additional leads besides the standard 12. This will help “diagnosis of a heart attack and modification of some of the criteria on how much ST elevation or depression needs to be present before you can be comfortable that this is actually related to acute ischemia,” he said.
Ultimate goal for clinical practice
With a more precise definition in place, the confusion that is currently dealt with in clinical practice would be minimized, Alpert said.
“Right now, one doctor may tell a patient he had a heart attack and another doctor takes over and tells him there was no heart attack. So what do you tell this patient?” he said. “That kind of [indecision] in the clinical setting can be a nightmare, as it’s certainly a nightmare for the patient.”
Alpert also said this indecision has consequences with insurance companies and clinical research as well. “Insurance companies go crazy over this, as one doctor may label many more patients as having an MI than another doctor,” he said. “And with clinical trials, one trial defines it one way and another trial defines it another way. So the question then becomes how can we make any comparisons? With this in mind, it becomes easier to see why confusion reigns and why it is not good for the industry, the science or the patient.”
Although ending this confusion is one part of the goal for a new universal definition of MI, Jaffe said he is also hoping that it will give clinicians some leeway to use their own judgment.
“One of the things that has made clinicians unhappy is that the troponin [assay], for many, has been viewed as something they have to use and that they are not allowed to use judgment with because this is myocardial injury; therefore, they must follow a protocol,” he said. “It’s likely that clinicians will appreciate an increased degree of flexibility, at least until we develop better metrics. The challenge is to provide guidelines for the use of clinical judgment so it is used well.
Updates to the universal definition of MI are expected to be published in early 2012. – by Brian Ellis
Alpert J. J Am Coll Cardiol. 2000;36:959-969.
Thygesen K. Eur Heart J. 2007;28:2525-2538.
Disclosure: Drs. Alpert and Chaitman reported no relevant financial disclosures. Dr. Jaffe has acted as consultant for numerous companies that develop and manufacture blood tests.
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