Today's BMJ

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New definition of myocardial infarction
Features new subtypes of infarction and puts high demands on diagnostic assays


The evolution of the definition of acute myocardial infarction tells a fascinating story of medical progress. Between the publication of the initial World Health Organization’s classification in 1979,1 and that published by the redefinition committee of the American College of Cardiology, American Heart Association, and European Society of Cardiology in 2000, much of our diagnostic reasoning changed.2 Biochemistry now takes centre stage, and the measurement of cardiac troponins has substantially increased diagnostic sensitivity.

Cardiologists predicted that these changes in diagnostic criteria and sensitivity would increase the incidence of acute myocardial infarction.3 They also predicted that the redefinition would have implications for individual patients and healthcare expenditure. Their predictions turned out to be correct, at least in part. A national registry in Norway found a 33% increase in acute myocardial infarction after the implementation of the 2000 criteria,4 and the Swedish Nationwide Centre of Epidemiology documented an abrupt 14% increase.5

Interest in the definition of acute myocardial infarction has recently been revived by the publication by the redefinition committee of the "universal definition of myocardial infarction."6 This guideline represents both consolidation and innovation—consolidation because the key importance of troponins is firmly established; innovation because for the first time the committee has established subtypes of infarction.

In principle, with regard to biomarkers, the 2007 definition of spontaneous acute myocardial infarction is the same as in the 2000 document. It requires a rise and fall of troponin values with at least one measurement above the upper 99th centile, a coefficient of variation (CV) <10% at this cut-off point, and the presence of myocardial ischaemia.

The subtypes of infarction are defined as follows (see box). Type 1 is the classic type of acute myocardial infarction triggered by rupture of an atherosclerotic plaque and subsequent thrombosis in a coronary artery. Type 2 reflects a mismatch between myocardial oxygen supply and demand, with no signs of coronary thrombosis. Type 3 is reserved for acute cardiac arrest, which in most cases is an infarction. Types 4 and 5 are peri-procedural infarctions, which occur during primary percutaneous coronary interventions or a coronary artery bypass graft, respectively. This new classification is a bold innovation.




Clinical classification of different types of myocardial infarction

Type 1—Spontaneous myocardial infarction related to ischaemia caused by a primary coronary event, such as plaque fissuring or rupture

Type 2—Myocardial infarction secondary to ischaemia resulting from an imbalance between oxygen demand and supply, such as coronary spasm

Type 3—Sudden death from cardiac disease with symptoms of myocardial ischaemia, accompanied by new ST elevation or left bundle branch block, or verified coronary thrombus by angiography. In this type of myocardial infarction death occurs before blood samples can be obtained

Type 4—Myocardial infarction associated with primary percutaneous coronary intervention

Type 5—Myocardial infarction associated with coronary artery bypass graft






What are the weaknesses of the new definition? Many laboratories cannot achieve a diagnostic precision of <10% CV at the 99th centile for a given troponin I or troponin T assay. Moreover, clinicians are entirely dependent on the assay manufacturer’s reported precision—the document refers readers to a website maintained by the International Federation for Clinical Chemistry,6 which lists the intra-lot variations established by the manufacturer. This has led to considerable uncertainty about whether to use the 99th centile as the cut-off point or whether to use a higher cut-off value. This decision is made more difficult by many assay manufacturers recommending their own cut-off value, regardless of the 99th centile and 10% CV requirements. These challenges call for a close collaboration between clinical chemistry and cardiology departments, so that the new definition can be implemented under conditions that both parties feel comfortable with.

Because the ability to subclassify myocardial infarction increases our diagnostic repertoire considerably, we urgently need to update what the word "infarction" actually means. For instance, a type 2 infarction does not necessarily carry a poor prognosis, and drugs that are normally prescribed for infarctions may not be needed. This message must be conveyed to a wide range of people, including general practitioners, specialists, trialists, healthcare authorities, life insurers, epidemiologists, and politicians.

The new universal definition of myocardial infarction should be implemented in clinical practice as soon as possible. However, clinical chemical expertise will be needed to ensure that a given hospital laboratory can deliver the required diagnostic precision of a CV <10% at the upper 99th centile. Most importantly, knowledge should be disseminated about the new classification of infarctions.

Cite this as: BMJ 2008;337:a3078




Dan Atar, professor and head of cardiology

[Gilarov]

Действительно, наибольший интерес вызывает 2-й тип ИМ. Все ли случаи повышения уровня тропонина (например, при ХПН) вне рамок истинного ИМ надо рассматривать как этот тип? Любой некроз миокарда - это ИМ или нет? А дальше - больше. Уже созданы тест-системы, выявляющие не нано-, а пикограммы тропонина. И показано, что даже такое повышение его уровня ухудшает прогноз. 2 интересные статьи в одном из последних номеров EHJ.
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