The new definition takes into account not only more precise measurement of biomarkers, but also defines MI as a cause of sudden death, MI in the setting of percutaneous coronary interventions, MI in coronary artery bypass patients, and a subtype of MI related to stent thrombosis.
The definition, published online by the European Heart Journal, was endorsed by the American College of Cardiology, the American Heart Association, the European Society of Cardiology, and the World Heart Federation.
It was drafted by a task force co-chaired by Kristian Thygesen, M.D., of Aarhus University Hospital, Joseph Alpert, M.D., of the University of Arizona, and Harvey White, M.D., of Auckland City Hospital in New Zealand.
Dr. Thygesen and colleagues wrote that because the new definition has a higher sensitivity than previous definitions, more cases of MI are likely to be identified, which will allow "appropriate secondary prevention."
In the most literal -- and simplest -- terms MI describes the death of heart cells caused by an interruption in the flow of blood to those cells, but in clinical practice defining MI is not a simple matter.
The universal definition states that the term myocardial infraction "should be used when there is evidence of myocardial necrosis in a clinical setting consistent with myocardial ischemia."
In that setting, any one of the these criteria would meet the diagnosis for MI:
- 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 together with evidence of myocardial ischemia with at least one of these -- symptoms of ischemia, ECG changes indicative of new ischemia such as new ST-T changes or new left bundle branch block; development of pathological Q waves in the ECG; or imaging evidence of new loss of viable myocardium, or new regional wall motion abnormality.
- Sudden unexpected cardiac death, involving cardiac arrest, often with symptoms suggestive of myocardial ischemia, and accompanied by new ST elevation or new left bundle branch block, and/or evidence of fresh thrombus by coronary angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood.
- For percutaneous coronary interventions in patients with normal baseline troponins, elevations of cardiac biomarkers above the 99th percentile upper reference limit are indicative of peri-procedural myocardial necrosis. By convention, increases of biomarkers greater than 3 X 99th percentile upper reference limit have been designated as defining PCI-related MI, a subtype related to stent thrombosis is recognized.
- For CABG patients with normal baseline troponin values, elevations of cardiac biomarkers above the 99th percentile upper reference limit are indicative of peri-procedural myocardial necrosis. By convention, increases of biomarkers greater than 5 x 99th percentile upper reference limit plus either new pathological Q waves or new left bundle branch block, or angiographically documented new graft or native coronary occlusion, or imaging evidence of new loss of viable myocardium have been designated as defining CABG-related myocardial infarction.
- Pathological findings of acute myocardial infarction.
Moreover, any one of the following criteria could be used to identify a prior MI:
- Development of new pathological Q wave with or without symptoms.
- Imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract, in the absence of a non-ischemic cause.
- Pathological findings of a healed or healing myocardial infarction.
Sidney Smith, M.D., of the University of North Carolina in Chapel Hill, said the first stab at defining MI was the result of a consensus conference of clinicians convened by the ACC and ESC in 1999, which agreed on a definition on the basis of clinical symptoms as well as pathology, electrocardiographic changes, biomarkers, and imaging studies.
But the "epidemiologic community was really not extensively involved in that paper and epidemiologists correctly pointed out that any change in MI definition by using more sensitive measures could have a major impact on disease prevalence," Dr. Smith said. "So in 2003 there was a second paper -- this time one that was drafted with input from epidemiologists -- that defined MI."
As "more sensitive measures of troponin and improved imaging became available, along with the critical need for inclusion of percutaneous coronary intervention criteria, there was a clear need for this latest updated definition," he said.
Dr. Smith, who served as chief science officer at the AHA when the original definition was published, now chairs the AHA/ACC percutaneous coronary intervention guidelines committee.
Moreover, "increasing the specificity of diagnostic criteria for myocardial infarction will result in more accurate diagnosis but will not exclude the presence of coronary artery disease, the case of which may benefit from secondary prevention."
|Dr. Thygesen declared no financial conflicts. Dr. Alpert said he received consulting fees from Sanofi-Aventis, Exeter Continuing Medical Education Company and Novartis. Dr. White said he received financial support from Alexion, Eli Lilly, Sanofi-Aventis, Merck Sharpe & Dohme, The Medicines Co., Neuren Pharmaceuticals, GlaxoSmithKline, Pfizer, Roche, Fournier Laboratories, Johnson & Johnson, Proctor & Gamble, Schering Plough, Janssen Cileg, and the National Institutes of Health. Expenses for the task force and for preparation of the manuscript were provided entirely by the ESC/ACC/AHA/WHF.|
- Reviewed by Zalman S. Agus, MD Emeritus Professor at the University of Pennsylvania School of Medicine