Third Universal Definition of Myocardial Infarction

Abstract

Criteria for acute myocardial infarction The term acute myocardial infarction (MI) should be used when there is evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischemia. Under these conditions any one of the following criteria meets the diagnosis for MI: ● Detection of a rise and/or fall of cardiac biomarker values [preferably cardiac troponin (cTn)] with at least one value above the 99th percentile upper reference limit (URL) and with at least one of the following: y Symptoms of ischemia. y New or presumed new significant ST-segment–T wave (ST–T) changes or new left bundle branch block (LBBB). y Development of pathological Q waves in the ECG. y Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality. y Identification of an intracoronary thrombus by angiography or autopsy. ● Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic ECG changes or new LBBB, but death occurred before cardiac biomarkers were obtained, or before cardiac biomarker values would be increased. ● Percutaneous coronary intervention (PCI) related MI is arbitrarily defined by elevation of cTn values (5 99th percentile URL) in patients with normal baseline values (99th percentile URL) or a rise of cTn values 20% if the baseline values are elevated and are stable or falling. In addition, either (i) symptoms suggestive of myocardial ischemia or (ii) new ischemic ECG changes or (iii) angiographic findings consistent with a procedural complication or (iv) imaging demonstration of new loss of viable myocardium or new regional wall motion abnormality are required. ● Stent thrombosis associated with MI when detected by coronary angiography or autopsy in the setting of myocardial ischemia and with a rise and/or fall of cardiac biomarker values with at least one value above the 99th percentile URL. ● Coronary artery bypass grafting (CABG) related MI is arbitrarily defined by elevation of cardiac biomarker values (10 99th percentile URL) in patients with normal baseline cTn values (99th percentile URL). In addition, either (i) new pathological Q waves or new LBBB, or (ii) angiographic documented new graft or new native coronary artery occlusion, or (iii) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality. Criteria for prior myocardial infarction Any one of the following criteria meets the diagnosis for prior MI: ● Pathological Q waves with or without symptoms in the absence of non-ischemic causes. ● 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 prior MI

Prevalence and Clinical Significance of Discordant Changes in Fractional and Coronary Flow Reserve After Elective Percutaneous Coronary Intervention

“…In 234 territories from 234 patients, 63 patients (26.9%) showed a post‐PCI cardiac troponin I (cTnI) level >5 times the upper reference limit (≥1.0 ng/mL) based on blood samples taken at an average of 20.1±2.4 hours after PCI. The institutional 99th percentile upper reference limit for diagnosing acute coronary syndrome is 0.20 ng/mL, and PCI‐related myocardial injury was defined as a cTnI level >1.0 ng/mL (0.20 ng/mL; institutional upper reference limit ×5) based on the third universal definition of myocardial infraction 22. In these 63 patients, 4 had distal embolization exhibiting a transient slow flow or no reflow at the time of PCI with ECG changes, and 10 showed side‐branch occlusion (>1.5 mm in diameter) during PCI with wall motion abnormality detected by ultrasound examination after PCI and/or ECG changes.…”

Short‐Term Exposure to Fine Particulate Matter Air Pollution Is Preferentially Associated With the Risk of ST‐Segment Elevation Acute Coronary Events

“…A recent randomized, double‐blind, crossover intervention study of healthy adults from Shanghai, China, for example, reported that substantial reductions in PM 2.5 exposures for 48 hours from air purification resulted in cardiopulmonary benefits, including decreases in several circulating inflammatory and thrombogenic biomarkers and lower systolic and diastolic blood pressure 27. Given these implied adverse mechanisms, in the context of universal definition and clinical classification of MI,28 these results suggest that there are differential effects of PM 2.5 exposures on different types of MI. It is likely, for example, that MI events that occur in those with no CAD by angiogram would be classified as type 2 MI, and these events would be less likely to be associated with short‐term elevated exposure to PM 2.5 air pollution than type 1 (or even possibly type 3) MI events.…”

Trends in Mortality Following Acute Myocardial Infarction Among Dialysis Patients in the United States Over 15 Years

“…Establishing an accurate diagnosis of NSTEMI in dialysis patients can be problematic because troponin increases and nonspecific electrocardiographic abnormalities are common and typical symptoms of acute coronary syndrome are less frequent,5 but prevalence of obstructive coronary artery disease is high. Consequently, differentiating type 1 (or spontaneous) AMI from type 2 AMI (caused by supply/demand mismatch), particularly in the context of chronic baseline troponin elevation, can be difficult 18. These diagnostic challenges, compounded by the transition of the preferred biomarker from creatinine kinase to higher sensitivity troponin assays, could potentially contribute to the remarkable uptick in diagnostic codes for NSTEMI between 1993 and 2008.…”