The International Classification of Diseases (ICD)—both versions 9 and 10—has not previously designated codes to identify the six types of myocardial infarction (MI) included in the Third Universal Definition of Myocardial Infarction, which was published in Circulation on Oct. 16, 2012. As of Oct. 1, 2017, that will change with the implementation of the 2018 International Classification of Diseases, 10th Revision, Clinical Modification (ICD-10-CM).
This month's column will discuss the definitions of and distinctions among the six types of MI. Next month's column will explore the new codes and coding rules for them.
For types 1, 2, and 4b, MI is defined as myocardial necrosis identified by a rise and/or fall of cardiac biomarkers to or from a level greater than the 99th percentile of the upper reference limit. Cardiac biomarkers include cardiac troponin I or T, MB fraction of creatinine phosphokinase (CK-MB), and myoglobin. Cardiac troponin is the most reliable biomarker for all types of MI because it has high myocardial specificity and high clinical sensitivity.
Types 1 and 2 are by far the most commonly encountered in clinical practice. Type 1 is the classic spontaneous MI, primarily due to coronary artery disease (CAD) with atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection causing intraluminal thrombosis. Occasionally type 1 occurs in the absence of CAD with spontaneous thrombosis of a coronary artery (particularly in women). Type 1 includes Q-wave infarction, ST-elevation MI and non-ST elevation MI.
Type 2 MI is commonly known as supply/demand infarction where the supply of oxygenated blood to the myocardium does not meet the physiologic demand for oxygen (supply/demand mismatch or ischemic imbalance), causing myocardial necrosis primarily due to a condition other than CAD. Common examples include severe anemia, tachyarrhythmia, hypertensive emergency, and shock states. Also included as type 2 are nonthrombotic occlusions like coronary spasm or embolism from another site.
Demand ischemia is supposed to be reserved to describe supply/demand mismatch causing ischemia without necrosis where biomarkers remain below the 99th percentile of the upper reference limit, but the term is often used by clinicians to describe what is technically a type 2 MI. As will be discussed next month, a clinically correct distinction between demand ischemia and type 2 MI is crucial because demand ischemia has far less impact on the severity classification.
Type 3 MI is rarely encountered since biomarkers are usually obtained, but sometimes the patient dies of an MI before the biomarkers have risen above the 99th percentile of the upper reference limit. The MI may have been identified by symptoms that suggested MI and were associated with presumed new changes on electrocardiogram, such as Q-waves, ST elevation, or new left bundle-branch block.
Type 4 MI identifies a complication related to percutaneous coronary intervention (PCI) or a coronary stent. Type 4a is an MI related to PCI. It has a complicated technical definition with six separate criteria, including one that requires an elevation of cardiac troponin to a level five times greater than the 99th percentile of the upper reference limit from a normal preprocedural baseline. Documentation of type 4a is best left to the cardiologist performing the PCI. Type 4b is simply MI associated with acute stent thrombosis.
Type 5 is MI related to coronary artery bypass grafting. It also has a complex technical definition best left to the expertise of the cardiac surgeon performing the procedure. There are four separate diagnostic criteria, one of which is an elevation of biomarkers (not limited to troponin as for type 4a) to a level 10 times greater than the 99th percentile of the upper reference limit from a normal preoperative baseline (Table).
In summary, the Third Universal Definition of Myocardial Infarction has defined six types of MI. The two most commonly encountered are type 1 (primarily due to CAD) and type 2 (primarily due to myocardial supply/demand mismatch). For these two types, MI is defined as myocardial necrosis identified by a rise and/or fall of cardiac biomarkers to or from a level greater than the 99th percentile of the upper reference limit.