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Biochemical or electrocardiographic evidence of acute myocardial injury
The identification of myocardial injury is an important problem in the critical care setting. Biomarkers have been used to detect myocardial injury since 1954. Since then, the sensitivity of serologic techniques has increased dramatically. Although increased sensitivity has allowed clinicians to detect smaller amounts of myocardial necrosis, this has also posed several interpretive challenges. What constitutes significant myocardial damage? How should evidence of myocardial necrosis be interpreted in the absence of classical clinical criteria for myocardial infarction? In response to some of these challenges, a task force has formulated a universal definition of myocardial infarction, updated in 2018 ( Table 29.1 ). These definitions rely on both electrocardiographic and biochemical information and stress that, in addition to biochemical findings, the diagnosis of myocardial infarction (MI) requires symptoms or characteristic electrocardiogram (ECG) changes or findings from imaging, angiography, or autopsy. The most important distinction for the clinician is between type 1 MIs (plaque rupture) and type 2 MIs (demand ischemia leading to infarction).
TABLE 29.1
Clinical Classification and Definition of Different Types of Myocardial Infarctions
From Thygesen K, Alpert JS, Jaffe AS, et al. Fourth universal definition of myocardial infarction. Circulation. 2018;138(20):e618–e651.
| Type 1: MI Caused by Atherothrombotic CAD and Usually Precipitated by Atherosclerotic Plaque Disruption (Rupture or Erosion) |
Detection of a rise and/or fall of cTn values with at least one value above the 99th percentile URL and with at least one of the following:
|
| Type 2: Myocardial Injury in the Context of a Mismatch Between Oxygen Supply and Demand |
Detection of a rise and/or fall of cTn values with at least one value above the 99th percentile URL and evidence of an imbalance between myocardial oxygen supply and demand unrelated to acute coronary atherothrombosis, requiring at least one of the following:
|
| TYPE 3: Cardiac Death in Patients with Symptoms Suggestive of Myocardial Ischemia and Presumed New Ischemic ECG Changes Before Ctn Values Become Available or Abnormal |
| Patients who suffer cardiac death, with symptoms suggestive of myocardial ischemia accompanied by presumed new ischemic ECG changes or ventricular fibrillation, but die before blood samples for biomarkers can be obtained, or before increases in cardiac biomarkers can be identified, or MI is detected by autopsy examination. |
| Type 4a: MI Associated with Percutaneous Coronary Intervention (≤48 Hours After the Index Procedure) |
Coronary intervention–related MI is arbitrarily defined by an elevation of cTn values more than five times the 99th percentile URL in patients with normal baseline values. In patients with elevated preprocedure cTn in whom the cTn levels are stable (<20% variation) or falling, the postprocedure cTn must rise by >20%. However, the absolute postprocedural value must still be at least five times the 99th percentile URL. In addition, one of the following elements is required:
|
| TYPE 4b: Stent/Scaffold Thrombosis Associated with Percutaneous Coronary Intervention |
| TYPE 4c: Restenosis Associated with Percutaneous Coronary Intervention |
| TYPE 5: MI Associated with CABG (≤48 Hours After the Index Procedure) |
CABG-related MI is arbitrarily defined as elevation of cTn values >10 times the 99th percentile URL in patients with normal baseline cTn values. In patients with elevated preprocedure cTn in whom cTn levels are stable (<20% variation) or falling, the postprocedure cTn must rise by >20%. However, the absolute postprocedural value still must be >10 times the 99th percentile URL. In addition, one of the following elements is required:
|
CABG , Coronary artery bypass grafting; cTn , cardiac troponin; ECG , electrocardiogram; MI , myocardial infarction; URL , upper reference limit.
Electrocardiographic evidence
Acute coronary syndromes (ACSs) are a group of conditions characterized by acute myocardial ischemia resulting from inadequacy of myocardial blood flow. The ACSs are classified by clinical, biochemical, and electrocardiographic data, initially dividing patients by ECG into those with ST elevation myocardial infarction (STEMI), who should be considered for immediate revascularization, and those without (non-ST elevation [NSTE-ACS]). Patients with suspected ACS must have an ECG obtained and interpreted within 10 minutes of presentation. Criteria for the diagnosis of STEMI include new ST elevation ≥0.1 mV at the J-point in at least two contiguous leads (except V 2–3 ) or new left bundle branch block (LBBB). , (In leads V 2–3 cut points are higher: ≥0.15 mV in women, ≥0.2 mV in men ≥40, and ≥0.25 mV in men <40.)
Many conditions that mimic STEMI lead to false positives. An early repolarization pattern with up to 3-mm ST elevation in leads V 1–3 can be seen in some healthy individuals, typically in young men. Preexcitation, bundle branch block, pericarditis, pulmonary embolism, subarachnoid hemorrhage, metabolic disturbances (e.g., hyperkalemia and hypothermia), and left ventricular aneurysms can be associated with ST elevation in the absence of acute myocardial ischemia. On the other hand, some conditions can lead to false negatives, including prior MI, paced rhythm, and LBBB when acute ischemia is not recognized. These pitfalls are common, both in the real world and in large clinical trials.
“Nondiagnostic” ECGs are common in the setting of true acute MI, characterizing up to 8% of such patients, with nonspecific changes occurring in another third. These nondiagnostic ECG findings may be the result of occlusion of only small vessels or insensitivity of the 12-lead ECG to ischemia in the lateral or posterior myocardial territory. Supplemental leads, such as V 7–9 , can improve sensitivity. If ischemia is strongly suspected without ECG changes, serial ECGs or ECGs with additional leads should be performed to increase the sensitivity of MI detection relative to single ECGs.
ST-segment depression on an ECG identifies patients with ACS at high risk, as this is associated with the severity of coronary artery disease (CAD). T-wave changes can also be prognostic. Patients presenting to the emergency department with ACS and isolated T-wave changes have a lower risk for adverse outcomes than those with ST depression but are at higher risk than those with a normal ECG. In asymptomatic patients, most T-wave changes are nonspecific. However, in the intensive care unit (ICU), some patterns are strongly associated with myocardial ischemia. Marked symmetric precordial T-wave inversions ≥2 mm suggest acute ischemia, usually the result of a critical stenosis of the left anterior descending artery.
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