28 Biochemical or Electrocardiographic Evidence of Acute Myocardial Injury
The identification of myocardial injury is an important problem in the critical care setting. The development of more sensitive serologic techniques, while allowing the clinician to detect smaller amounts of myocardial necrosis, can pose 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 was organized to formulate a universal definition of myocardial infarction, and what emerged from the collaboration was a clinical classification of different types of myocardial infarction (Table 28-1).1 Of the five types, the most pertinent in the critical care setting are type I (plaque rupture) and type II (demand ischemia leading to infarction). These definitions rely on both electrocardiographic and biochemical information.1 As previously, diagnosis of type I infarction requires a compatible clinical scenario and either biochemical or electrocardiographic evidence.
TABLE 28-1 Clinical Classification of Different Types of Myocardial Infarction
| Type 1 |
| Spontaneous myocardial infarction related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection |
| Type 2 |
| Myocardial infarction secondary to ischemia due to either increased oxygen demand or decreased supply (e.g., coronary artery spasm, coronary embolism, anemia, arrhythmias, hypertension, hypotension) |
| Type 3 |
| Sudden unexpected cardiac death including cardiac arrest, often with symptoms suggestive of myocardial ischemia, accompanied by presumably new ST elevation, new left bundle branch block, or evidence of fresh coronary thrombus by angiography or autopsy |
| Type 4a |
| Myocardial infarction associated with percutaneous coronary intervention |
| Type 4b |
| Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy |
| Type 5 |
| Myocardial infarction associated with coronary artery bypass grafting |
From Thygesen K, Alpert JS, White HD, et al. Universal definition of myocardial infarction. Circulation. 2007;116(22):2634-2653.
Electrocardiographic Evidence
Acute coronary syndromes are classified by the initial electrocardiogram (ECG), and patients are divided into three groups: those with ST-elevation myocardial infarction (STEMI), those without ST elevation but with enzyme evidence of myocardial damage (non–ST-elevation myocardial infarction, or NSTEMI), and those with unstable angina. Classification according to the presenting ECG coincides with current treatment strategies, since patients presenting with ST elevation benefit from immediate reperfusion. An ECG in patients with suspected acute coronary syndrome (ACS) should be obtained and interpreted within 10 minutes of presentation.2
Criteria for the diagnosis of STEMI include1–3:
A number of potential pitfalls can contribute to misinterpretation of the ECG. Many conditions can mimic STEMI and lead to false positives. An early repolarization pattern with ≤ 3 mm ST elevation in leads V1 to V3 can be seen in healthy individuals, usually young men. Preexcitation, bundle branch block, pericarditis, pulmonary embolism, subarachnoid hemorrhage, metabolic disturbances such as hyperkalemia, hypothermia, and left ventricular (LV) aneurysm 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 myocardial infarction (MI), paced rhythm, and LBBB when acute ischemia is not recognized. These pitfalls are common in the real world and in large clinical trials. For example, when ECGs from the GUSTO IIB trial were reviewed by expert readers at a core laboratory, 15% of patients with STEMI were found to have been misclassified as NSTEMI, and these patients had a 21% higher mortality rate.4
“Nondiagnostic” ECGs are common in the setting of acute MI. Up to 18% of patients subsequently determined to have MI have a normal ECG, and an additional 25% have nonspecific changes. These nondiagnostic ECG findings may be due to occlusion of small vessels only or to insensitivity of the 12-lead ECG to ischemia in the lateral or posterior LV territory. Visualization in the horizontal plane can be extended laterally and posteriorly by the addition of leads V7 to V9 and rightward by the addition of V4R and V5R. Systematic 15-lead ECG to include V4R, V8, and V9 has been suggested to increase the sensitivity of diagnosing ST elevation from 47% to 59% without decreasing specificity.5 In fact, an 80-lead body surface mapping system has been shown to increase sensitivity and specificity of ECG diagnosis of ischemia, but challenges with rapid application at the bedside remain.6 If ischemia is strongly suspected, but changes are not seen on standard leads, obtaining an ECG with additional leads should be considered.3
ST-segment depression on ECG identifies patients with ACS at high risk. In the TIMI risk score, which has been shown to predict the likelihood of death and ischemic events, ST-segment changes, along with advanced age and prior coronary artery disease, show the strongest association with severe epicardial disease.7
The significance of T-wave changes is directly related to the pretest probability of disease. Large studies in asymptomatic patients show that most T-wave changes are nonspecific. In the coronary care unit, however, 87% of patients with only T-wave inversions across the precordium will have a significant left anterior descending (LAD) coronary artery stenosis by angiography. Among patients presenting to the emergency department with ACS, those with isolated T-wave changes have lower risk than those with ST depression but higher risk than those with a normal ECG.8
Cardiac Biomarkers
With cardiac cell death, proteins are released into the blood, and detection of these proteins has played a key role in establishing the diagnosis of ACS, risk stratification, and prediction of outcome. Beginning early in the 1970s, creatine kinase (CK) and its isoenzyme, MB, became the biomarkers of choice to establish myocardial injury and infarction. The sensitivity of CK-MB for diagnosis of MI at 6 hours is 91%, but at 2 and 4 hours, sensitivity is only 21% and 46%.9 The poor performance of CK-MB early in the course of MI led to the continued search for biomarkers that could diagnose MI early. Myoglobin was a contender for just such a role, because serum levels increase earlier than CK-MB, but the degree to which early sensitivity is increased is uncertain, and myoglobin lacks specificity.10
These biomarkers have now been superseded by troponin T and I, parts of the troponin-tropomyosin complex in cardiac myocytes. Troponin elevations are highly specific for myocardial cellular injury, except for infrequent false positives due to fibrin interference or cross-reacting antibodies.11 Troponin is also much more sensitive than CK-MB because of its higher concentration in cardiac muscle; minor cardiac injury can elevate levels.11 Even small increases in circulating troponin values correlate with adverse outcomes in the short and long term.11 In non–ST-elevation ACS, elevated troponin levels not only predict increased risk but also identify the patients most likely to benefit from more aggressive antiplatelet strategies using IIb/IIIa inhibitors, use of low-molecular-weight heparin, and an early invasive strategy with coronary angiography and revascularization when appropriate.3
The challenge for the clinician, and in particular the intensivist, is that while elevation of serum troponin concentration is highly specific for myocardial cell damage, not all of that damage is a consequence of rupture of an atherosclerotic plaque. Other causes of elevated troponin, many of which are common in the intensive care unit (ICU), are listed in Table 28-2.
TABLE 28-2 Nonischemic Conditions Commonly Associated with Elevated Cardiac Troponin
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