ST elevation myocardial infarction electrocardiogram

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 * Associate Editors-In-Chief:

Overview
A primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad, symptomatic emergency department populations. The 12 lead ECG is used to classify patients into one of three groups: A normal ECG does not rule out the presence of acute myocardial infarction. Sometimes the earliest presentation of acute myocardial infarction is instead the presence of a hyperacute T wave. In clinical practice, hyperacute T waves are rarely seen, because they exists for only 2-30 minutes after the onset of infarction. Hyperacute T waves need to be distinguished from the peaked T waves associated with hyperkalemia.
 * Those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with thrombolytics or primary PCI),
 * Those with ST segment depression or T wave inversion (suspicious for ischemia), and
 * Those with a so-called non-diagnostic or normal ECG.

Definition of ST Elevation
The electrocardiographic definition of ST elevation MI requires the following: at least 1 mm (0.1 mV) of ST segment elevation in 2 or more anatomically contiguous leads. While these criteria are sensitive, they are not specific as thromboctic coronary occlusion is not the most common cause of ST segment elevation in chest pain patients.

Differential Diagnosis of Causes of ST Segment Elevation in the Absence of Myonecrosis
ST Segment Elevation Does Not Always Signify a Myocardial Infarction. ST segment elevation should alert the clinician to the possibility of myocardial injury, however, there are a variety of conditions that cause ST segment elevation which are not associated with myonecrosis. Indeed, over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation in at least one precordial lead. The clinician must therefore be well versed in recognizing the so-called ECG mimics of acute myocardial infarction, which include left ventricular hypertrophy, left bundle branch block, paced rhythm, benign early repolarization, pericarditis, hyperkalemia, and ventricular aneurysm.

Left bundle branch block and pacing can interfere with the electrocardiographic diagnosis of acute myocadial infarction. The GUSTO investigators Sgarbossa et al. developed a set of criteria for identifying acute myocardial infarction in the presence of left bundle branch block and paced rhythm. They include concordant ST segment elevation > 1 mm (0.1 mV), discordant ST segment elevation > 5 mm (0.5 mV), and concordant ST segment depression in the left precordial leads. The presence of reciprocal changes on the 12 lead ECG may help distinguish true acute myocardial infarction from the mimics of acute myocardial infarction. The contour of the ST segment may also be helpful, with a straight or upwardly convex (non-concave) ST segment favoring the diagnosis of acute myocardial infarction.

Acute epicardial artery occlusion by thrombus is certainly one cause of ST segment elevation, but other causes of ST segment elevation which are not associated with myonecrosis include the following: (listed in alphabetical order)


 * Aneurysm of the ventricle can result in persistent ST segment elevation that can be exacerbated with tachycardia.


 * Arrhythmogenic right ventricular cardiomyopathy


 * Balloon inflation in a coronary artery during percutaneous coronary intervention


 * Brugada syndrome


 * Transthoracic cardioversion


 * Coronary artery rupture during percutaneous coronary intervention


 * Early repolarization is a normal variant that can result in ST segment elevation. It is more common in males of younger age. The ST elevation is exacerbated by bradycardia.


 * Hyperkalemia known as the "dialyzable current of njury" hyperkalemia may cause hyperacute ECG changes due to changes in membrane polarity


 * Left bundle branch block is associated with ST segment elevation in those leads that are discordant to the QRS. Stated differently, if the QRS is predominantly of a negative deflection, it is normal to observe ST segment elevation in the same leads. The presence of ST elevation in leads where the QRS deflection is upright (concordance) may be a marker of myocardial injury.


 * Myopericarditis can cause injury to the subepicardial myocytes and ST segment elevation.


 * Myocarditis can cause injury to the subepicardial myocytes and ST segment elevation.


 * Pericardiocentesis when the needle comes into contact with the myocardium, there can be ST segment elevation reflecting local injury of the myocardium.


 * Pericarditis can cause injury to the subepicardial myocytes and ST elevation.


 * Pulmonary Embolism


 * Prinzmetal's angina is associated with ST segment elevation due to transient epicardial coronary artery spasm either in the absence or presence of atherosclerosis. If the condition persists long enough, myonecrosis can be observed.


 * Stroke Intracranial hemorrhage can in some cases cause ST segment elevation due to direct myocyte injury from a hyperadrenergic stimulation emanating from the central nervous system.

Differential Diagnosis of Causes of ST Segment Elevation in the Presence of Myonecrosis (STEMI)
While plaque rupture is the most common cause of ST segment elevation MI, other conditions can cause ST elevation and myocardial necrosis. In order to expeditiously treat an alternate underlying cause of myonecrosis, it is important to rapidly identify conditions other than plaque rupture that may also cause ST elevation and myonecrosis. Indeed, the management of some of these conditions might be differ substantially from that of plaque rupture: cocaine induced STEMI would not be treated with beta-blockers, and myocardial contusion would not be treated with an antithrombin. These conditions include the following:

Limitations of the 12 lead ECG
While clinicians are widely familar with the 12 lead ECG, there are limitations to its sensitivity and specificity in detecting myocardial injury due to thrombotic vessel occlusion. A single static ECG represents a brief sample in time. In STEMI, the culprit artery is often opening and closing or "winking and blinking" due to cyclic flow variations with the clot dissolving and reforming again. Furthermore, patients with acute coronary syndromes often have rapidly changing supply versus demand characteristics. As a clinical example, one of the authors (CM Gibson) once saw a patient with 6 hours of chest pain who had non-specific ECG changes. 15 minutes later the patient complained of worsening chest pain, and at that time the ECG showed ST elevation. Had the second ECG with ST elevation been instead the first ECG that was reviewed, it would have been concluded that the patient was infarcting for over 6 hours, when instead, the artery was occluded for 15 minutes at most during the recent episode of chest pain. Because a single ECG may not accurately represent evolving myocardial injury, it is standard practice to obtain serial 12 lead ECGs, particularly if the first ECG is obtained during a pain-free episode. Alternatively, many emergency departments and chest pain centers use computers capable of continuous ST segment monitoring. While the standard 12 lead ECG is well designed to detect anterior ischemia, by virtue of the fact that it samples only electrical vectors from the front left chest wall, the 12 lead ECG may miss right ventricular and posterior infarctions. In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG or ST segment depression in the anterior precordial leads. The use of non-standard ECG leads like right-sided lead V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. Newer technologies such as the 80 lead ECG have demonstrated greater sensitivity in detecting RV and posterior infarcts compared with the 12 lead ECG. The failure to identify patients with ST elevation MI delays care and has a negative effect on the quality of patient care.

Localization of the Culprit Artery Based Upon the 12 lead ECG
While the ECG leads that are involved with ST elevation and depression are often used to predict the potential location of the culprit artery, teh sensitivity and specificity of these techniques are often poor. New technologies such as 80 lead ECGs may prove to be more useful in this regard. Identification of the potential culprit artery can be important in guiding patient management. In particular, the ECG should be used to identify patients with a right ventricular infarct where nitrate administration is contraindicated. The 12 lead ECG can also be used to identify the most appropriate artery to perform angiography on first when performing primary angioplasty.



Evolution of ST Segment Elevation
As the myocardial infarction evolves, there may be loss of R wave height and development of pathological Q waves. T wave inversion may persist for months or even permanently following acute myocardial infarction. Typically, however, the T wave recovers, leaving a pathological Q wave as the only remaining evidence that an acute myocardial infarction has occurred. Understanding the typical time course of ST changes in acute MI is critical in distinguishing STEMI from pericarditis and other conditions.

Measurement of the Magnitude of ST Elevation: 60 Milliseconds after the J point
The optimal time after the J point to measure ST elevation is debated. This example shows the technique of measuring the magnitude of ST elevation 60 milliseconds or 1.5 small boxes after the J point.



Distinguishing Early Repolarization and Other Normal Variants from Pathologic ST Elevation
Early repolarization is an electrocardiographic pattern that can mimic the changes of ST elevation myocardial infarction. It is often seen in younger males. As the example below shows, there is often a notch (shown in red) where the QRS and ST segments join.