Abstract
This chapter introduces the findings and utility of echocardiography in managing acute myocardial infarction (MI). This includes establishing the diagnosis, recognizing patterns of dysfunction visualized during MI, and recognizing urgent consequences that may occur acutely during an MI.
Keywords
acute MI, coronary artery disease, echocardiography, myocardial infarction, wall motion abnormalities
Introduction
Acute myocardial infarction (MI), the classic “heart attack,” is caused by the sudden loss of blood flow and oxygenation to the heart muscle due to complete occlusion of a coronary artery. The risk factors, clinical presentation, and serial changes in electrocardiogram (ECG) and serologic markers as myocardium is damaged are well known. For the physician and technologist, echocardiography often plays a critical role in the early diagnosis and management of the patient, but it should be used judiciously.
In the setting of suspected acute MI, echocardiography is appropriate to evaluate (1) a patient with acute chest pain, with suspected MI but a nondiagnostic ECG (particularly if the scan can be performed during pain), (2) a patient who has had recent chest pain and other features or laboratory markers indicative of ongoing myocardial infarction who is currently chest pain–free, and (3) to evaluate for a suspected complication of MI such as myocardial or valve disruption, right or left heart failure, or tamponade (see Chapter 19 ). Importantly, when a patient’s symptoms and ECG are clearly indicative of an ongoing acute MI, there is no need to obtain an echo in the acute setting, when the focus should be on progression towards definitive therapy (i.e., opening the coronary artery). Atypical symptoms, as may occur in women, those with diabetes, or the elderly, may benefit from an echocardiogram early on when there is sufficient suspicion. The following section addresses considerations in imaging a patient in the setting of acute MI (0–48 hours after presentation), focusing primarily on diagnosis, ventricular function, and recognition of critical complications.
Establishing the Diagnosis, Extent, and Location of Myocardial Infarction
When a coronary artery is occluded, echocardiography will demonstrate changes in the left ventricular (LV) myocardial wall motion within 30 seconds, even before chest pain or ECG changes occur. Instead of a normokinetic area, myocardium that is starved of oxygen will thicken to a lesser degree and become hypokinetic.
There are five degrees of myocardial wall motion ( Table 18.1 ): normokinesis, hyperkinesis, hypokinesis, akinesis , and dyskinesis . Normokinetic motion is the systolic thickening of the ventricular wall, usually increasing by at least 30%–50% due to shortening of the myocardial cells that are arranged in concentric spirally oriented layers around the barrel and apex of the left ventricle. 
show normal parasternal long and short-axis views of the left ventricle with normokinesis of all segments. Hyperkinesis (unusually brisk or exaggerated thickening) is seen when the left ventricle is adapting overall to increased demand, such as in exercise, stress, or hyperadrenergic states. In cases where there is recent focal LV dysfunction, the remaining uninjured myocardial segments may become hyperkinetic as a compensatory mechanism for maintaining overall stroke volume and cardiac output.
| Wall Motion Type | Thickening | Tissue | Wall Motion Score (ASE MODEL) |
|---|---|---|---|
| Hyperkinetic | >50% | Compensatory/hyperadrenergic state | — |
| Normokinetic | 30%–50% | Normal perfusion and function | 1 |
| Hypokinetic | <30% | Ischemic or nontransmural infarct | 2 |
| Akinetic | None | Transmural infarct (or stunned or hibernating) | 3 |
| Dyskinetic | Bulges outwards (paradoxically) | Infarcted and fibrosed | 4 |
| Aneurysmal | Thinned and bulges outwards | Extensive infarct/fibrosed area | 5 |
show examples of these varying degrees of kinesis. The latter three types of wall motion, hypokinesis, akinesis, and dyskinesis (see 
respectively), are indicative of dysfunctional myocardium and hence termed “wall motion abnormalities (WMA).” Hypokinetic segments thicken less than 30% in systole and indicate dysfunctional myocardium. Akinetic segments do not thicken at all. Dyskinetic segments actually bulge away from the LV center in systole. If there is a large area of both myocardial thinning (<6 mm in thickness) and dyskinesis, this implies that there is an extensive fibrotic scar that has replaced functioning myocardium, and these areas are deemed aneurysmal (see 
). The most severe degrees of dysfunction (akinesis and dyskinesis) occur with prolonged injury, as ischemic myocardium can no longer contract, die, and become replaced by fibrocytes. Oftentimes, the presence of preserved remaining normo- or hyperkinetic myocardium surrounding a discrete wall motion abnormality can create hinge points , which better delineate the poorly contractile segments (see 
).
There are various classification schemes assigning numerical values to these types of segmental WMAs, with 1 representing normal or hyperkinetic segments and 5 representing the most dysfunctional aneurysmal segments. The sum of these scores for a 17-segment model will give a quantitative assessment of overall LV systolic function.
Importantly, the degree of kinesis is primarily an indicator of full-thickness myocardial contractility at the indicator segment. Taken without clinical context, a hypo- or akinetic segment may indicate any state along the spectrum that includes acute ischemia, subendocardial or subepicardial injury, stunned myocardium (i.e., reperfused but still not fully functioning cells), and hibernating (chronically underperfused, barely metabolically active but still viable) myocardium to completed transmural infarct. Additional techniques and agents may be required to distinguish among these states (see Chapters 12 , 27 ). Myocardial dysfunction due to other causes than hypoxia may also cause WMA.
As a caveat, there is a “fake-out” wall motion abnormality termed “pseudodyskinesis.” This is the apparent systolic paradoxical bulging of the entire inferior ventricular wall in systole, best seen on short-axis windows, which can be misinterpreted to be true dyskinesis ( 
). In fact, slowing the playback speed of the loop to carefully inspect the actual thickening between the epicardium and endocardium will reveal that the inferior wall is flattened (distorting the normal circular cross-sectional shape of the left ventricle) in diastole by external compression from the abdominal organs. In systole, it assumes the usual circular profile and hence gives the appearance that the wall is bulging radially outwards in systole. Pseudodyskinesis is frequently observed in patients with liver failure and ascites.
The coronary artery that is occluded will dictate which ventricular segments have abnormal function. For reference, the normal coronary tree as it relates to the entire heart, particularly the left ventricle, is shown by 3D computed tomography (CT) angiography in Fig. 18.1 , with the corresponding 360-degree view in 
.
