Echocardiography in Patients with Myocardial Infarction

Wall Motion and Electrocardiographic Infarct Location

ECG changes do not always correlate with the quantity of damaged myocardium, and the extent of the dysfunction often is considerably greater than expected relative to the size of the necrotic area, because it encompasses not only the zone of the actual infarct but also stunned and hibernating segments and dysfunction from previous coronary events. Consequently, echocardiography is a better predictor of the extent and location of the MI and associated ventricular dysfunction than the ECG. This observation is especially true in inferior MI, because the septum is not assessed well by electrocardiographic modalities. When an anterior MI is identified on the ECG, at least one of the anterior segments will exhibit RWMA on echocardiography, with the extent of the dysfunction being determined by the level at which the obstruction occurs in the left anterior descending coronary artery. If the obstruction is located proximal to the first septal perforator, all of the segments of the anterior septum, the anterior wall, and the apex will be affected, whereas obstruction distal to the first septal perforator usually spares the basal segments of the anterior septum and anterior wall. The sensitivity and specificity of the 12-lead ECG for the detection of an apical MI are low despite meeting several well-characterized ECG criteria, whereas apical involvement is clearly identified and quantified by echocardiography. The presence of Q waves is associated with a larger area and more severe degree of apical dysfunction, and persistent ST-segment elevation may be associated with a left ventricular aneurysm on the echocardiogram.

Echocardiography and Coronary Anatomy

Using correlative studies with coronary angiography and echocardiography in patients with acute MI, the specific coronary artery perfusing each segment of the left ventricle was determined ( Figure 31-2 ).

The early stage of a nonrevascularized acute MI is characterized on echocardiography by decreased amplitude of regional endocardial excursion with normal wall thickness, followed in 4 to 6 weeks by wall thinning in the affected region and often increased echogenicity secondary to a fibrotic response. Studies have found good correlation between histologic evidence of infarction and the presence of segmental dysfunction on echocardiography in more than 90% of cases. Experimentally, necrosis of 20% or less of the wall thickness results in a decrease in systolic thickening of approximately 50%, whereas necrosis of more than 20% of the thickness is uniformly associated with systolic thinning, with the extent of RWMAs shown by echocardiography shortly after coronary occlusion (up to 2 days) correlating well with actual infarct size. Echocardiography can overestimate infarct size, however, because of contractile abnormalities (“tethering”) in the noninfarcted myocardium immediately adjacent to the severely ischemic regions. Accordingly, transthoracic imaging (i.e., transthoracic echocardiography [TTE]) can identify the location and extent of myocardial infarction ( Video 31-1, Video 31-2, Video 31-3, Video 31-4, Video 31-5 ).

Echocardiography After Reperfusion Therapy

Restoration of antegrade flow after pharmacologic or mechanical reperfusion usually is associated with improved wall motion, fewer complications, and decreased mortality. The extent of functional recovery is related to the duration of the occlusion, the extent of the ischemic zone, and the success of reperfusion. Recovery usually occurs 24 hours to 10 days after reperfusion but may take up to 6 weeks if stunning is present (see Chapter 4 and Chapter 32 ). The stunned myocardium has had, by definition, flow restored (by angioplasty or thrombolysis or spontaneously) yet remains temporarily dysfunctional. Echocardiography combined with low-dose inotropic stimulation with dobutamine (5 to 10 μg/kg/min) can be used to distinguish stunned myocardium after revascularization from nonviable myocardium (see Stress Echocardiography ). Patency of the infarct-related coronary artery, as seen within days of the acute MI, has been associated with an improvement in regional function and attenuation of left ventricular dilation 1 to 6 months after the initial event; by contrast, adverse remodeling of the left ventricular wall will continue to increase in patients without successful reperfusion.

Angiographic restoration of flow in an epicardial artery does not accurately reflect perfusion at the microvascular level. The lack of myocardial reperfusion despite restored epicardial flow is referred to as the “no-reflow” phenomenon (see Chapter 24 ). Adequacy of myocardial blood flow after either pharmacologic or mechanical revascularization can be assessed using contrast echocardiography of the myocardium, in addition to the classic clinical and ECG parameters. Myocardial contrast techniques have shown good correlation with angiographic methods of assessing microvascular reperfusion in patients with acute MI, such as the corrected Thrombolysis In Myocardial Infarction (TIMI) frame count (cTFC), TIMI myocardial perfusion grade (TMPG), and TIMI myocardial blush grade.

Evaluation of Systolic Left Ventricular Function

A reduced left ventricular ejection fraction (LVEF) after MI is a strong predictor of poor outcome. An immediate decline in left ventricular systolic function may be observed with onset of necrosis, but further adverse remodeling of the left ventricle due to infarct expansion also can occur (see Chapter 4 and Chapter 36 ). Such remodeling is characterized by the enlargement of the primary hypokinetic/akinetic zone and left ventricular dilation, potentially leading to the development of heart failure. Initially enlarged left ventricular volumes are suggestive of extensive myocardial injury, but sequential echocardiograms may be required for detection of adverse left ventricular remodeling; left ventricular systolic function also can improve over time after a reperfused MI. In patients with at least moderate ventricular dysfunction early after MI, reevaluation of LVEF approximately 40 days later is needed to determine whether implantation of a cardiac defibrillator is warranted (see Chapter 28 ).

Qualitative and Semiquantitative Evaluation of Left Ventricular Systolic Function

Global and regional ventricular function can be evaluated with echocardiography. A few seconds after coronary occlusion, decreases in the amplitude of endocardial excursion and wall thickening become apparent in the area supplied by the obstructed artery; the abnormality is defined as hypokinesis when contraction normally is directed but reduced in magnitude, akinesis when it is absent, or dyskinesis when systolic bulging is present.

Wall Motion Score Index

Semiquantitative assessment of regional left ventricular contraction is provided by the wall motion score index (WMSI). The American Heart Association (AHA), as part of an effort to unify wall motion analysis among various imaging modalities, recommended a 17-segment model when perfusion is assessed, but the 16-segment model ( Figure 31-2 ) remains clinically recommended for functional imaging, because the apical cap does not contract. The various echocardiographic views permit visualization of regions of the myocardium perfused by the different coronary artery branches ( Figure 31-3 ). Professional society recommendations suggest that a score be assigned to each segment according to its contractility, as follows: (1) normal or hyperkinetic, (2) hypokinetic, (3) akinetic (absent or negligible thickening), and (4) dyskinetic (systolic thinning or stretching, e.g., aneurysm). In contrast with previous recommendations, clinicians should refrain from assigning a separate wall motion score for aneurysm; furthermore, no specific score has been designated for compensatory hyperkinesis. The WMSI is equal to the sum of the regional scores divided by the number of evaluable segments and can range between 1 (for normal ventricular contraction) and 3.9 (for severe systolic dysfunction) ( Figure 31-4 ). A good correlation exists between the echocardiographic WMSI and the LVEF measured by radionuclide ventriculography. A WMSI of 1.7 or higher usually suggests dysfunction involving greater than 20% of the left ventricle after acute MI. In addition, the WMSI has important prognostic value, with a significantly higher mortality rate in the group with the most abnormal score than in patients with favorable ones (61% versus 3%).

Because CAD causes segmental dysfunction, which can be accompanied by compensatory hyperkinesis of nonischemic segments, regional assessment of systolic function is more sensitive than global approaches. Nevertheless, determination of the LVEF is part of a standard examination. The correlation between the visual echocardiographic estimation and the radionuclide determination of LVEF is good, but visual assessment requires experience, and clinicians should validate their own performance with quantitative methods.