Echocardiography in Acute Coronary Syndrome
Eyal Herzog
Dan Halpern
Farooq A. Chaudhry
The last few decades have witnessed remarkable progress in the understanding of the pathophysiology of acute coronary syndrome (ACS). This, in turn, has led to advances in various imaging techniques for diagnosis and therapeutic options. Developments in the field of echocardiography have paralleled the progress made in ACS. The initial use of echocardiography was to detect pericardial effusions and cardiac tumors. However, the current applications of various forms of echocardiography include an extended list of pathologic and therapeutic indications. Advances in echocardiographic techniques and instrumentation have rivaled those in management of ACS.1 This chapter focuses on the role of echocardiography in ACS.
ASSESSMENT OF REGIONAL SYSTOLIC FUNCTION IN ACUTE CORONARY SYNDROME
Occlusion of an epicardial coronary artery at the time of ACS may lead to a loss of contractile function in the myocardial segments subtended by that vessel. The magnitude and duration of wall motion abnormalities depend on the severity, extent, and duration of the coronary occlusion.
In unstable angina (UA), left and right ventricular wall motion maybe normal unless transthoracic echocardiography happens to be performed during an episode of chest pain.
Non-ST-elevation myocardial infarction (NSTEMI) usually results from an occlusion of a coronary branch vessel often in an elderly patient with preexisting collateral coronary circulation. Typically the loss of contractile function is restricted to the subendocardial layer that is most vulnerable to ischemia. However, on standard echocardiography, the contractility loss may be observed in the entire thickness of the affected myocardial segment. This overestimation of contractile loss is attributed to tethering (an apparent passive loss of contractility in normal segments owing to contractile loss in an adjacent area).
ST-elevation myocardial infarction (STEMI) often results from an acute occlusion of a major coronary vessel and tends to occur in a younger age group compared with NSTEMI. If the total session of coronary flow lasts for >3 to 6 hours, myocardial necrosis will occur and the myocardium in the affected segments will be replaced with a fibrous tissue over the ensuing weeks.2
The magnitude of regional contractile loss in ACS is usually assessed semi-quantitatively. It is usually interpreted clinically as follows2:
Interpretation of wall motion abnormalities:
Normal
Contractility preserved
Hypokinesis
Partial loss of contractility
Akinesis
Complete loss of contractility
Dyskinesis
Paradoxical movement of the affected segment away from the center of the ventricle during systole
Aneurysmal
Outward movement of the affected segment during both systole and diastole
Extent and location of affected segments
Suspected coronary artery distribution (left anterior descending artery vs. right coronary artery vs. left circumflex artery).
ASSESSMENT OF GLOBAL SYSTOLIC FUNCTION IN ACUTE CORONARY SYNDROME
Global ventricular systolic function in ACS is assessed through either wall motion scoring and global ventricular ejection fraction.
WALL MOTION SCORING
Wall motion scoring analysis assigns a numeric value to the degree of contractile dysfunction in each segment. Most common scoring criteria are seen in Table 5.1.
Once all segments are assigned individual scores, total score is calculated as a sum of individual scores. A wall motion score index (WMSI) in then calculated as a ratio between the total score over the number of evaluated segments. The WMSI is a dimensionless index.
For a fully visualized normal ventricle the total score is 17 (all segments have normal contractility). Because all 17 segments are evaluated, the WMSI of a normal heart is 17/17 = 1. For abnormal ventricles, the higher the WMSI, the more significant is the abnormal wall motion.
TABLE 5.1 Left Ventricular Wall Motion Scoring | |||||||||||||||
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ASSESSMENT OF VENTRICULAR EJECTION FRACTION
Numerous studies have consistently shown left ventricular ejection fraction (LVEF) as one of the most powerful predictors of future mortality and morbidity in patients with heart disease.3 LVEF is the single most powerful predictor of mortality and the risk for developing life-threatening ventricular arrhythmias after myocardial infarction.4 Furthermore, once the ACS resolves, the residual LVEF is important for treatment options as LVEF cutoff values are built into recommendations for both medical and electrical device therapies. Even with treatment and clinical stabilization of heart failure, there is an inverse, almost linear, relationship between LVEF and survival in the patient whose LVEF is <45% (Figure 5.1).5
By definition, LVEF is the percentage of the end-diastolic volume that is ejected with each systole as the stroke volume. Thus, to calculate the LVEF one needs to estimate the end-systolic and end-diastolic volume of the left ventricle.
For two-dimensional echocardiography, biplane Simpson’s rule is routinely used for estimation of LVEF.6,7 Most modern ultrasound systems provide a semiautomated software package for the Simpson’s rule analysis. Operators are usually required to trace only the left ventricular endocardial border at end-diastolic and end-systolic in the apical four-chamber and two-chamber views; the software package then automatically calculates the left ventricular end-diastolic volume, end-systolic volume, and LVEF (Figure 5.2).
With the advent of real-time three-dimensional (RT3D) transthoracic techniques, left ventricular volumes and LVEF can now be calculated with greater accuracy than is possible with the biplane Simpson’s rule (Figure 5.3). RT3D-derived left ventricular volume data are now comparable to those obtained by cardiac magnetic resonance imaging, the prior gold standard for such calculations.7
Thus, whenever available, left ventricular volumes and LVEF in ACS should be calculated from an RT3D system. The biplane Simpson’s rule should be the next best method for such calculations when only a two-dimensional ultrasound system is available.
THE ISCHEMIC CASCADE
The ischemic cascade refers to a sequence of events that occurs in the myocardium after the onset of ischemia.8 Myocardial perfusion is determined by coronary blood flow and myocardial oxygen consumption. Any imbalance in this supply and demand relationship results in myocardial ischemia.9 The mechanical, electrographic, and clinical events that follow the development of ischemia were formally described in 1985 by Hauser et al.,10
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