The myocardium has its own independent blood supply and drainage (Fig. 4.1). Two coronary arteries originate from the aortic root: The left main coronary artery from the left coronary sinus, and the right coronary artery (RCA) from the right coronary sinus, both adjacent to the respective left or right cusp of the aortic valve.

The left main coronary artery bifurcates at around 10 mm from its origin into the left anterior descending (LAD) and the left circumflex (LCX) coronary arteries. The LAD runs along the anterior interventricular sulcus passing the ventricular apex to reach the posterior interventricular sulcus. On its way to the apex, it gives rise to the diagonal branches and septal arteries. It thereby supplies the left ventricular (LV) anterior wall, the apex, and the anterior part of the interventricular septum.

The LCX runs along the left atrioventricular sulcus and gives rise to a large marginal branch and the posterolateral branches supplying the lateral wall. In patients with left-dominant coronary distribution, the distal LCX extends as a posterolateral branch to supply part of the inferior LV wall.

The RCA runs along the right atrioventricular sulcus, where its middle section gives off the right ventricular (RV) acute marginal branches. These acute marginal branches supply the RV free wall and the conduction system including the sinus and atrioventricular node. The RCA bifurcates into the posterior descending artery and the right posterolateral branch. Their supply territory is the inferolateral RV wall, the inferior part of the interventricular septum, and the inferior wall of the LV.

There are three major variations of coronary distribution. These distribution types affect the posterior descending artery and posterolateral branch which supply the inferior septum and inferior wall of the LV
(Figs. 4.1, 4.2, 4.3, 4.5). The right-dominant coronary distribution type is the most common (80% to 85%), where supply originates from the RCA. In left-dominant systems supply is via the LCX artery. A balanced or codominant type is present in about 5% of individuals, where the posterior descending artery and the posterolateral branch receive supply from both the RCA and from the LCX. Recent imaging studies, however, have altered traditional concepts of coronary perfusion zones as well as reveal the significant individual variation in coronary supply to the myocardial segments. For example, the apical segments are now understood in the majority of cases to be supplied by the LAD with the LCX and RCA seen in a minority of individuals.
The greatest overlap in coronary artery distribution occurs in the inferolateral region corresponding either to RCA or LCX territories, as well as the inferoseptal region that may be supplied by the LAD artery, RCA, or even a left-dominant LCX artery. Figure 4.2 incorporates these recent findings and emphasizes the large amount of myocardium supplied by the LAD artery and potential for substantial infarct size with LAD occlusion (1). The coronary distribution can be defined by cardiac catheterization and this information is valuable when communicating regional wall contraction abnormalities (RWCAs) to the surgeon.

Although echocardiographic diagnosis of coronary artery stenosis is not a daily practice, it can be clinically valuable for assessing proximal vessel disease when coronary angiography is not practical (i.e., during emergent cardiac surgery) (5,10). Indicators are increased echo density, suggesting calcification of the vascular
intima, and velocity acceleration with turbulent color Doppler flow signals. The following velocities have been published as threshold for hemodynamically relevant stenosis (>50%): left main coronary artery >140 cm/s, LAD >90 cm/s, LCX >110 cm/s (11). The percentage reduction in vessel diameter or increase in diastolic velocity-time integral at the site of stenosis compared to the normal segment proximal to the stenosis correlates well with the degree of stenosis diagnosed by coronary angiography.

The echocardiographer must be aware of the various presentations of ischemic tissue, including myocardial stunning and hibernation, which complicate the echocardiographic assessment of myocardial viability. Acute ischemia results from severe reductions in coronary blood flow and is associated with reductions in wall thickening and endocardial inward motion (14). Stunned myocardium occurs following an acute episode of ischemia when a potentially reversible RWCA transiently persists despite full restoration of blood flow. Hibernation is a chronic ischemic condition where RWCAs persist in viable myocardium with marginal resting blood flow. LV function may improve markedly and mortality may be reduced following successful coronary revascularization. The time course of recovery is variable.

The echocardiographic appearance of stunning and hibernation during resting conditions is similar to acutely ischemic myocardium (Table 4.1) (23,24). Echocardiography and other imaging techniques can be used in combination with clinical algorithms for differentiation of myocardial ischemia, hibernation, stunning, and nonviable infarcted tissue (25,26). Dobutamine stress echocardiography is used for the detection of viable hibernating myocardium. Viable myocardium shows improved regional contractile function (inotropic reserve) in response to low dose dobutamine administration. For patients with ischemic heart disease, dobutamine stress echocardiography predicts the likelihood of LV functional recovery following revascularization. In addition, in patients with LV dysfunction, caused by myocardial infarction, dobutamine stress echocardiography is useful for evaluating the presence of hibernating myocardium due to a residual stenosis that warrants intervention. Patients with LV dysfunction who demonstrate myocardial viability with dobutamine stress echocardiography have a better survival with revascularization than with medical therapy (27). A key message is that an RWCA is not always caused by acute ischemia but may reflect stunning, hibernation, and/or nonviable infarcted tissue.

The 17-segment model of LV topographical anatomy (Fig. 4.2) (30) provides a common nomenclature across imaging specialties to define the LV segmental anatomy. Using the 17-segment model in the setting of perioperative TEE has the advantage of applying the same topographical concept for describing regional function
of the LV as in transthoracic echocardiography, cardiovascular magnetic resonance imaging, nuclear cardiology, and cardiac computed tomography (30). It also serves as the basis for correlating the location of RWCAs with coronary perfusion.

The 17-segment model divides the LV along its longitudinal axis into three levels plus the apical cap (Fig. 4.2). The basal and mid (midpapillary) levels are subdivided into six segments: the anteroseptal, anterior, anterolateral, inferolateral (formerly “posterior”), inferior, and inferoseptal segments. The apical level is subdivided into anterior, lateral, inferior, and septal segments.

The three standard ME views (31) (ME four chamber, ME two chamber, and ME long axis) (Figs. 4.3, 4.4, 4.5) together allow visualization of all 17 segments. Although all the three views theoretically visualize the distant apical slice (segment 17), often the echo imaging plane transects the ventricle above the true apex and the TEE image is “foreshortened.” X-plane or multiplane mode may be useful for detecting foreshortening. To obtain correct alignment of the imaging plane along the long axis of the LV, the echocardiographer should focus on obtaining the maximum long-axis dimension in each view. A reliable indicator of a “true” long axis is the lack of movement of the apical epicardium toward the TEE probe during systole. The reason is that the entire LV moves into an apical direction during systole with little displacement of the apex (32). Favorable settings include a low ultrasound frequency (usually no higher than 6 MHz), because the apex is in the far field of the TEE image; a focal zone placed in the area of the apex; and optimized gain settings in that field.

The transgastric (TG) short-axis views (basal, mid, and apical) allow visualizing of 16 segments excluding the apical cap. The TG basal and midpapillary short-axis views each show the entire radius of six segments and are unique in that myocardial territories perfused by all the three main coronary arteries are visualized (Fig. 4.2). Although ischemia monitoring in TG midpapillary short-axis view is popular, using this view alone is inadequate, because ischemia caused by stenosis in an artery more distal to this plane will be missed. Repeated assessment of multiple views is essential as limiting the examination to the TG midpapillary SAX view alone will miss the majority of RWCAs (33). We advise comprehensive monitoring of all the 17 segments for ischemia utilizing both ME and TG imaging planes.

The coronary perfusion to the 17 LV segments is shown in Figures 4.2, 4.3, 4.4, 4.5. Many segments have a consistent coronary artery perfusion. Recent imaging studies, however, have altered traditional concepts of coronary perfusion zones as well as reveal the significant individual variation in coronary supply to the myocardial segments. For example, the apical segments are now understood in the majority of cases to be supplied by the LAD with the LCX and RCA seen in a minority of individuals. The greatest overlap in coronary artery distribution occurs in the inferolateral region corresponding either to RCA or LCX territories, as well as the inferoseptal region that may be supplied by the LAD artery, RCA, or even a left-dominant LCX artery. Figure 4.2 incorporates these recent findings and emphasizes the large amount of myocardium supplied by the LAD artery and potential for substantial infarct size with LAD occlusion (1). In those segments with physiologic variability in coronary supply, the culprit coronary artery of an RWCA can often be identified by examining neighboring segments whose coronary supply is known. For example, the combination of ischemia in the anterolateral and inferolateral walls is consistent with a left-dominant or codominant LCX occlusive disease while the presence of anterolateral ischemia without inferolateral wall ischemia is specific for a nondominant LCX occlusion.