Coronary Anatomy, Ischemic Heart Disease & Wall-Motion Abnormalities

Coronary Artery Anatomy and Perfusion Territories

The left ventricle is perfused by three major epicardial arteries, all originating from the aortic root just above the sinuses of Valsalva. The left main coronary artery (LMCA) arises from the left coronary sinus and travels a short course before bifurcating into the left anterior descending (LAD) and left circumflex (LCx) arteries (a ramus intermedius branch is present in roughly a third of patients). The right coronary artery (RCA) arises separately from the right coronary sinus.

• LAD — travels the anterior interventricular groove, giving off septal perforator branches (supplying the anterior two-thirds of the interventricular septum) and diagonal branches (supplying the anterolateral wall). The LAD territory covers the anterior wall, anteroseptal wall, and typically wraps around to supply the apex.
• LCx — travels the left atrioventricular groove, giving off obtuse marginal (OM) branches. It supplies the lateral wall, and in a left-dominant circulation also supplies the posterior wall.
• RCA — travels the right atrioventricular groove, giving off acute marginal branches to the right ventricular free wall. In the roughly 85% of hearts that are right-dominant, the RCA terminates as the posterior descending artery (PDA), supplying the inferior wall, inferoseptal wall, and posteromedial papillary muscle. Coronary dominance is defined strictly by which artery gives rise to the PDA (right-dominant approximately 85%, left-dominant approximately 8%, codominant approximately 7%).

Because a single vessel typically feeds a contiguous group of segments, an acute occlusion produces a regional, not global, contraction abnormality that respects a coronary distribution. This is the physiologic basis for using echocardiography as a rapid, bedside ischemia detector, often positive before ECG changes or biomarker elevation. Older reports sometimes label the basal-to-mid inferolateral wall as the "posterior wall" — current ASE nomenclature retires that term in favor of inferolateral, since true isolated posterior-wall segments do not exist in the 17-segment model.

Ischemia, Infarction, Stunning, and Hibernation

• Ischemia — an acute oxygen supply and demand mismatch; contraction fails within seconds of flow interruption, well before cell death, and is fully reversible if flow is restored promptly.
• Infarction — irreversible myocyte necrosis following sufficiently prolonged severe ischemia.
• Myocardial stunning — transient post-ischemic contractile dysfunction that persists despite restoration of normal, or near-normal, resting coronary flow; resolves spontaneously over hours to days without any intervention.
• Hibernation — chronic contractile dysfunction driven by persistently reduced resting flow, or by repetitive stunning; the myocardium is alive but down-regulates function to match reduced supply, and can recover contractile function if revascularized (assessed with dobutamine stress echo, section 9.2).

Distinguishing these four states matters clinically: a stunned or hibernating segment is a target for medical optimization or revascularization, while a truly infarcted, scarred segment will not regain function regardless of intervention.

The 17-Segment Model and Wall-Motion Scoring

ASE's standardized left ventricular model divides the ventricle into 17 segments: 6 basal, 6 mid-cavity, 4 apical, and 1 apical cap. Each segment is assigned to a dominant coronary territory, although the apex is a watershed zone that can be supplied by any of the three vessels depending on individual anatomy — a "wrap-around" LAD supplies the apex and part of the inferior wall in some patients, which can blur territory-based localization at the apex specifically.

Each segment is graded on endocardial excursion and myocardial thickening using a 4-point scale:

The wall-motion score index (WMSI) is the sum of all individual segment scores divided by the number of segments scored:

WMSI = (sum of segment scores) divided by (number of segments assessed)

A fully normal study yields a WMSI of 1.0 (17 divided by 17); any value above 1.0 reflects regional dysfunction, and the magnitude correlates with infarct size, ejection fraction, and prognosis. A higher WMSI at presentation, and at hospital discharge, predicts worse long-term outcomes after myocardial infarction, independent of the overall ejection fraction.

Territory Correlation

Recognizing and Reporting RWMA

When scanning for ischemia, compare each segment to its neighbors and to the opposite wall — for example, septum versus lateral wall. Dysfunction confined to a single coronary distribution favors an ischemic cause, whereas diffuse, non-territorial hypokinesis favors a non-ischemic cardiomyopathy instead. Because RWMA extent approximates infarct size, WMSI is also used clinically to estimate global ejection fraction when endocardial border definition limits volumetric Simpson measurement. Sonographers should always report the number and location of abnormal segments, not just an overall ejection fraction, since regional detail changes clinical management, such as localizing a likely culprit vessel before diagnostic catheterization or planning revascularization strategy with the referring cardiologist.