15.3 Ischemic Heart Disease, Coronary Territories, Stress Response, and Complications
Key Takeaways
- Ischemia is identified by new or worsening regional thickening and excursion during adequate stress, confirmed side-by-side in matched orthogonal views.
- Standard coronary maps are probabilistic because dominance, branch anatomy, grafts, collaterals, and multivessel disease create overlapping segmental territories.
- Stress interpretation includes workload or dose, achieved heart rate, blood pressure, symptoms, ECG, global response, image timing, enhancing-agent use, and explicit adequacy limitations.
- Acute MR, septal or free-wall rupture, tamponade, aneurysm or pseudoaneurysm, thrombus, RV infarction, and ventricular deterioration require systematic assessment and urgent communication when critical.
Map regional function before assigning a vessel
Ischemia reduces systolic wall thickening and inward endocardial excursion before a global EF change is required. At rest, assess all 17 LV segments from parasternal long- and short-axis and apical four-, two-, and long-axis views. Grade each segment as normal or hyperkinetic, hypokinetic, akinetic, dyskinetic, or aneurysmal, and confirm an abnormality in more than one plane. Motion without thickening may reflect translation or tethering rather than contraction. Compare prior studies and the ECG, but do not force a territorial diagnosis from one poorly seen segment.
Typical maps associate anterior and anteroseptal regions and much of the apex with the LAD; inferolateral regions with the circumflex; and inferior regions with the RCA. These are teaching patterns, not fixed anatomy. Coronary dominance, a wraparound LAD, branch size, collaterals, prior bypass grafts, and individual variation create overlap. Basal and mid inferoseptal segments may be supplied by the RCA or LAD, while inferolateral segments may be RCA or circumflex. Multivessel or left-main disease can produce diffuse or multiterritory change. Describe the observed segments first, then state the likely territory with appropriate uncertainty. Angiography or CT, not an echo map alone, defines coronary anatomy.
| Pattern | Likely interpretation | Limitation to challenge |
|---|---|---|
| New reduced thickening in contiguous segments during adequate stress | Inducible ischemic response | Confirm side-by-side in orthogonal views and exclude dropout or translation |
| Severe resting abnormality unchanged with stress | Fixed response, often scar or limited viability | Prior infarction, image quality, and stress adequacy affect confidence |
| Resting dysfunction improves at low-dose dobutamine | Contractile reserve or viability | Tethering and slight isolated change are less convincing than adjacent segments |
| Improvement at low dose followed by worsening at high dose | Biphasic response suggesting viable myocardium with flow-limiting disease | Requires staged acquisition and correct matching of the same tissue |
| Akinesis becomes dyskinesis | Often passive mechanical response of infarcted tissue | Do not automatically label this change new ischemia |
Compare rest and stress under matched conditions
Use the same views, depth, sector orientation, focus, and display format at baseline and stress. Optimize frame rate while preserving the endocardial border and acquire representative beats without postectopic augmentation. Side-by-side synchronized loops help distinguish true change from a different plane. An ultrasound-enhancing agent should be used under protocol when two or more contiguous segments cannot be seen or an entire coronary territory is incomplete. Contrast improves border definition but attenuation, near-field artifact, swirling, or inadequate opacification still requires correction.
Exercise is preferred when the patient can exercise because workload, symptoms, ECG, heart rate, and blood pressure add physiologic and prognostic information. With treadmill testing, obtain postexercise images immediately, generally within 1–2 minutes, because transient abnormalities can normalize rapidly. Bicycle imaging can be performed during incremental stages and peak stress. Dobutamine uses staged imaging to evaluate contractile reserve and inducible ischemia when exercise is unsuitable. Follow the laboratory's medication, monitoring, dosing, and termination protocol; the sonographer does not independently alter drugs or endpoints.
A normal response includes preserved regional function with increased contractility and usually reduced end-systolic size, although the degree depends on treadmill, bicycle, or dobutamine loading. Ischemia is a new wall-motion abnormality in a segment normal at rest or worsening of a preexisting abnormality during stress. Assess thickening more heavily than excursion. Report the stage or heart rate at first change, extent, severity, recovery, global EF and cavity response, workload or dose, symptoms, ECG, and blood pressure. Failure to reach adequate workload or target heart rate reduces sensitivity; a negative but inadequate test cannot be called fully reassuring.
Recognize mimics and discordant responses
LBBB, ventricular pacing, prior surgery, RV pressure loading, hypertensive response, cardiomyopathy, and excessive translational motion can create nonischemic abnormalities. Basal inferior or septal excursion may look reduced because of fibrous tethering while thickening remains preserved. A hypertensive response or cardiomyopathy may blunt global hyperkinesis without an epicardial territorial pattern. Foreshortening can make the apex appear akinetic; switching planes between rest and peak can manufacture improvement or worsening. Microvascular disease may also produce symptoms or a blunted response without a classic focal pattern. Strain and perfusion imaging can add evidence but remain tracking-, vendor-, load-, and artifact-dependent. No EF, strain value, ECG change, or isolated segment independently establishes or excludes ischemia.
Stress testing requires continuous attention to the patient as well as the images. Monitor rhythm, blood pressure, symptoms, oxygenation when indicated, and test stage. New or worsening wall-motion abnormality, hypotension, severe hypertension, significant arrhythmia, severe symptoms, or protocol endpoint requires immediate action by the supervising team. Preserve diagnostic images without delaying safety response. Document whether peak imaging preceded recovery or occurred after heart rate had substantially fallen.
Search for ischemic complications
Acute infarction can cause regional dysfunction, reduced EF, and low output, but mechanical complications are the urgent echo targets. Papillary muscle ischemia or rupture can produce acute severe eccentric MR and pulmonary edema. Ventricular septal rupture produces a new left-to-right color jet and high-velocity systolic Doppler signal. Free-wall rupture may cause new pericardial blood, tamponade physiology, or sudden collapse. A true LV aneurysm has a broad neck and scarred dyskinetic wall; a pseudoaneurysm represents contained rupture and commonly has a narrower communication. Inspect akinetic apical regions for thrombus using enhancing agent when indicated. Also assess RV infarction, pericardial effusion, remodeling, functional MR, and ventricular function.
A new postinfarct shunt, suspected free-wall or papillary rupture, rapidly accumulating effusion, severe MR, mobile thrombus, or profound ventricular deterioration requires immediate communication through laboratory policy. Report anatomy and hemodynamics rather than recommending surgery from the scanning room. A defensible ischemia examination combines regional evidence, stress adequacy and timing, explicit coronary-territory uncertainty, clinical monitoring, and a systematic search for complications.
Coronary territories overlap
Name the abnormal segments and confirm them in orthogonal views before suggesting a vessel. Dominance, wraparound branches, grafts, collaterals, and individual anatomy mean an echo territory cannot define coronary anatomy by itself.
At adequate exercise stress, two contiguous inferior and inferolateral segments develop new reduced thickening confirmed in orthogonal views. What is the best interpretation?
Two days after an acute infarction, a patient becomes hypotensive and a new rapidly enlarging pericardial effusion with right-sided chamber compression appears. What is the priority?