Area of the Heart Affected by LAD Occlusion
Occlusion of the left anterior descending (LAD) artery invariably causes anterior wall ischemia/infarction, affecting the anterior and lateral walls of the left ventricle, the interventricular septum, and potentially the cardiac apex depending on the location and extent of the occlusion. 1
Specific Myocardial Territories Based on Occlusion Location
Proximal LAD Occlusion (Above First Septal and First Diagonal Branches)
This produces the most extensive myocardial damage, involving:
- Basal portion of the left ventricle 1
- Anterior wall of the left ventricle 1
- Lateral wall of the left ventricle 1
- Interventricular septum (including basal septum) 1
- Cardiac apex (when LAD wraps around) 1
The ST-segment spatial vector is directed superiorly and to the left, producing ST elevation in leads V1-V4, I, aVL, and often aVR, with reciprocal ST depression in leads II, III, aVF, and often V5. 1, 2
Mid-LAD Occlusion (Between First Septal and First Diagonal Branches)
This affects a smaller territory because the basal interventricular septum is spared:
- Anterior wall of the left ventricle 1
- Lateral wall of the left ventricle 1
- Cardiac apex (when LAD extends to apex) 1
The basal septum remains viable, so ST elevation does not occur in lead V1. 1, 2 ST elevation appears in leads V2-V4 and aVL, with reciprocal ST depression in lead III. 2
Distal LAD Occlusion (Below First Septal and First Diagonal Branches)
This produces the most limited infarct territory:
The basal left ventricle is not involved, and the ST-segment vector is oriented more inferiorly. 1 ST elevation is most prominent in leads V3-V6 and less prominent in V2, with no ST elevation in V1, aVR, or aVL, and no reciprocal ST depression in inferior leads. 1, 2 Paradoxically, ST elevation may occur in leads II, III, and aVF due to inferior orientation of the ST vector. 1, 2
Critical Anatomic Variations Affecting Infarct Size
LAD Length and Apical Supply
The length of the LAD is a critical determinant of infarct size and prognosis. 4, 5
Type C (wrap-around) LAD: Extends beyond the apex to supply the inferoapical segment of the left ventricle, occurring in 87% of left coronary dominance and 47% of right coronary dominance. 5 Proximal occlusion of wrap-around LAD carries significantly higher mortality (28% vs 2.4%) compared to shorter LAD. 4
Type B LAD: Reaches the apex but does not supply the inferoapical segment. 5
Type A (short) LAD: Terminates before the cardiac apex, with the apex supplied by either the posterior descending artery from the right coronary artery or, rarely, by an obtuse marginal branch from the left circumflex. 6, 5
Women more frequently have long LADs that wrap around the apex compared to men, irrespective of coronary dominance. 5
Clinical Pitfalls and Caveats
Mimics of LAD Occlusion
Stanford Type A aortic dissection can produce anterior ST elevation through mechanisms other than LAD occlusion, including:
- Aortic valve distortion with acute severe aortic regurgitation causing global myocardial ischemia 7
- Hemopericardium and cardiac tamponade producing diffuse ST elevation 7
- Global hypoperfusion from dissection-related shock 7
Before proceeding to cardiac catheterization for presumed LAD occlusion, assess for chest pain radiating to the back (present in 47% of Type A dissections), pulse deficits, blood pressure differentials between extremities, and consider bedside echocardiography and CT angiography if clinical suspicion exists. 7 Delayed surgical intervention for misdiagnosed Type A dissection increases mortality by 1% per hour. 7
Anatomic Variants
Dual LAD variants exist in which two branches supply the usual LAD distribution—a short LAD terminating proximally in the anterior interventricular sulcus and a long LAD with variable course returning to the sulcus distally. 8 Recognition is critical for surgical planning and angiographic interpretation. 8