ST Depressions with PVCs in V1, aVL, and V3 and Their Relationship to Chronic RCA Occlusion and Ventricular Tachycardia
ST depressions in leads V1, aVL, and V3 with PVCs can indeed correlate with chronic right coronary artery (RCA) occlusion, and this electrical instability can predispose patients to ventricular tachycardia due to myocardial scarring and altered repolarization patterns in the affected territory.
ECG Patterns in RCA Occlusion
The ECG manifestations of RCA occlusion have distinct patterns that can help identify the affected vessel:
- When the RCA is occluded, the spatial vector of the ST segment is usually directed more to the right than when the left circumflex artery (LCx) is occluded 1
- This typically results in greater ST-segment elevation in lead III than in lead II and is often associated with ST-segment depression in leads I and aVL 1
- ST depression in leads V1-V3 can occur with occlusion of either the RCA or LCx, traditionally referred to as "posterior ischemia" or "posterolateral ischemia" 1, 2
Distinguishing RCA vs. LCx Occlusion
The pattern of ST changes can help differentiate between RCA and LCx occlusion:
- ST depression in leads I and aVL ≥ 0.1 mV is a key indicator for RCA occlusion 3
- When the LCx is occluded, the ST segment may be elevated to a greater extent in lead II than in lead III and may be isoelectric or elevated in leads I and aVL 1
- ST depression in V3 with a ratio of ST depression in V3 to ST elevation in III > 1.2 is more suggestive of LCx occlusion 3
Chronic RCA Occlusion and Risk of Ventricular Tachycardia
Chronic occlusion of the RCA can lead to ventricular tachycardia through several mechanisms:
- Myocardial Scarring: Chronic occlusion leads to fibrosis and scarring, creating a substrate for reentrant arrhythmias
- Electrical Remodeling: Areas of ischemia adjacent to scarred tissue have altered repolarization properties
- PVCs as Triggers: PVCs originating from the border zones between normal and scarred myocardium can trigger ventricular tachycardia
Relationship Between ST Depression, PVCs, and Ventricular Tachycardia
The presence of ST depressions with PVCs in leads V1, aVL, and V3 suggests:
- Ongoing ischemia or altered repolarization in the territory of the RCA
- Electrical instability that can serve as a substrate for ventricular tachycardia
- Potential right ventricular involvement, which is associated with higher arrhythmic risk
When a patient with chronic RCA occlusion spontaneously develops ventricular tachycardia, several factors may be involved:
- Acute ischemia superimposed on chronic occlusion (due to thrombosis or loss of collateral flow)
- Electrolyte disturbances affecting already compromised myocardium
- Autonomic fluctuations triggering arrhythmias in vulnerable substrate
- PVCs serving as triggers for reentrant circuits
Clinical Implications and Management
For patients presenting with ST depressions in V1, aVL, and V3 with PVCs:
- Urgent Evaluation: These findings warrant immediate assessment for posterior myocardial infarction or RCA/LCx occlusion 2
- Consider Posterior Leads: Recording leads V7-V9 can help identify posterior involvement, with ST elevation ≥0.5 mm confirming posterior MI 2
- Right-Sided ECG: Obtain right precordial leads (V3R, V4R) to assess for right ventricular involvement, which affects management and prognosis 2
- Coronary Angiography: Early coronary angiography is recommended to determine the culprit vessel and extent of disease 2
Pitfalls to Avoid
- Failing to recognize that ST depression in V1-V3 may represent posterior MI, which requires STEMI management protocols 2
- Overlooking right ventricular involvement, which significantly impacts morbidity and mortality 2
- Missing the diagnosis of RCA occlusion by not assessing ST depression patterns in leads I and aVL 3
- Delaying ECG acquisition, as ST changes in right-sided leads can disappear rapidly 2
In summary, the pattern of ST depressions in V1, aVL, and V3 with PVCs can be indicative of chronic RCA occlusion. The development of ventricular tachycardia in this setting likely represents the interaction between a vulnerable myocardial substrate (scarring from chronic occlusion) and triggers (PVCs), potentially exacerbated by acute changes in perfusion, electrolytes, or autonomic tone.