What is the significance of ST depression in leads V2‑V6 with ST elevation in lead V1?

ST Depression in V2-V6 with ST Elevation in V1: Posterior Wall Myocardial Infarction

This ECG pattern represents acute posterior (or posterolateral) wall myocardial infarction, where the ST depression in anterior precordial leads V1-V3 (and extending to V4-V6) is the reciprocal mirror image of ST elevation occurring in the posterior wall—a region not directly visualized by standard 12-lead ECG. 1

Understanding the Spatial Vector Concept

The key to interpreting this pattern is recognizing that ST depression in the anterior precordial leads is electrocardiographically equivalent to posterior ST elevation from a spatial vector perspective. 1 The American Heart Association guidelines explicitly state that acute posterior wall infarction can be diagnosed from reciprocal ST-segment depression evident in precordial leads V1 through V3. 1

• The posterior wall of the left ventricle is not directly "seen" by standard precordial leads 1
• When posterior myocardial injury occurs, the ST vector points posteriorly (away from V1-V3) 1
• This manifests as ST depression in the anterior leads—the reciprocal of true posterior ST elevation 1

Critical Diagnostic Features

The most specific early ECG finding of posterolateral infarction is maximal ST segment depression in precordial leads V2 and V3 as the sole ECG finding during chest pain in the first 24 hours. 2 Research demonstrates that:

• ST depression isolated to V2-V3 without reciprocal changes may represent the initial ECG finding of posterolateral infarction 2
• In 40% of patients with isolated precordial ST depression, electrocardiographic evidence of posterior MI evolves within 3 days 3
• These patients have significantly higher peak CK values (1,051 vs 663 IU, p<0.009) compared to anterior non-Q-wave MI 3

Identifying the Culprit Vessel

The pattern of ST depression in V2-V6 with ST elevation in V1 suggests occlusion of either the right coronary artery (RCA) or left circumflex artery (LCx), depending on which vessel is dominant and supplies the posterior descending branch. 1

Distinguishing RCA from LCx Occlusion:

• ST depression in leads V1-V3 accompanying inferior wall infarction (ST elevation in II, III, aVF) cannot definitively distinguish between RCA and LCx occlusion 1
• However, absence of such anterior ST depression is more suggestive of RCA than LCx occlusion 1
• When LCx is occluded, the spatial ST vector in the frontal plane is more likely directed to the left than with RCA occlusion 1

Immediate Clinical Actions Required

Record posterior chest leads V7, V8, and V9 immediately to confirm posterior wall ST elevation. 1 The American Heart Association recommends:

• Place V7 at the posterior axillary line 1
• Place V8 below the scapula 1
• Place V9 at the paravertebral border 1
• All three leads should be in the same horizontal plane as V6 1
• ST elevation >0.05 mV (0.5 mm) in V7-V9 confirms posterior STEMI 1

If inferior wall changes are present (ST elevation in II, III, aVF), immediately record right-sided leads V3R and V4R to assess for right ventricular involvement. 1 This is critical because:

• ST elevation ≥0.1 mV in V4R indicates right ventricular infarction 1
• Right ventricular involvement is associated with greater in-hospital complications 1
• The diagnostic window for RV infarction is narrow—ST elevation in right-sided leads persists for much shorter duration than inferior lead changes 1

Treatment Implications: STEMI vs NSTEMI

This is where clinical management becomes critically nuanced. The American Heart Association explicitly states that "anterior ST depression during infarction from a spatial vector perspective may be electrocardiographically equivalent to posterior ST elevation, but it may be quite different in terms of a literal interpretation of treatment." 1

Current Treatment Guidelines:

• If posterior leads V7-V9 show ST elevation ≥0.5 mm, this qualifies as STEMI requiring immediate reperfusion therapy (primary PCI preferred) 1, 4
• Without documented posterior ST elevation on V7-V9, isolated anterior ST depression is typically managed as NSTEMI with early invasive strategy within 24-72 hours 5
• Recent guidelines for acute coronary syndromes differ significantly between ST-elevation and non-ST-elevation infarction 1

Evolution and Later ECG Findings

Other ECG findings compatible with posterolateral infarction are relatively delayed manifestations appearing after the initial ST depression. 2 These include:

• Appearance of Q waves in leads V5 and V6 2
• Increased R/S ratio in leads V1 and V2 (tall R waves) 1, 2
• Diminution of R wave amplitude in leads I, aVL, V5, and V6 2
• In 78% of cases, posterior MI evolution occurs by day 3 without re-elevation of cardiac enzymes 3

Common Pitfalls to Avoid

Do not dismiss anterior precordial ST depression as "non-STEMI" or "subendocardial ischemia" without recording posterior leads V7-V9. 1, 2 Critical errors include:

• Failing to recognize that ST depression in V1-V3 may represent the reciprocal of posterior STEMI 1
• Delaying posterior lead recording—some cases show ST elevation only in posterior leads 1
• Missing right ventricular involvement by not recording V3R/V4R when inferior changes are present 1
• If RV infarction is confirmed, avoid aggressive fluid resuscitation and nitrates—these patients are preload-dependent and may develop cardiogenic shock or profound hypotension 4, 5

High-Risk Features Requiring Aggressive Management

Research demonstrates that patients with precordial ST depression who develop posterior MI have:

• Significantly larger infarct size (peak CK 1,051 vs 663 IU) 3
• Greater mean precordial ST depression in V1-V3 (p<0.01) 3
• More lateral extension of perfusion defects 6
• Larger anterior injury vectors 6

Measure cardiac troponin immediately and repeat at 6-12 hours; troponin elevation confirms myocardial necrosis and mandates invasive strategy. 5