AWMI+TPWMI

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AWMI + TPWMI: Anterior Wall MI vs. True Posterior Wall MI


I. ANTERIOR WALL MYOCARDIAL INFARCTION (AWMI)

Coronary Territory

The anterior wall of the left ventricle is supplied by the left anterior descending (LAD) artery. LAD occlusion is the most common cause of AWMI and produces the largest infarcts - often leading to extensive LV dysfunction and cardiogenic shock.

ECG Criteria (STEMI)

From Tintinalli's Table 49-4:
SubtypeECG Changes
AnteroseptalST elevation in V1, V2, (± V3)
AnteriorST elevation in V1, V2, V3, V4
AnterolateralST elevation in V1-V6, I, and aVL
Lateral onlyST elevation in I and aVL
Reciprocal changes: ST depression in inferior leads (II, III, aVF). ST elevation in aVR can also accompany extensive anterior STEMI and suggests proximal LAD or left main occlusion.

Sequence of ECG Changes in AWMI

  1. Hyperacute T waves - tall, peaked T waves in V1-V4 (earliest sign, often missed)
  2. ST elevation - upsloping then convex/tombstone elevation in V1-V4
  3. Q wave development - pathological Q waves (>0.04 s, >25% of R wave) in affected leads
  4. T wave inversion - after ST normalizes
  5. Persistent ST elevation - when present beyond 2 weeks suggests LV aneurysm / large akinetic area

Key Complications of AWMI

  • Cardiogenic shock - most common cause is large anterior wall MI (LAD territory)
  • LV aneurysm / thrombus - occurs most often post-anterior MI; LV thrombus warrants anticoagulation (warfarin preferred; DOACs have conflicting evidence)
  • VSD (interventricular septal rupture) - more common in anterior MI than inferior
  • Complete heart block - anterior MI causes block in distal His-Purkinje system → wide complex escape rhythms, poor prognosis
  • New LBBB - suggests large anterior MI, worse prognosis
  • Bundle branch / hemiblock - new development = extensive anterior MI

II. TRUE POSTERIOR WALL MI (TPWMI)

Coronary Territory

The true posterior wall (inferobasal LV) is supplied by the posterior descending artery (PDA), which arises from:
  • The right coronary artery (RCA) in right-dominant systems (most common)
  • The left circumflex (LCx) in left-dominant systems
TPWMI almost always accompanies inferior MI or inferolateral MI. It rarely occurs in isolation.

Why It's "True Posterior"

The standard 12-lead ECG does not directly face the posterior wall - V1 and V2 are the "mirror image" leads. Therefore, TPWMI produces reciprocal/mirror changes in V1-V2, not primary ST elevation.

ECG Criteria for TPWMI

From Rosen's Emergency Medicine and Tintinalli's Table 49-4:
In V1-V2 (reciprocal / mirror changes):
  1. Tall, wide R wave (R ≥ 0.04 s) - the mirror image of a posterior Q wave
  2. R/S ratio ≥ 1 in V1
  3. Horizontal ST depression (not upsloping)
  4. Upright (tall) T wave - "positive T wave" in V1-V2 during an acute event
The combination of horizontal ST depression + upright T wave in V1-V2 increases diagnostic accuracy significantly.
Posterior leads (V7, V8, V9) - direct imaging:
  • Placed at the posterior chest (V7 = posterior axillary line, V8 = tip of scapula, V9 = paraspinal)
  • Show ST elevation ≥ 0.5 mm, directly confirming TPWMI
  • V8 and V9 have subtle ST elevation (as shown in the image below)
Posterior leads V8 and V9 showing subtle ST elevation in acute posterior MI
Posterior leads V8 and V9: arrows indicate ST elevation consistent with acute posterior wall MI - Rosen's Emergency Medicine

Important Clinical Notes on TPWMI

  • Tall R in V1 may be delayed - emergence can lag behind the infarct because it represents a developing posterior Q wave in mirror
  • Cardiac MRI evidence suggests many so-called "posterior" infarctions (with tall R in V1-V2) are actually lateral LV wall MIs - a consensus document has proposed reclassifying them as "inferobasal MI"
  • Patients with inferior MI who also have ST depression in V1-V3 or ST elevation in V8-V9 have: larger infarct zones, lower ejection fractions, higher morbidity and mortality than isolated inferior MI
  • Fibrinolysis indication: ST depression in ≥2 precordial leads (V1-V4) as a sign of posterior STEMI is a recognized indication for fibrinolytic therapy

III. Side-by-Side Comparison

FeatureAWMITPWMI
ArteryLADPDA (from RCA or LCx)
Primary ECG leadsV1-V4 (± I, aVL)No direct standard lead; V7-V9 (posterior)
Standard 12-lead signST elevation V1-V4ST depression + tall R + upright T in V1-V2
Pathological Q wavesV1-V4Not seen in standard leads (mirror R wave instead)
Reciprocal changesST depression in II, III, aVFST elevation appears in V7-V9 if checked
Key complicationCardiogenic shock, VSD, LV thrombus, LBBBUsually accompanies inferior MI; larger infarct zone
PrognosisWorst prognosis among STEMI locationsWorse than isolated inferior MI
ManagementPrimary PCI / fibrinolysisPrimary PCI; fibrinolysis indicated for V1-V4 depression

IV. Management Principles (Both)

  • Primary PCI is the treatment of choice when available within the recommended time window (door-to-balloon ≤90 min)
  • Fibrinolysis (TNK preferred - single bolus, most fibrin-specific, 80x more resistant to PAI-1 than t-PA) when PCI unavailable within time target
    • TPWMI with ST depression in ≥2 precordial leads (V1-V4) qualifies as a fibrinolysis indication
  • Antiplatelet + anticoagulation combined with reperfusion strategy
  • Avoid nitrates in suspected RV infarction (often accompanies inferior/posterior MI) as nitrate-induced hypotension can be severe

Sources: Tintinalli's Emergency Medicine (Table 49-4, p.378) - Rosen's Emergency Medicine (Fig. 64.13, Posterior Leads section) - The Washington Manual of Medical Therapeutics
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