What is the significance of poor R (r wave) progression on an electrocardiogram (ECG) in patients with a history of coronary artery disease (CAD)?

Poor R Wave Progression on ECG: Clinical Significance in Coronary Artery Disease

Poor R wave progression (PRWP) is a highly significant ECG finding in patients with coronary artery disease that strongly predicts sudden cardiac death, anterior myocardial infarction, and left anterior descending artery stenosis, requiring immediate cardiac evaluation and risk stratification. 1

Definition and Diagnostic Criteria

PRWP is defined as R-wave amplitude ≤0.3 mV in lead V3 with R-wave amplitude in V2 ≤ R-wave amplitude in V3. 1 The DePace criteria systematically identify this pattern and should be applied when evaluating precordial leads. 2

A more specific variant called reversed R wave progression (RRWP) occurs when RV2 < RV1, RV3 < RV2, or RV4 < RV3, and this pattern is even more strongly associated with cardiac pathology. 3

Prognostic Significance in CAD Patients

Mortality Risk

In patients with established CAD, PRWP carries particularly grave prognostic implications:

• Sudden cardiac death risk increases 2.6-fold (HR 2.62; 95% CI 1.38-4.98) in CAD patients with PRWP compared to those without. 1
• Cardiac mortality increases 1.7-fold (HR 1.71; 95% CI 1.19-2.46) specifically in the CAD subgroup. 1
• All-cause mortality increases 1.3-fold (HR 1.29; 95% CI 1.08-1.54) in the general population with PRWP. 1

The association with sudden cardiac death is significant only in patients with CAD, not in those without coronary disease, making this finding particularly actionable in your patient population. 1

Anatomic Correlation

PRWP demonstrates strong anatomic specificity:

• 85% of patients with RRWP who undergo cardiac evaluation have significant cardiac disease. 3
• Among those with ischemic heart disease, 100% have left anterior descending (LAD) artery stenosis. 3
• 41% have prior anterior myocardial infarction, and an additional 17% have ischemic heart disease without prior MI. 3

Distinguishing Anterior MI from Other Causes

Key Discriminating Features

PRWP has four major causes that must be distinguished: anterior MI, left ventricular hypertrophy, right ventricular hypertrophy, and normal variant with diminished anterior forces. 4

The QRS axis is critical for interpretation:

• PRWP with a normal QRS axis (-30° to 100°) is significantly more associated with non-ST-elevation MI (NSTEMI) in hospitalized patients (p <0.0001). 2
• Patients with NSTEMI and PRWP who have a normal QRS axis are older (mean age 71.3 years) compared to those with axis deviation (mean age 64.3 years). 2

Established Q Waves

Q waves ≥0.04 seconds suggest prior MI and indicate high likelihood of significant CAD, though they are less helpful for diagnosing acute unstable angina. 5 Isolated Q waves in lead III may be normal, especially without repolarization abnormalities in inferior leads. 5

Quantifying Myocardial Damage

The sum of R-wave amplitude across V1-V6 inversely correlates with infarct size (r = -0.56, p <0.001) and positively correlates with left ventricular ejection fraction (r = 0.45, p <0.001) in patients with prior anterior MI. 6

Patients with PRWP (RV3 ≤3 mm) have:

• Larger perfusion defects (sum of defect score 17.5 ± 8.6 vs 7.6 ± 10.3, p <0.001) 6
• Lower LVEF (46.1 ± 9.8% vs 55.2 ± 12.9%, p <0.01) compared to anterior MI patients without PRWP 6

This means residual R-wave amplitude reflects myocardial salvage and ventricular function in the coronary intervention era. 6

Clinical Action Algorithm

Immediate Evaluation Required

When PRWP is identified in a patient with known or suspected CAD:

1. Compare with prior ECGs to determine if this represents a new finding, which would suggest acute ischemia or recent infarction. 5

2. Assess for accompanying ST-segment and T-wave changes:

   • ST-segment depression >1 mm in two or more contiguous leads is highly suggestive of acute coronary syndrome. 5
   • Deep symmetrical T-wave inversion in anterior chest leads suggests significant proximal LAD stenosis. 5

3. Obtain cardiac biomarkers (troponin T or I) to distinguish acute from chronic findings. 5

4. Evaluate for signs of left ventricular dysfunction (rales, S3 gallop, acute mitral regurgitation), which indicate severe underlying CAD and high risk of poor outcomes. 5

Risk Stratification

High-risk features requiring urgent intervention:

• New PRWP with ongoing chest pain >20 minutes 7
• PRWP with hemodynamic instability 7
• PRWP with elevated cardiac troponins 7
• RRWP pattern (even more specific than standard PRWP) 3

Diagnostic Workup

• Echocardiography to assess wall motion abnormalities (anterior wall hypokinesis strongly suggests LAD disease) and quantify left ventricular function. 3, 6
• Coronary angiography should be strongly considered given the 100% association with LAD stenosis in ischemic heart disease patients with RRWP. 3
• Myocardial perfusion imaging can quantify infarct size and correlates with R-wave amplitude. 6

Critical Pitfalls to Avoid

• Do not dismiss PRWP as "non-specific" in CAD patients—it carries significant prognostic weight for sudden cardiac death. 1
• Do not assume PRWP always indicates prior MI—only 41% of RRWP cases represent prior infarction, though 58% have ischemic heart disease. 3
• A completely normal ECG does not exclude acute coronary syndrome—1-6% of patients with normal ECGs have MI or unstable angina. 5
• Consider posterior MI (approximately 4% of acute MI), which may present with increased R-wave amplitude in V1-V2 rather than PRWP, representing the Q-wave equivalent. 5
• Verify lead placement before attributing clinical significance, as electrode misplacement can create apparent PRWP. 8

Alternative Diagnoses to Consider

When PRWP is present without CAD:

• Dilated cardiomyopathy (7% of RRWP cases) 3
• Hypertrophic cardiomyopathy (3% of RRWP cases) 3
• Left ventricular hypertrophy 5, 4
• Right ventricular hypertrophy 4
• Pulmonary embolism (3% of RRWP cases) 3
• Normal variant (only 24% of RRWP cases) 3