What are the causes of poor R wave progression?

Causes of Poor R Wave Progression

Poor R wave progression results from four primary causes: electrode misplacement (the most common), prior anterior myocardial infarction, left ventricular hypertrophy, and right ventricular hypertrophy, with a small percentage representing normal anatomic variation. 1

Technical/Artifactual Causes (Must Exclude First)

Electrode misplacement is the most frequent cause and must be systematically excluded before considering pathological etiologies. 1

• Superior displacement of V1 and V2 electrodes (placed in the 2nd or 3rd intercostal space instead of the 4th) reduces R-wave amplitude by approximately 0.1 mV per interspace, creating artifactual poor R wave progression that can mimic anterior infarction. 2, 1

• Superior misplacement produces rSr' complexes with T-wave inversion resembling lead aVR, which should alert you to incorrect placement. 2, 1

• Precordial lead transposition (V1 with V2, or within V1-V3) causes reversed R-wave progression with distorted P-wave and T-wave progression in the same leads. 1

• Inferior placement of V3 and V4 in patients with low diaphragm position (common in obstructive pulmonary disease) positions these leads above ventricular boundaries, recording negative deflections that simulate anterior infarction. 2, 1

Pathological Cardiac Causes

Prior Anterior Myocardial Infarction

This is the most clinically significant pathological cause, particularly when accompanied by pathological Q waves. 2, 1

• Anterior MI accounts for approximately 41% of cases with reversed R wave progression (a more specific finding than simple poor progression). 3

• Loss of precordial R wave amplitude occurs with acute myocardial ischemia and established infarction. 2

• Q waves ≥0.02 seconds or QS complexes in V2-V3 indicate prior anterior MI. 2

• In Takotsubo syndrome, anterior Q-waves or poor R-wave progression without ST-elevation occurs in approximately 15% of cases (versus 69% in anterior STEMI), representing electrical stunning rather than infarction. 2

Left Ventricular Hypertrophy

LVH produces poor R wave progression through increased posterior forces that diminish anterior R wave amplitude. 1, 4

• The diagnosis becomes challenging when LBBB coexists, as both alter QRS patterns. 2

• In complete LBBB, poor R wave progression is expected due to altered depolarization sequence (broad notched R waves in lateral leads, absent Q waves in I, V5, V6). 2

• Voltage criteria for LVH in athletes represent physiologic adaptation and do not require further evaluation when isolated. 1

Right Ventricular Hypertrophy

RVH shifts the QRS vector rightward and anteriorly, producing poor R wave progression. 1, 4

• Up to 13% of athletes fulfill Sokolow-Lyon criteria for RVH, representing normal physiologic adaptation when isolated. 1

• In acute cor pulmonale or pulmonary embolism, poor R wave progression may occur acutely. 2

Cardiomyopathies

• Dilated cardiomyopathy accounts for 7% of cases with reversed R wave progression. 3

• Hypertrophic cardiomyopathy produces Q waves or QS complexes through myocardial fibrosis in the absence of coronary artery disease. 2

• Pre-excitation, obstructive cardiomyopathy, cardiac amyloidosis, and myocarditis can all produce poor R wave progression. 2

Normal Variant

Poor R wave progression occurs in approximately 8% of apparently normal individuals without cardiac disease, likely representing one tail of the normal distribution of cardiac electrical axes. 5

• This normal variant shows no correlation with age, sex, height, weight, body surface area, thoracic skeletal abnormalities, or mitral valve prolapse. 5

• The positive predictive value for coronary artery disease in the general population is only approximately 7.3%. 1

Systematic Evaluation Approach

Step 1: Verify Electrode Placement

• Confirm V1 and V2 are in the 4th intercostal space at the sternal borders, not superiorly displaced. 2, 1
• Ensure V4 is at the 5th intercostal space, midclavicular line, with V5 and V6 following horizontally (not along the intercostal space). 2

Step 2: Assess Associated ECG Findings

• Look for pathological Q waves (≥0.02 sec in V2-V3 or ≥0.03 sec and ≥0.1 mV in other leads). 2
• Evaluate QRS axis: Normal axis (-30° to +100°) with poor R wave progression is more significantly associated with NSTEMI than axis deviation. 6
• Check for ST-segment depression (uncommon in Takotsubo syndrome but present in >30% of ACS patients). 2
• Assess for bundle branch blocks, particularly LBBB (QRS ≥120 ms, broad notched R in I, aVL, V5-V6). 2

Step 3: Consider Clinical Context

• Age and cardiac risk factors: Young athletes with isolated voltage criteria likely represent physiologic adaptation. 1
• Symptoms: Chest pain, dyspnea, or syncope warrant aggressive evaluation. 2
• History of cardiac disease: Prior MI, known cardiomyopathy, or pulmonary disease. 2, 3

Step 4: Determine Need for Further Testing

• Reversed R wave progression (RV2 < RV1, RV3 < RV2, or RV4 < RV3) is highly specific for cardiac disease, particularly ischemic heart disease with LAD stenosis (present in 58% of cases), and warrants cardiac imaging. 3
• Echocardiography, cardiac MRI, or stress testing indicated when high clinical suspicion exists despite normal variant appearance. 1
• In patients with poor R wave progression and NSTEMI, 82% have normal QRS axis, making this a useful discriminator. 6