How can secondary ST‑T changes be differentiated from the criteria for Wellens syndrome?

Differentiating Secondary ST-T Changes from Wellens Criteria

Secondary ST-T changes result from altered ventricular depolarization (bundle branch blocks, ventricular hypertrophy, pacing) and are directed opposite to the QRS vector, whereas Wellens syndrome represents primary repolarization abnormalities with deeply inverted or biphasic T waves in V1-V4 that indicate critical proximal LAD stenosis—the key distinction is that secondary changes follow predictable QRS-discordant patterns while Wellens changes occur with normal QRS complexes and precordial R-wave progression. 1, 2, 3

Understanding Secondary ST-T Changes

Secondary repolarization abnormalities occur as a direct consequence of altered ventricular conduction, not from changes in myocyte repolarization itself. 1

Characteristic Features of Secondary Changes

• In left bundle branch block (LBBB): ST-segment and T-wave vectors are directed opposite to the mean QRS vector—if the QRS is predominantly negative in a lead, expect the T wave to be positive, and vice versa. 1

• In right bundle branch block (RBBB): ST-T changes are directed opposite to the slow terminal component (the terminal R' wave) of the QRS complex, typically producing T-wave inversion in V1-V3 where the terminal forces are positive. 1

• In ventricular hypertrophy: ST-T changes are directed opposite to the increased QRS voltage—left ventricular hypertrophy with tall R waves in V5-V6 produces ST depression and T-wave inversion in those leads (the "strain pattern"). 1

• Magnitude relationship: The degree of ST-T change is proportional to the magnitude of QRS waveform changes when excitation pathways are altered. 1

Temporal Characteristics

• Transient conduction changes (ectopic beats, transient bundle branch blocks) produce secondary ST-T changes that revert promptly to baseline once normal conduction resumes. 1

• Prolonged conduction changes (chronic pacing, persistent bundle branch block) may take hours to days to develop full secondary repolarization changes and similarly long to dissipate after conduction normalizes. 1

Wellens Syndrome: Primary Repolarization Abnormality

Wellens syndrome represents a high-risk pattern of primary repolarization changes indicating critical proximal LAD stenosis, not secondary to QRS abnormalities. 2, 3, 4

Diagnostic Criteria for Wellens Syndrome

• History of anginal chest pain (though ECG changes are typically seen during pain-free periods). 3, 4

• Little or no cardiac enzyme elevation at the time of ECG recognition. 3, 5

• Normal or minimally elevated cardiac biomarkers initially, though high-sensitivity troponin may be positive. 4

• No pathologic precordial ST-segment elevation (distinguishes from acute STEMI). 3, 5

• Preserved precordial R-wave progression (no loss of R waves, normal QRS complexes). 3, 5

Two ECG Patterns of Wellens Syndrome

Type A (25% of cases): Biphasic T waves (initially positive, then negative) in leads V2-V3, often extending to V1 and V4. 2, 6, 3, 4

Type B (75% of cases): Deeply inverted, symmetrical T waves in leads V1-V3 (or V1-V4), typically ≥2 mm in depth. 7, 2, 6, 3

Critical Distinguishing Features

• Normal QRS duration and morphology: Wellens changes occur with normal ventricular depolarization (QRS typically 80-100 ms), unlike secondary changes that require abnormal QRS patterns. 7, 3

• Persistent T-wave abnormalities: The T-wave changes may persist for hours to weeks, even during asymptomatic periods, and are best recognized outside episodes of chest pain. 6, 3, 5

• Anterior lead distribution: Changes are confined to precordial leads V1-V4, reflecting the LAD territory. 2, 6, 3

• Symmetrical, deep inversions: When inverted, Wellens T waves are characteristically symmetrical and often ≥2 mm deep, unlike the asymmetric inversions of secondary changes. 7, 3, 4

Algorithmic Approach to Differentiation

Step 1: Assess QRS Morphology and Duration

• If QRS is widened (≥120 ms) with LBBB or RBBB pattern: ST-T changes are likely secondary. Check if T-wave direction is opposite to the terminal QRS forces. 1

• If QRS is normal (<120 ms) with preserved R-wave progression: Consider primary repolarization abnormality, including Wellens syndrome. 3, 5

Step 2: Evaluate T-Wave Vector Relationship to QRS

• Secondary changes: T-wave vector is predictably opposite to QRS vector (LBBB) or terminal QRS component (RBBB). 1

• Wellens syndrome: T-wave changes occur despite normal QRS vectors—the T-wave abnormality is independent of QRS direction. 3, 4

Step 3: Examine Lead Distribution

• Secondary changes in RBBB: T-wave inversion typically in V1-V2 (where terminal R' is positive), with upright T waves in lateral leads. 1

• Secondary changes in LBBB: T-wave inversion in lateral leads (I, aVL, V5-V6) where QRS is predominantly positive. 1

• Wellens syndrome: Biphasic or deeply inverted T waves specifically in V1-V3 or V1-V4, with characteristic symmetry. 2, 6, 3

Step 4: Assess Clinical Context

• Recent onset of conduction abnormality: Suggests secondary changes, especially if ST-T changes appeared simultaneously with QRS changes. 1

• History of angina with pain-free ECG: Classic for Wellens syndrome, where T-wave changes persist after chest pain resolves. 3, 5, 4

• Cardiac biomarkers: Wellens typically shows minimal or no elevation initially, though high-sensitivity troponin may be mildly positive. 3, 4

Step 5: Compare with Prior ECGs

• Secondary changes: If prior ECG showed normal conduction with normal ST-T segments, and current ECG shows new bundle branch block with concordant ST-T changes, diagnosis is secondary repolarization abnormality. 1

• Wellens syndrome: Prior ECGs may show normal findings or evolving T-wave changes over hours to weeks in the same precordial leads despite stable QRS morphology. 6, 3

Common Pitfalls and How to Avoid Them

Pitfall 1: Assuming All Anterior T-Wave Inversions Are Secondary to RBBB

• Avoidance: In RBBB, secondary T-wave inversion should be confined to V1-V2 and be relatively shallow. Deep, symmetrical inversions extending to V3-V4 with normal R-wave progression suggest Wellens syndrome, not secondary changes. 1, 7, 3

Pitfall 2: Missing Wellens Syndrome in Patients with Ventricular Hypertrophy

• Avoidance: Primary and secondary repolarization abnormalities can coexist—ventricular hypertrophy may have baseline ST-T changes, but new, deeply inverted T waves in V1-V4 that don't follow the expected pattern for hypertrophy warrant evaluation for superimposed ischemia. 1

Pitfall 3: Dismissing Biphasic T Waves as Nonspecific

• Avoidance: Biphasic T waves (Type A Wellens pattern) in V2-V3 are highly specific for critical LAD stenosis and should never be dismissed as nonspecific, especially with a history of chest pain. 2, 3, 4

Pitfall 4: Failing to Recognize Wellens During Asymptomatic Periods

• Avoidance: Wellens T-wave changes are characteristically present during pain-free intervals and may persist for weeks—absence of current symptoms does not exclude the diagnosis. 6, 3, 5

Pitfall 5: Over-Relying on Cardiac Biomarkers

• Avoidance: Wellens syndrome is defined by minimal or no biomarker elevation at presentation, but this does not indicate low risk—these patients are at extremely high risk for extensive anterior MI without urgent revascularization. 3, 5, 4

Clinical Significance and Management Implications

• Secondary ST-T changes do not indicate myocardial ischemia or require urgent intervention—they reflect altered conduction pathways and resolve when normal conduction returns. 1

• Wellens syndrome indicates critical proximal LAD stenosis (typically 80-95% stenosis) and portends anterior wall myocardial infarction in the majority of untreated cases—urgent coronary angiography and revascularization are mandatory. 2, 3, 5, 4

• Exercise stress testing is contraindicated in suspected Wellens syndrome, as it may precipitate acute MI. 4

• With successful revascularization, Wellens T-wave changes resolve and the ECG normalizes. 3, 5