What is the appropriate acute management for a pain‑free patient with Wellen syndrome characterized by deep symmetric T‑wave inversions in V2‑V3 and minimal ST‑segment elevation?

Wellens Syndrome: Urgent Management Protocol

A pain-free patient with Wellens syndrome—characterized by deep symmetric T-wave inversions in V2-V3—requires immediate coronary angiography with revascularization, not stress testing or conservative management, because this ECG pattern indicates critical proximal LAD stenosis with imminent risk of massive anterior wall myocardial infarction. 1

Immediate Recognition and Risk Assessment

Wellens syndrome is a pre-infarction state that will progress to extensive anterior wall MI in the majority of untreated cases, making early recognition life-saving. 2 The absence of chest pain at presentation is typical and reflects the presence of collateral circulation, but does not reduce risk. 1

Diagnostic ECG Criteria

• Deep symmetric T-wave inversions ≥2 mm in leads V2-V4 (often extending to V5) are the hallmark finding. 1, 3
• Biphasic T-waves in V2-V3 represent an alternative pattern (Type A Wellens), while deeply inverted T-waves represent Type B. 4, 2
• QT prolongation frequently accompanies these T-wave changes. 1
• The ECG pattern is highly specific for critical proximal LAD stenosis with anterior wall hypokinesia present in approximately 88% of cases. 5

Critical Clinical Context

• Patients typically present with recent chest pain that has resolved at the time of evaluation. 3, 6
• Cardiac biomarkers may be normal or minimally elevated on initial presentation. 3, 2
• The ECG pattern may persist for days to weeks after symptom resolution. 6

Immediate Management Steps (First 10 Minutes)

1. Establish IV access and continuous cardiac monitoring immediately. 1
2. Administer aspirin 162-325 mg without delay. 1
3. Measure vital signs and assess hemodynamic stability. 1
4. Obtain serial cardiac biomarkers (high-sensitivity troponin), though normal values do not exclude the diagnosis. 7, 2
5. Initiate dual antiplatelet therapy (aspirin plus P2Y12 inhibitor such as ticagrelor or prasugrel). 8, 3
6. Start anticoagulation (unfractionated heparin or enoxaparin). 8
7. Administer statin therapy immediately. 3

Definitive Management: Urgent Invasive Strategy

Proceed directly to urgent coronary angiography within hours, not days, regardless of TIMI risk score or biomarker levels. 1 This is a Class I indication for immediate invasive management under ESC guidelines for non-ST-elevation ACS with ongoing ischemia. 7

Why Urgent Angiography Is Mandatory

• Revascularization reverses both the T-wave inversions and wall motion abnormalities, preventing progression to massive anterior MI. 5, 1
• Medical management alone carries high risk of progression to extensive myocardial infarction with marked left ventricular dysfunction and death. 5, 9
• The critical stenosis is typically located in the proximal or mid-LAD artery. 1, 4

Revascularization Options

• Percutaneous coronary intervention (PCI) with drug-eluting stents is the primary approach for isolated LAD lesions. 3, 2
• Coronary artery bypass grafting (CABG) should be considered for multivessel disease. 1, 4
• Intravascular ultrasound may be used to confirm plaque rupture and guide stent sizing. 3

Critical Contraindications and Pitfalls

Do NOT Perform Stress Testing

Stress testing is contraindicated and dangerous in Wellens syndrome—these patients require direct angiography. 1 Exercise testing may precipitate acute MI in this high-risk population. 2

Do NOT Administer Fibrinolytic Therapy

Fibrinolytic therapy is contraindicated in this non-STEMI presentation and will not address the underlying critical stenosis. 1

Do NOT Delay for Risk Stratification

Traditional risk scores (TIMI, GRACE) should not delay angiography in patients with this specific ECG pattern, as Wellens syndrome represents a distinct high-risk entity. 1

Essential Differential Diagnoses to Exclude

While proceeding to angiography, consider these mimics:

• Intracranial hemorrhage produces similar deep T-wave inversions with QT prolongation; obtain focused neurological examination. 5, 1
• Takotsubo cardiomyopathy will show normal coronaries on angiography with apical ballooning on echocardiography. 1
• Pulmonary embolism may cause right-sided precordial T-wave changes; assess for dyspnea, tachycardia, and hypoxia. 5, 1
• Tricyclic antidepressant or phenothiazine toxicity can cause deep T-wave inversions; review medication history. 5

Post-Revascularization Management

• Beta-blocker therapy should be initiated as tolerated. 1
• ACE inhibitor or ARB should be started, particularly if anterior wall dysfunction is present. 1
• High-intensity statin therapy should be continued. 3
• Dual antiplatelet therapy for 12 months post-PCI. 3
• Successful revascularization typically results in complete resolution of symptoms and ECG changes. 1

Anatomical and Pathophysiological Insights

• The presence of collateral circulation explains why patients are often pain-free at presentation despite critical stenosis. 1
• Plaque rupture with thrombosis is the typical underlying pathology. 3
• The ECG pattern reflects reperfusion injury after transient occlusion, not ongoing ischemia, which is why biomarkers may be normal. 5

Key Prognostic Points

• Early recognition and revascularization prevent progression to extensive anterior MI in the vast majority of cases. 3, 2
• Delayed or missed diagnosis results in massive anterior wall infarction with marked left ventricular dysfunction and high mortality. 9, 2
• The spectrum of Wellens syndrome is wide, with biphasic T-waves being the rarest and most easily missed pattern. 2