Wellens Syndrome

Wellens syndrome is a pattern of characteristic T-wave changes in V2 and V3 (sometimes V1 to V4) that signals critical stenosis of the proximal left anterior descending artery. It is found in the pain free interval after an episode of unstable angina, and it predicts extensive anterior infarction within days to weeks if untreated.

It is found in about 14 to 18% of patients admitted with unstable angina. Cardiac markers are normal or slightly raised, and the ECG does not meet ST-elevation criteria, so the pattern is easy to dismiss.

Two types exist. Type A (about 25%) shows biphasic T waves with an initial positive and terminal negative deflection. Type B (about 75%) shows deeply and symmetrically inverted T waves.

Without revascularisation, most patients develop anterior infarction, often within a week.

Pathophysiology.

A critical proximal left anterior descending stenosis, often with transient thrombosis or spasm, causes intermittent ischaemia that resolves spontaneously. Reperfusion changes ventricular repolarisation, and the T-wave inversion reflects ischaemia with reperfusion of the anterior wall.

Because the lesion is a thrombus prone proximal plaque with a large myocardial territory at risk, plaque disruption can produce anterior infarction and cardiogenic shock.

A recent history of anginal chest pain, which usually has resolved when the ECG is recorded. Examination is often normal. Some patients have ongoing pain or heart failure. Risk factors are those of coronary disease.

Wellens syndrome is diagnosed by all of the following:

• Characteristic T-wave changes in V2 and V3 (biphasic type A, or deeply inverted type B).
• Isoelectric or minimally elevated ST segment (under 1 mm).
• No precordial Q waves and normal precordial R-wave progression.
• Recent anginal pain, now settled.
• Normal or only slightly raised cardiac troponin.

Further tests: serial ECGs and troponin (high sensitivity assay), echocardiography (anterior hypokinesia may be mild), and early coronary angiography. Exercise stress testing and pharmacological stress testing are contraindicated because they can precipitate infarction.

Differential diagnosis.

• Apical hypertrophic cardiomyopathy and left ventricular hypertrophy with strain.
• Pulmonary embolism, Takotsubo syndrome and myocarditis.
• Raised intracranial pressure and subarachnoid haemorrhage (cerebral T waves).
• Normal juvenile T-wave inversion, bundle branch block, digoxin effect and Wellens like patterns from other causes.

Treat as high risk unstable coronary syndrome. Admit to a coronary care unit with continuous ECG monitoring and bed rest. Do not perform stress testing.

Antithrombotic therapy.

• Aspirin 150 to 300 mg orally loading dose, then 75 to 100 mg daily.
• Ticagrelor 180 mg orally loading dose then 90 mg twice daily (or prasugrel 60 mg loading dose after anatomy is known, then 10 mg daily, 5 mg when weight is under 60 kg or age is 75 or over; or clopidogrel 600 mg loading dose, then 75 mg daily).
• Anticoagulation: enoxaparin 1 mg/kg subcutaneously every 12 hours (once daily when creatinine clearance is under 30 mL/min), or fondaparinux 2.5 mg subcutaneously daily (avoid when creatinine clearance is under 20 mL/min), or unfractionated heparin 60 to 70 units/kg bolus (maximum 5000 units) then 12 to 15 units/kg/h (maximum 1000 units/h), aPTT 1.5 to 2.5 times control. Use unfractionated heparin when angiography is imminent and in severe renal impairment.

Anti-ischaemic therapy.

• Glyceryl trinitrate 400 to 800 microgram sublingually for pain, or 10 to 200 microgram/min intravenously, increased every 5 to 10 minutes, avoiding systolic blood pressure under 90 mmHg.
• Metoprolol 25 to 50 mg orally twice daily (avoid in heart failure, hypotension, bradycardia or block).
• Atorvastatin 80 mg orally once daily from admission.

Early invasive strategy. Coronary angiography within 24 hours. Immediate angiography (under 2 hours) for recurrent or refractory pain, haemodynamic instability, arrhythmia or heart failure. Revascularise the proximal left anterior descending lesion by percutaneous intervention, or bypass grafting for left main or multivessel disease by heart team decision.

Secondary prevention. Dual antiplatelet therapy for 12 months after an acute coronary syndrome (shorter in high bleeding risk), then single antiplatelet therapy. Atorvastatin 40 to 80 mg daily with ezetimibe 10 mg daily if LDL cholesterol stays over 1.4 mmol/L. Ramipril 2.5 mg daily titrated to 10 mg for ejection fraction 40% or under, hypertension, diabetes or kidney disease. Omeprazole 20 mg daily while on dual antiplatelet therapy. Smoking cessation, blood pressure and glucose control, and cardiac rehabilitation.

Monitoring. Continuous ECG, repeat ECG every 6 to 8 hours and with any pain, troponin at 0 and 1 to 3 hours then repeated, echocardiography within 48 hours, creatinine and platelets daily on heparin, T-wave evolution after revascularisation.

Referral and escalation. Refer every patient on the same day for cardiology review and angiography. Treat recurrent pain, ST elevation, arrhythmia or heart failure as an emergency requiring immediate catheter laboratory activation.

Special groups.

• Older adults and frailty: lower fondaparinux and enoxaparin doses by renal function; assess bleeding risk before dual antiplatelet therapy.
• Kidney impairment: use unfractionated heparin when creatinine clearance is under 30 mL/min, and limit contrast.
• Pregnancy: spontaneous coronary artery dissection should be considered; avoid fibrinolysis and manage in a tertiary centre.
• Region specific: where angiography is not available within 24 hours, treat medically and transfer early.