Wellens’ syndrome describes a characteristic pattern of ECG T-wave changes in association with critical narrowing of the left anterior descending coronary artery. Failure to diagnose this condition, with subsequent inappropriate management, may have fatal consequences. A case of Wellens’ syndrome is reported in a young man presenting with “atypical chest pain” and the significance of its prompt recognition is discussed.
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A man in his mid-30s who had previously been fit and well presented with a one-week history of intermittent central chest pain. This was localised, tight in nature and each episode lasted from a few seconds to a minute. There were no associated symptoms and his pain was not precipitated by exertion. His only positive cardiac risk factor was smoking. He was initially seen in an emergency department (ED) and after baseline investigations (including ECG), he was reassured and discharged home with a diagnosis of gastrointestinal reflux. The frequency and severity of the episodes of pain increased over the following days at which point he re-presented to a different ED.
At the time of his second presentation, he was pain free. Examination was unremarkable. His initial ECG showed sinus rhythm, normal QRS and biphasic T waves in leads V2–V3 (fig 1). He developed chest pain while in the ED and a repeat ECG revealed frequent ventricular ectopics (fig 2). He was admitted for observation and remained pain free. Cardiac enzyme levels, including troponin I, were within the normal range. The patient underwent a Bruce protocol exercise tolerance test (ETT). This was terminated at approximately 9 minutes due to chest discomfort and pathological ECG changes showing greater than a 2 mm ST depression in leads V5–V6.
The patient was transferred to the cardiac catheterisation laboratory for coronary angiography. This revealed a single vessel disease with 90% stenosis of the proximal left anterior descending coronary artery (LAD). Ventriculography demonstrated a normal left ventricle with an ejection fraction of 85%. He underwent successful transluminal coronary angioplasty with stent deployment.
At 3 months follow-up, the patient was well with no recurrence of his chest pain.
Chest pain is one of the chief presenting complaints among patients attending ED. ED clinicians must be able to evaluate these patients and identify those with an underlying life-threatening cause. Although junior physicians are often able to recognise ECG changes associated with ischaemic disease,1 many are still unaware of Wellens’ syndrome and fail to realise its prognostic significance. Without prompt diagnosis and aggressive intervention, patients with Wellens’ syndrome may go on to develop extensive anterior wall myocardial infarction, the majority occurring within a matter of days.2
The characteristic T-wave abnormalities suggestive of LAD stenosis were first reported by Wellens and colleagues in 1982.2 This was substantiated by a larger prospective study in 1988, which showed that in the subgroup of patients admitted with unstable angina who demonstrated these ECG changes, coronary angiography confirmed at least a 50% narrowing of the LAD in all these patients.3 In addition, the initial study also showed that 75% of patients who were medically treated without angiographic investigation went on to develop an extensive anterior wall myocardial infarction within a mean of 8.5 days.2 These results imply that Wellens’ T-wave pattern is highly specific for identifying high-risk patients.
Two patterns of T-wave changes are indicative of Wellens’ syndrome. In 75% of cases the T waves in the precordial leads (V1–V4) are deeply inverted with symmetric contours.2 3 4 This T-wave pattern is well recognised by junior doctors. In the less common, poorly recognised variant, the T wave has a characteristic upsloping followed by downsloping pattern in V2–V3. This is described as a biphasic T wave, which was the finding in our patient (fig 1).
The criteria for Wellens’ syndrome are as follows: previous history of chest pain; normal or minimally elevated cardiac enzymes; no pathological precordial Q waves or loss of R waves; little or no elevation of ST segment; symmetric and deep T-wave inversion or biphasic T-wave leads V2–V3 (may extend to V5 and V6); tight proximal LAD stenosis.
In our case report, the patient was young and described a history of chest pain that was not typical of ischaemic heart disease. With normal cardiac enzyme levels, it is easily understandable that a junior ED doctor may erroneously make a diagnosis of “atypical chest pain” and attribute ECG findings to “non-specific T-wave changes”.
The initial ECG clearly shows biphasic T waves in V2–V3. It is important to note that this occurred during a pain-free period.5 This is characteristic of Wellens’ syndrome. Ventricular arrhythmias were present during an episode of chest pain in our patient. This is not classic of Wellens’ syndrome in which the T-wave changes typically normalise at this time.5 6
ETT is contraindicated and a fatal outcome has been reported in a patient with Wellens’ syndrome who underwent the test.4
In our case the diagnosis was initially missed and despite being admitted on the second occasion with the diagnostic ECG pattern, the patient was sent for an ETT. This reflects the lack of awareness among doctors of Wellens’ syndrome and a poor understanding of the significant implications of the diagnosis.
Our case report highlights the problem that Wellens’ syndrome continues to be a diagnostic pitfall. Its recognition is invaluable in the risk stratification of patient with unstable angina and allows early, potentially life-saving interventions.
Competing interests None.
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