Discussion

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.

The recommendation now for patient with Wellens’ syndrome is for early cardiac catheterisation and subsequent angioplasty or coronary bypass surgery.4 5

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.