Harbinger of infarction

Case description

A 79-year-old woman with a history of asthma and hypertension presents to the ED complaining of increasing shortness of breath (SOB) and productive cough for the past 3 days. She denies chest pain, syncope, presyncope, hemoptysis, abdominal pain, or nausea and vomiting. Her respiratory rate is 20 breaths/min; oxygen saturation is 88% on room air. Vital signs are otherwise within normal limits and she is afebrile. Results of routine bloodwork, including troponin testing, are unremarkable; a chest x-ray scan shows chronic hyperinflation without active intrathoracic pathology. Results of an electrocardiogram (ECG) are interpreted as “nonspecific T-wave abnormalities” (Figure 1). No previous ECG is available for comparison. The clinical impression is a chronic obstructive pulmonary disease exacerbation and is managed accordingly. The next morning her SOB has improved and she is discharged. She returns within 24 hours with increasing SOB and develops central chest pain while in the ED. Another ECG is completed (Figure 2).

While the patient’s second ECG (Figure 2) demonstrates an obvious ST-segment elevation myocardial infarction (MI) in the anterior leads, a closer inspection of her initial ECG (Figure 1) reveals anterior lead T-wave abnormalities in keeping with Wellens syndrome.

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Figure 1

Electrocardiographic interpretation: Sinus with a first-degree atrioventricular block; right atrial enlargement; left ventricular hypertrophy, ST-segment elevation in leads V₂–V₃ (approximately 1 mm); biphasic T waves in leads V₂–V₄; and U waves in leads V₂–V₄.

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Figure 2

Anteroseptal ST-segment elevation myocardial infarction

Wellens syndrome

Patients with Wellens syndrome (or left anterior descending [LAD] coronary T-wave syndrome) show a collection of ECG findings most commonly recognized as deeply inverted T waves across the anterior precordial leads, often while asymptomatic. In 1982, de Zwaan et al first demonstrated that these ECG abnormalities correlated with high-grade lesions of the LAD artery in patients with unstable angina.¹ Box 1 shows the criteria for Wellens syndrome.

Wellens syndrome is represented by 2 different types of T-wave abnormalities, both suggesting substantial “preinfarction” lesions. Physicians working in the ED must be alert for deeply inverted T waves across the anterior precordial leads; however, this finding might only represent 75% to 80% of Wellens syndrome cases; the remaining 20% to 25% show much more subtle findings of smaller biphasic T waves across the anterior leads, most commonly leads V₂ to V₃ and occasionally leads V₁ and V₄ to V₆.²

While the differential diagnosis for T-wave inversions is broad, abnormalities found in Wellens syndrome are particularly concerning because they often occur in asymptomatic patients, they might pseudonormalize in those presenting with cardiac chest pain or dyspnea, and they will not typically elevate cardiac enzymes. The concern is that ECGs might be interpreted as “nonspecific ST-segment or T-wave changes” in patients with identified risk factors for coronary artery disease who are then sent for outpatient EST.³

Numerous cases in the literature describe patients with these ECG abnormalities sent for EST who experience fatal MI during testing.^2,4,5 As cardiac enzyme test results are often negative or within the upper limit of normal, ECG interpretation might be the only clue to the safest disposition of these patients. These ECG abnormalities can be found in a range of patients, including those as young as 39 years of age⁶ and those with previously stented LAD lesions or recurrent Wellens syndrome.⁷

While medical management might alleviate symptoms, these lesions often progress quickly to MI of a large territory of the anterior wall; in the original study, 75% of patients who received medical management without cardiac catheterization progressed to MI in a mean of 8.5 days.¹ If these patients are identified in the ED, they should be sent for cardiology consultation and should not be discharged or sent for EST. These ECG abnormalities alone, even if symptoms resolve, warrant cardiac catheterization.⁵

While the pathophysiology of Wellens syndrome ECG manifestations in relation to proximal LAD lesions is not fully understood, and it has been suggested that development of T-wave inversion with resolution of symptoms represents a phase of reperfusion, a relationship between ECG repolarization abnormalities and left ventricular myocardial edema has also been proposed; this might explain cases of T-wave abnormalities similar to those in Wellens syndrome associated with reversible left ventricle dysfunction, such as Takotsubo cardiomyopathy or intracranial bleeding, rather than just nonreversible ischemic damage.⁸

Regardless of the underlying mechanism, ED physicians must consider the ECG manifestations of Wellens syndrome in determining the safest disposition of patients being assessed for coronary artery disease.

Case resolution

The patient’s condition deteriorates. She becomes hypotensive and is intubated owing to impending respiratory failure. She is taken for cardiac catheterization and the results show a critical lesion of the proximal LAD, which is stented. She is admitted to the critical care unit and is discharged after an uneventful recovery.