Background
Wellens syndrome was first described in the early 1980s by de Zwaan, Wellens, and colleagues, who identified a subset of patients with unstable angina who had specific precordial T-wave changes and subsequently developed a large anterior wall myocardial infarction (MI). [1] Wellens syndrome refers to these specific electrocardiographic (ECG) abnormalities in the precordial T-wave segment, which are associated with critical stenosis of the proximal left anterior descending (LAD) coronary artery.
Wellens syndrome is also referred to as LAD coronary T-wave syndrome. [2, 3] Syndrome criteria include the following:
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Characteristic T-wave changes
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History of anginal chest pain
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Normal or minimally elevated cardiac enzyme levels
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ECG without Q waves, without significant ST-segment elevation, and with normal precordial R-wave progression
Recognition of this ECG abnormality is of paramount importance because this syndrome represents a preinfarction stage of coronary artery disease (CAD) that often progresses to a devastating anterior wall MI.
Pathophysiology
Wellens syndrome represents critical stenosis of the proximal LAD artery. The LAD arises from the left coronary artery and travels in the interventricular groove along the anterior portion of the heart to the apex. This groove is situated between the right and left ventricles of the heart. The LAD gives rise to 2 main branches, the diagonals and the septal perforators. [4]
A lesion in the proximal LAD can have severe consequences, as suggested by the common nickname given to this lesion: “widow maker.” The LAD supplies the anterior wall of the heart, including both ventricles, as well as the septum. An occlusion in this vessel can result in serious ventricular dysfunction, thus placing the patient at serious risk for congestive heart failure (CHF) and death.
Etiology
Wellens syndrome is a preinfarction stage of CAD. Thus, the causes of Wellens syndrome are similar to the conditions that cause CAD, including the following:
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Atherosclerotic plaque
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Coronary artery vasospasm (cocaine is one possible cause)
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Increased cardiac demand
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Generalized hypoxia
Risk factors for Wellens syndrome are essentially those of CAD and include the following:
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Smoking history
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Diabetes mellitus
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Hypertension
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Increased age
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Hypercholesterolemia
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Hyperlipidemia
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Metabolic syndrome
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Family history of premature heart disease
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Occupational stress
Epidemiology and Prognosis
The characteristic ECG pattern of Wellens syndrome is relatively common in patients who have symptoms consistent with unstable angina. Of patients admitted with unstable angina, this ECG pattern is present in 14-18%. [1, 5]
Wellens syndrome represents critical proximal LAD disease; accordingly, its natural progression leads to anterior wall MI. This progression is so likely that medical management alone is not enough to stop the natural process. Evolution to an anterior wall MI is rapid, with a mean time of 8.5 days from the onset of Wellens syndrome to infarction. [1]
If anterior wall MI occurs, there is the potential for substantial morbidity or mortality. Thus, it is of utmost importance to recognize this pattern early.
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This ECG represents a patient who came in to the emergency department with 8/10 chest pain. The patient had old right bundle-branch block (RBBB) and left ventricular hypertrophy (LVH), and this compared similarly to his previous ECGs.
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Classic Wellens syndrome T-wave changes. ECG was repeated on a patient who came in to the emergency department with 8/10 chest pain after becoming pain free secondary to medications. Notice the deep T waves in V3-V5 and slight biphasic T wave in V6 in this chest pain– free ECG. The patient had negative cardiac enzyme levels and later had a stent placed in the proximal left anterior descending (LAD) artery.
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A 57-year-old with 4/10 pressurelike chest pain. Improvement with treatment by EMS. The patient had this ECG on arrival. Notice perhaps the beginning of a small biphasic T wave in V2.
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Pain-free ECG of a 57-year-old patient who presented with 4/10 pressurelike chest pain. Notice after the patient was treated with medications and pain subsided, the ECG shows T-wave inversion in V2 and biphasic T waves in V3-V5. This more closely resembles the less common presentation of Wellens syndrome with a biphasic T-wave pattern. This patient had a cardiac catheterization that showed a subtotal occlusion of the proximal left anterior descending (LAD) artery, which was stented, and the patient did well.
