Recognizing Wellens Syndrome in Emergency Medical Care – A Case Report

Introduction

Acute coronary syndrome remains one of the leading causes of mortality and morbidity globally, often requiring urgent medical intervention [1]. It is most commonly diagnosed through clinical examination, electrocardiogram (ECG) findings, and laboratory markers, but within the spectrum of this syndrome, there are subtle forms that should not be overlooked. Wellens syndrome is one such example, in which a patient may exhibit ECG changes that are not typical for myocardial ischemia, and may even have negative cardiac biomarkers [2].

Wellens syndrome, as a characteristic electrocardiographic pattern, indicates a critical stenosis in the proximal portion of the left anterior descending (LAD) coronary artery, which carries a high risk of developing an anterior wall myocardial infarction if left untreated [3]. Classic Wellens syndrome is associated with LAD sub-occlusion; however, similar changes may occur in the right coronary artery (RCA) or the left circumflex artery, as well as in lateral or posterior leads. It is also important to recognize the limitations regarding the specificity and sensitivity of Wellens-type ECG changes, as other clinical conditions and coronary lesions can mimic this pattern [4].

The diagnostic criteria for Wellens syndrome are:

Two ECG patterns have been described:

Case Report

In October 2024, a 55-year-old female patient presented to emergency medical services due to severe chest pain described as a tightening sensation radiating to the neck and back, accompanied by feelings of shortness of breath. She reported having experienced similar episodes of chest tightness earlier the same day. The initial episode began suddenly while she was at rest, lasting approximately 20 minutes, and was partially relieved by rest before recurring twice more within the same day. She denied any specific triggers, and noted that deep breathing and mild physical activity aggravated the discomfort. In her personal medical history she denied any cardiovascular or other chronic diseases, as well as any drug allergies. She reported being a smoker for the past 30 years (20 cigarettes per day) and denied alcohol consumption. She also denied illicit drug use. She had no history of hypertension, diabetes mellitus, or dyslipidemia, and there was no family history of premature coronary artery disease. At the time of examination, the patient was conscious, oriented, afebrile, non-cyanotic, non-icteric, and tachypneic, and showed no signs of hemorrhagic syndrome or peripheral lymphadenopathy. Auscultation of the lungs revealed normal breath sounds without any pathological phenomena. Cardiac auscultation showed a regular heart rhythm with no pathological murmurs and normal arterial pulsations. Her blood pressure was measured at 160/80 mmHg. Baseline laboratory investigations, including complete blood count, renal function tests, and electrolytes, were within normal limits. Differential diagnoses at this stage included unstable angina, pericarditis, and pulmonary embolism. An ECG was performed immediately, showing a sinus rhythm with a heart rate of 84 beats per minute, and no ST-segment changes (Figure 1).

Afterward, the patient was prescribed symptomatic treatment consisting of analgesics and antihypertensive medication, and was placed under observation for further monitoring.

During the monitoring, the patient reported that the pain had subsided and that she was feeling significantly better. A second, control ECG was performed after the complete relief of symptoms, which showed biphasic, inverted T waves in the precordial leads V2, V3, V4, and V5. This ECG finding can be characterized as Wellens pattern Type A (Figure 2).

Upon recognizing the Wellens pattern on the ECG, the patient was transported with medical escort to the admitting internal medicine clinic at the general hospital, where she was hospitalized in the coronary care unit.

Therapy was initiated according to the NSTEMI (non-ST-elevation myocardial infarction) protocol. Her key laboratory parameters for diagnosis were as follows: Troponin I: 459.91 pg/mL (reference value <45.20 pg/mL); pro-BNP 3252.0 pg/mL (reference value <450 pg/mL). The coronary angiography report indicated that a right transradial approach was used. The left anterior descending coronary artery (LAD) was of large caliber, supplying the anterior wall and interventricular septum, and was diffusely narrowed by 40% proximally, with 2 levels of subocclusion in the medial part, and no stenoses further along the course. The first and second diagonal branches of the LAD were of medium caliber and were ostially suboccluded, with no stenoses further along.

The left circumflex artery, of medium caliber and supplying the lateral wall, showed a 50% ostial stenosis, with no stenoses proximally. The obtuse marginal branch 1 was ostially suboccluded, and its large lateral branch was also ostially suboccluded. The obtuse marginal branch 2 had a 50% medial stenosis.

The RCA, of large caliber and supplying the inferior wall, presented a 70% medial stenosis, and suboccluded distally before the crux, with no further stenoses along its course. The patient was indicated for surgical myocardial revascularization – bypass of the LAD, ramus intermedius, circumflex artery, and RCA.

Discussion

Risk factors for Wellens syndrome are similar to those seen in acute coronary syndrome, including hypertension, diabetes, dyslipidemia, obesity, a sedentary lifestyle, and smoking. Wellens syndrome is caused by transient obstruction of the LAD. As such, Wellens syndrome is considered a pre-infarction state. Although the exact mechanism behind the characteristic ECG changes in Wellens syndrome is not fully understood, it is believed that coronary artery spasms are responsible for these specific changes. It is also believed that transmural ischemia and subsequent reperfusion cause myocardial edema, which leads to the changes seen on the ECG [7–9].

In Wellens syndrome, 2 patterns of T waves are observed, Type A and Type B. In Type A, biphasic T waves are seen in 25% of cases and are biphasically inverted, while deeply inverted T waves are found in Type B, which accounts for 75% of cases. These T waves are usually observed in the V2 and V3 leads, but they can also appear in V1, V4, V5, and V6. As the disease progresses, Type A T waves may evolve into Type B T waves. ECG patterns can develop even when patients are pain-free [7].

The patient described in this case report presented with a characteristic clinical picture of acute coronary syndrome, marked by severe chest pain described as a tightening sensation and episodes of shortness of breath. Although, according to de Zwaan et al [2], she met all the clinical criteria for the diagnosis of Wellens syndrome (a previous history of chest pain, a normal ECG during pain episodes, and typical Wellens ECG changes in the absence of pain), coronary angiography showed only moderate (40%) proximal narrowing of the LAD. This is functionally significant in the context of the patient’s symptoms and ECG findings, which were characteristic of Wellens syndrome. The most significant stenosis was found in the RCA (70%). Significant stenosis was also present in the circumflex artery (50%) and its branches. These findings suggest that Wellens-type ECG changes can occasionally be associated with multi-vessel coronary artery disease and may not always correspond to a single critical LAD lesion.

Wellens-type ECG changes are most often linked to critical proximal LAD stenosis, yet in this patient, LAD narrowing was only moderate, with severe sub-occlusive lesions present in other coronary vessels. ECG patterns can result from ischemia in non-LAD territories, including the RCA or obtuse marginal branches [10]. Such atypical presentations have also been described in other clinical contexts. Prousi et al reported a case of a patient with COVID-19 pneumonia in whom the presence of Wellens-type ECG changes enabled early initiation of NSTEMI therapy despite the absence of significant LAD stenosis on initial angiography [11]. This reinforces that ECG patterns can arise in the setting of systemic illnesses causing secondary myocardial ischemia, and highlights the importance of considering a broad differential diagnosis when interpreting these changes. The 2020 European Society of Cardiology guidelines for the management of acute coronary syndromes without persistent ST-segment elevation emphasize that ECG changes alone should not be relied upon to identify the culprit vessel, especially in multi-vessel disease, which may explain the findings in this case [10].

Given this, can Wellens syndrome still be diagnosed based on ECG changes and clinical criteria, despite only moderate stenosis of the LAD artery?

Conclusions

Accurate and timely recognition of Wellens syndrome plays a crucial role in the management of every patient presenting to emergency services with chest pain, as Wellens syndrome can rapidly progress to myocardial infarction. This case highlights that Wellens-type ECG changes may occur even in the presence of moderate LAD stenosis, particularly when other significant coronary lesions are present. Integrating ECG interpretation with comprehensive angiographic assessment is essential for accurate diagnosis and risk stratification. Continuous monitoring, repeated ECG evaluation during pain-free phases, and early intervention remain key to improving patient outcomes. This case underlines the importance of considering multi-vessel disease in the differential diagnosis of Wellens syndrome, thereby broadening clinical awareness and guiding optimal management.

Given the multi-vessel involvement and the patient’s clinical presentation, the Wellens-type ECG changes were interpreted as a manifestation of combined coronary artery disease rather than isolated critical LAD stenosis. This aligns with previously reported cases of pseudo-Wellens pattern in multi-vessel disease [9].