Recognizing Wellens Syndrome in a Family Practice Setting

    


    


    Figure 1: Arrows depict T-wave inversion pattern in V2-V5, but no ST-Elevation Myocardial Infarction (STEMI) pattern.

    

In the Emergency Department (ED), the patient denied any chest pain or shortness of breath. The ECG performed in the ED was interpreted as sinus bradycardia with bifascicular block. Cardiac enzymes and electrolytes were within normal limits. The patient was discharged home with outpatient follow-up with their primary care physician and referral to cardiology.

Subsequent to the cardiology office visit, the patient underwent monitoring with a Holter monitor for a total duration of 7 days. Over this monitoring period, the patient experienced 4 episodes of ventricular tachycardia and 42 episodes of supraventricular tachycardia. Notably, no significant pauses or instances of high-grade atrioventricular block were observed during this monitoring period.

Following the 7-day Holter monitor evaluation, the patient underwent a pharmacological stress test, which revealed a left ventricular perfusion abnormality. Of note, there were no indications of ECG changes suggestive of ischemia, and the patient did not report any symptoms during the stress test. Given the abnormal findings on both the Holter monitor and the stress test, the patient was scheduled for a heart catheterization procedure with the possibility of angioplasty. During the heart catheterization, a severe stenosis exceeding 99% was identified in the midportion of the LAD. Subsequently, an angioplasty using a standard balloon was performed, and a drug-eluting stent was successfully placed in the midportion of the LAD which resolved the obstruction.

Discussion

The risk factors associated with Wellens syndrome overlap with those of conventional acute coronary syndrome, encompassing conditions such as diabetes mellitus, hypertension, increased age, hyperlipidemia, and smoking [1-3]. In line with other documented cases of Wellens syndrome [1-3], our patient shared similar risk factors.

Wellens syndrome represents a pre-infarction state. However, due to unstable coronary perfusion, these patients face a considerably elevated risk of a substantial anterior wall myocardial infarction or potential death [1-3].

While the precise electrophysiological mechanism underpinning the ECG alterations seen in Wellens syndrome remains uncertain, some hypotheses that coronary artery spasms and myocardial stunning may be account for the observed ECG variations [1-3]. Conversely, other researchers propose that the ECG modifications stem from repetitive transmural ischemia-perfusion episodes that may eventually culminate in myocardial infarction [3]. The possibility of plaque rupture also exists, which could swiftly result in complete obstruction of the left anterior descending coronary artery, precipitating a myocardial infarction.

Wellens syndrome presents itself in two distinct patterns, classified as Type A and Type B. Type A is characterized by biphasic T waves, displaying an initial positive deflection followed by terminal negativity, a pattern observed in about 25% of cases [1-2]. Conversely, Type B is characterized by symmetrically inverted T waves, a presentation seen in approximately 75% of cases [2-3]. In our patient's case, the presence of symmetrically inverted T waves in V2-V5 aligns most closely with the characteristics of Wellens syndrome Type B.

This patient displayed a pain-free presentation during evaluation in the outpatient primary care setting, as well as when further assessed in the emergency department on the same day. This aligns with the common observation that patients with Wellens syndrome frequently present to the emergency department without chest pain and often exhibit normal or only slightly elevated cardiac enzyme levels [1-3]. The absence of pain or clear signs of acute infarction led the emergency medicine team to refrain from immediate and aggressive interventions. This ominous and critical clinical presentation has been documented in several prior cases of Wellens syndrome [6-8]. Consequently, it becomes imperative for clinicians working in both inpatient and outpatient settings to understand and recognize Wellens syndrome's ECG patterns. This knowledge equips clinicians to make quicker and more informed clinical decisions, facilitating the implementation of essential aggressive interventions and ultimately improving patient outcomes and mortality rates.

Early intervention, facilitated by a multidisciplinary management approach encompassing evaluation, diagnosis, and treatment of Wellens Syndrome, has been well-documented to significantly enhance patient outcomes across various clinical settings [6-8]. For non-ST elevation acute coronary syndrome, particularly in patients without chest pain, like the one discussed in our case report, early percutaneous coronary interventions stand as the preferred treatment modality [1-3]. The Wellens pattern on ECG will typically return to baseline after treatment, as was clearly demonstrated in our patient's ECG eight weeks after the angioplasty procedure (Figure 2). Subsequent outcomes following catheterization have proven successful, mirroring our patient's experience, when appropriate interventions were undertaken. Delay in definitive treatment may precipitate an anterior wall infarction and potentially result in a fatal outcome [1- 3,9].

    


    


    Figure 2: ECG eight weeks after angioplasty procedure. Note the absence of T-wave changes previously demonstrated on the initial ECG prior to the angioplasty procedure.