Wellen’s Syndrome

Abishwin¹, Vetri Karunakaran²

¹Resident – Emergency Medicine, Kauvery hospital, Chennai

²Consultant – Emergency Medicine, Kauvery hospital, Chennai

Background

Wellen’s 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).Wellens syndrome refers to the 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. It is alternatively known as anterior, descending, T-wave. Recognizing this syndrome is crucial for clinicians, as it demands urgent intervention to prevent a potentially catastrophic outcome.

This article aims to provide a comprehensive understanding of Wellen’s syndrome, including its clinical significance, diagnostic criteria, management, and implications for patient care

Case presentation

A 49-year gentleman was brought to our ER around 3:20pm with C/o retro sternal burning sensation ×2 day followed by sudden onset of retro sternal chest pain since 3 pm next day, dull aching, not radiating, lasting for 20 min resolved after taking T. Dolo 650mg

H/o sweating (+)

Patient was asymptomatic since and came for further management

No H/O palpitation, orthopnoea, SOB, fever, LOC, syncope, giddiness, bowel or bladder disturbances

Comorbidities: none

No family h/o CAD, no drug/food allergies

Smoker, non-alcoholic

On examination

Patient was conscious, oriented, afebrile, hydration fair

PICCLE: Negative

Vitals

HR	113/min
BP	130/80 mmHg
RR	20/min
SpO2	99% in RA
CBG	105
GCS	E4V5M6 (15/15)
Temp	98.2°F

Systemic examination

CVS: S1S2 +, no murmur, JVP – normal

RS: B/L AE +. NVBS, no added sounds

PA: soft, non-tender, no organomegaly, BS +

CNS: moving all 4 limbs, NFND

Treatment at ER

Propped up position / IV Access

Maintaining Spo2 >94%

IV cannula secured –

Inj. Paracetamol 1g IV stat

Inj. Pantoprazole 40mg IVstat

Investigations advised

ECG, Trop-I, Echo

Trop I– 5.11 (positive)

Echo

Normal sized cardiac chambers

Trivial MR mild LVH

No TR / PAH

RWMA + LV apex hypokinetic

Normal LV systolic dysfunction (EF-55%)

Normal IVC size

Cardio team informed and PT shifted for CAG ASAP

CAG 95% occlusion in Proximal LAD

Plan: PTCI / Stenting to proximal LAD

Discussion

1. Pathophysiology

Wellens syndrome represents a pre-infarction state due to 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 and supplies the anterior wall of the heart, including both ventricles, as well as the septum.

A lesion in the proximal LAD can have severe consequences, as suggested by the common nickname given to this lesion: “widow maker.”

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

2. Etiology

The causes of Wellens syndrome are similar to any conditions that cause cardiac heart disease, including the following:

Atherosclerotic plaque
Coronary artery vasospasm
Hypoxia
Increase in cardiac demand

3. Risk factors

Diabetes mellitus
Family history of coronary heart disease
Hypertension
Increased age
Hyperlipidaemia
Metabolic syndrome
Occupational stress
Smoking

4. Diagnostic criteria

Diagnostic criteria for Wellens syndrome are as follows:

Deeply inverted T waves in leads V2 and V3 (may also be seen in leads V1, V4, V5, and V6) OR biphasic T waves (with initial positivity and terminal negativity) in V2 and V3
Isoelectric or minimally elevated ST segment, less than 1 mm (in other words, no signs of an acute anterior wall myocardial infarction)
Preservation of precordial R-wave progression and no precordial Q waves (in other words, no signs of old anterior wall infarct)
Recent history of angina
ECG pattern present in a pain-free state
Normal or slightly elevated cardiac markers

5. Types

Here are two patterns of T-wave abnormality in Wellens syndrome:

Type A – Biphasic, with initial positivity and terminal negativity (25% of cases)

Type B – Deeply and symmetrically inverted (75% of cases)

Treatment

ABC Approach
Initiate medical therapy to alleviate symptoms, stabilize the patient,
ECG– Serial examinations and pain-free tracings may be helpful
Administer aspirin or other antiplatelet agents to inhibit platelet aggregation and reduce the risk of thrombosis
Investigations (TROP I, ECHO, CBC, RFT, Blood Grouping, Serology)
Keep cardio team in loop and Shift the Pt. for cardiac interventions (CAG – PTCA/ CABG) ASAP

Key take aways

Early recognition of Wellens Syndrome

Recognize the characteristic ECG changes of Type 1 Wellens Syndrome (deeply inverted T waves in V2-V3) which are indicative of critical LAD stenosis and an impending anterior myocardial infarction.

Prompt and aggressive management

Initiate rapid and appropriate medical therapy including antiplatelets, anticoagulation, and beta-blockers.
Prioritize urgent coronary angiography to confirm the diagnosis and facilitate timely revascularization.

Importance of risk factor modification

Emphasize the importance of smoking cessation in reducing cardiovascular risk.
Manage other modifiable risk factors such as hypertension and hyperlipidaemia aggressively.

Emergency Department coordination

Effective communication and coordination with the cardiology team are crucial for timely intervention.
Ensure comprehensive discharge planning including medication adherence, lifestyle

References

De Zwaan C, Bar FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr. 103(4 Pt 2):730-6.
Nisbet BC, Zlupko G. Repeat Wellens’ syndrome: case report of critical proximal left anterior descending artery restenosis. J Emerg Med. 2010 Sep. 39(3):305-8
Moore KL, Dalley AF. Thorax. Clinically Oriented Anatomy. 4th ed. Baltimore, Maryland: Lippincott Williams & Wilkins; 1999. 135.
de Zwaan C, Bar FW, Janssen JH, et al. Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. Am Heart J. 1989 Mar. 117(3):657-65
Hsu YC, Hsu CW, Chen TC. Type B Wellens’ syndrome: Electrocardiogram patterns that clinicians should be aware of. Ci Ji Yi Xue Za Zhi. 2017 Apr-Jun. 29(2):127-8
Y-Hassan S. The pathogenesis of reversible T-wave inversions or large upright peaked T-waves: Sympathetic T-waves. Int J Cardiol. 2015 Jul 15. 191:237-43.
Singh B, Singh Y, Singla V, Nanjappa MC. Wellens’ syndrome: a classical electrocardiographic sign of impending myocardial infarction. BMJ Case Rep. 2013 Feb 18. 2013
Sowers N. Harbinger of infarction: Wellens syndrome electrocardiographic abnormalities in the emergency department. Can Fam Physician. 2013 Apr. 59(4):365-6
Rhinehardt, J., Brady, W. J., Perron, A. D., & Mattu, A. (2002). Electrocardiographic manifestations of Wellens’ syndrome. The American Journal of Emergency Medicine, 20(7), 638-643.
Fuster, V., Ryden, L. E., Cannom, D. S., Crijns, H. J., Curtis, A. B., Ellenbogen, K. A., … & Smith, S. C. (2006). ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines. European Heart Journal, 27(16), 1979-2030.

Dr. Vetri Karunakaran
Consultant – Emergency Medicine

Wellen’s Syndrome

Wellen’s Syndrome

Abishwin1, Vetri Karunakaran2

Journals

Abishwin¹, Vetri Karunakaran²