Wellens Syndrome
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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:
Characteristic T-wave changes
History of anginal chest pain
Normal or minimally elevated cardiac enzyme levels
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.
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.
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:
Atherosclerotic plaque
Coronary artery vasospasm (cocaine is one possible cause)
Increased cardiac demand
Generalized hypoxia
Risk factors for Wellens syndrome are essentially those of CAD and include the following:
Smoking history
Diabetes mellitus
Hypertension
Increased age
Hypercholesterolemia
Hyperlipidemia
Metabolic syndrome
Family history of premature heart disease
Occupational stress
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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Patel K, Alattar F, Koneru J, Shamoon F. ST-elevation myocardial infarction after pharmacologic Persantine stress test in a patient with Wellens’ syndrome. Case Rep Emerg Med. 2014. 2014:530451. [Medline]. [Full Text].
Moore KL, Dalley AF. Thorax. Clinically Oriented Anatomy. 4th ed. Baltimore, Maryland: Lippincott Williams & Wilkins; 1999. 135.
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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. [Medline].
Lin AN, Lin S, Gokhroo R, Misra D. Cocaine-induced pseudo-Wellens’ syndrome: a Wellens’ phenocopy. BMJ Case Rep. 2017 Dec 14. 2017:[Medline].
Abuarqoub A, Naranjo M, Shamoon F. Myocardial bridging with left ventricular hypertrophy presenting as Wellens pattern. Ann Transl Med. 2017 Oct. 5(20):401. [Medline]. [Full Text].
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Benjamin B Mattingly, MD Assistant Professor, Department of Emergency Medicine, Tufts University School of Medicine, Baystate Medical Center
Benjamin B Mattingly, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Kevin M Gentile, DO Attending Physician, Department of Emergency Medicine, USACS at Bristol Hospital
Kevin M Gentile, DO is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians
Disclosure: Nothing to disclose.
Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates
Disclosure: Nothing to disclose.
Edward Bessman, MD Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine
Edward Bessman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School
Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Wellens Syndrome
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