Case #16 — Cocaine-Induced Electrocardiographic Phenomenon

by Sundeep Kumar, MD, Luis Sanchez, MD, Ruthvik Srinivasamurthy, MD, and Patrick F. Mathias, MD, FACC

A 27-year-old white man presented at the hospital after recent cocaine use, reporting intermittent left-sided chest pain, diaphoresis, and dizziness. His vital signs were normal; results of physical examination were not noteworthy. Chest radiographic and cardiac enzyme test results were normal. His urine was positive for cocaine. An electrocardiogram (ECG) during a pain-free state revealed findings not present one month earlier: a prolonged QTc interval, new T-wave inversions, and biphasic T waves in leads V₂ and V₃ (Fig. 1, arrows).

Fig. 1

A transthoracic echocardiogram (TTE) showed nothing unusual, and a radionuclide myocardial perfusion imaging test revealed no inducible or reversible ischemic changes. At the patient’s follow-up visit one week later, the ECG changes had spontaneously resolved.

Which of the following is associated with these ECG findings?

A) Anterior postischemic changes/Wellens syndrome

B) Aberrant posterior descending artery

C) Left main coronary artery stenosis

D) Left circumflex coronary artery stenosis

Answer

A) Anterior postischemic changes/Wellens syndrome

Wellens syndrome, or left anterior descending coronary artery (LAD) T-wave syndrome, has a distinctive pattern in the precordial leads (V₁ through V₃): an isoelectric or minimally elevated takeoff of the ST segment from the QRS complex, a concave or straight ST segment passing into a negative T wave at a 60° to 90° angle, and a symmetrically inverted T wave.¹ Biphasic T-wave inversion in leads V₂ and V₃ was present in 24% of patients who had a variant of Wellens syndrome.² These ECG changes indicate postischemic reperfusion injury, typically related to critical narrowing of the LAD.

Wellens syndrome is associated with cardiac and noncardiac causes, including drug and medication use.³ Cocaine users may have ECG changes typical of Wellens syndrome, but as part of a vasospastic phenomenon, without underlying stenosis or reperfusion injury.^4,5 Accordingly, β-blockers should be prescribed cautiously, if at all. Our patient had normal myocardial perfusion and TTE results, so cocaine-induced coronary vasospasm plausibly explains the ECG changes. Knowing that a patient uses drugs can help to clinically differentiate true Wellens syndrome from cocaine-associated pseudo-Wellens.

References

1. 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; 103(4 Pt 2):730-6.
2. Tandy TK, Bottomy DP, Lewis JG. Wellens’ syndrome. Ann Emerg Med 1999;33(3):347-51.
3. Y-Hassan S. The pathogenesis of reversible T-wave inversions or large upright peaked T-waves: sympathetic T-waves. Int J Cardiol 2015;191:237-43.
4. Dhawan SS. Pseudo-Wellens’ syndrome after crack cocaine use. Can J Cardiol 2008;24(5):404.
5. Langston W, Pollack M. Pseudo-Wellens syndrome in a cocaine user. Am J Emerg Med 2006;24(1):122-3.