Article Text

  1. N. Koradia1,
  2. J. Jani1,
  3. S. Niranjan1,
  4. A. Khanna1
  1. 1Department of Cardiology, Coney Island Hospital, Brooklyn, NY.


Background Brugada syndrome has been linked to ventricular tachycardia, ventricular fibrillation, and sudden cardiac death. Right bundle branch block (RBBB) with coved or saddleback ST-segment elevations in leads V1 to V3 in the absence of any structural heart disease is the electrocardiographic (ECG) hallmark of Brugada syndrome. These changes can be augmented by selective α-adrenergic stimulation and sodium channel blockade. A few recently published case reports implicated cocaine as a possible inductor.

Case Presentation A 50-year-old homeless man with a history of active smoking presented to the ER not feeling well, with fever and abdominal pain. He denied any chest pain, difficulty breathing, palpitations, or syncope. He also denied any family history of sudden death. He initially denied any substance abuse, but his urine toxicology was positive for cocaine. His cardiovascular examination was unremarkable. His ECG demonstrated incomplete RBBB with coving ST elevations in leads V1 to V2 showing type 1 (definite) Brugada pattern. Compared to his prior ECG 2 months ago, these changes were new. An echocardiogram showed normal left and right ventricular function without any regional wall motion abnormalities. Within 24 hours, his ECG changes reverted back to normal. His cardiac enzymes remained within normal limits. He was treated for viral syndrome and subsequently discharged. Temporal association between cocaine use and Brugada pattern with its subsequent normalization clearly implicates cocaine as the cause.

Discussion Patients with cocaine use could have various ECG abnormalities, including ST-segment depressions or transient ST elevations. These findings are usually attributed to myocardial ischemia provoked by cocaine-induced vasospasm. In contract, our case describes a typical Brugada pattern on ECG in the absence of any biochemical or morphologic marker of myocardial ischemia. Various mechanisms have been postulated, including the sodium channel-blocking property of cocaine and inhibition of noradrenaline uptake, resulting in enhanced sympathetic activity. Currently, optimal management for incidental cocaine-induced Brugada pattern is not known. The role of EP study or AICD placement is controversial.

Conclusion This case report illustrates an important cardiovascular sign related to cocaine abuse. It also underlines the need for screening for cocaine in patients presenting with a transient Brugada pattern. Optimal management of incidental cocaine-induced Brugada pattern remains unclear. The role of EP study and AICD in such patients is controversial and warrants further research.

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