Cocaine-Induced QTc Prolongation
For several days, a 48-year-old woman had complained of chest pain. She also reported a syncopal episode of a few seconds’ duration, followed by consciousness without any associated confusion. She admitted smoking crack cocaine.
2 days before the onset of her symptoms. She had no other symptoms and took no medications.
The vital signs and the physical examination results were normal, as were basic chemistry and hematologic studies. The troponin T level was less than 0.03 µg/L on three occasions 8 hours apart.
A chest radiograph and a CT scan of the head were unremarkable. A 12-lead ECG showed a prolonged QTc interval of 634 ms with T wave inversions (A). Serial ECGs showed a decrease in the QTc interval to 483 ms before discharge (B). Coronary angiography revealed mild non-obstructive coronary artery disease.
Six months before this admission, her ECG showed a QTc interval of 445 ms with normal T waves (C).
Cocaine use is common in the United States and is a frequent cause of chest pain admissions in hospitals across the country. Typically, physicians are concerned about cocaine-induced coronary ischemia and myocardial infarction. Our goal is to emphasize other potential cardiovascular complications arising from cocaine use, which are often overlooked and can lead to significant morbidity and mortality.
Cocaine has a robust effect on the myocardial conducting system leading to electrical abnormalities, such as the ones observed in this patient. The literature contains evidence to suggest that cocaine causes QTc prolongation.1,2 The exact mechanism has not been established; however, there is some evidence that cocaine-induced sodium and potassium channel blockade may be responsible for this effect.3 Cocaine also leads to numerous other types of arrhythmias, such as Brugada syndrome, bundle branch block, ventricular fibrillation, ventricular tachycardia and accelerated idioventricular rhythm, heart block, torsades de pointes, and a variety of supraventricular tachycardias.4
This patient had dynamic changes in systolic dysfunction evident on two separate echocardiograms 4 months apart. Cocaine has also been shown to cause cardiomyopathy and myocarditis. Various mechanisms are responsible for these changes, such as myocardial ischemia, direct toxic effect of cocaine causing myocardial necrosis, tachycardia-induced cardiomyopathy, and autoimmune reaction to cocaine and levamisole (used as a cutting agent with cocaine).5
REFERENCES:
1. Magnano AR, Talathoti NB, Hallur R, et al. Effect of acute cocaine administration on the QTc interval of habitual users. Am J Cardiol. 2006;97(8):1244-1246.
2. Haigney MC, Alam S, Tebo S, et al. Intravenous cocaine and QT variability.
J Cardiovasc Electrophysiol. 2006;17(6):610-616.
3. Wood DM, Dargan PI, Hoffman RS. Management of cocaine-induced cardiac arrhythmias due to cardiac ion channel dysfunction. Clin Toxicol (Phila). 2009;47(1):14-23.
4. Om A, Ellenbogen KA, Vetrovec GW. Cocaine-induced bradyarrhythmias. Am Heart J. 1992;124(1):232-234.
5. Bertolet BD, Freund G, Martin CA, et al. Unrecognized left ventricular dysfunction in an apparently healthy cocaine abuse population. Clin Cardiol. 1990;13(5):323-328.