Cocaine use and acute left ventricular dysfunction

• Published in: The Lancet (North American edition) Vol. 357; no. 9268
• Main Authors: Missouris, C G, Swift, P A, Singer, DRJ
• Format: Journal Article
• Language: English
• Published: 19.05.2001
• ISSN: 0099-5355

A previously fit 36-year-old caucasian woman was admitted to the coronary care unit, in August, 1999, with a 2 hour history of central precordial chest pain associated with sweating and shaking. She had smoked 1/2 oz tobacco weekly for three years, and previously smoked cigarettes since age 15, but denied recreational drug use. Her mother had suffered from angina at the age of 56 years. On examination her resting heart rate was 125 beats/min and supine blood pressure was 102/67 mm Hg. There were no clinical signs of heart failure. The resting 12-lead electrocardiogram showed sinus tachycardia with normal electrical axis. There was widespread deep T-wave inversion in the anterior chest leads. Biochemical investigations including initial creatine kinase (116 IU/L) and cholesterol (5 mmol/L), were normal. Serial cardiac enzymes and troponin T measurement were also normal. Her plasma renin activity (PRA) and A-type natriuretic peptide (ANP) on admission were normal at 0 times 4 ng/L per s (normal range 0 times 14-0 times 69 ng/L per s) and 1 times 3 pmol/L (normal values 0 times 3-5 times 2 pmol/L), respectively. In view of the probable diagnosis of an unstable coronary syndrome she was treated with aspirin, oral metoprolol, intravenous nitrates, and subcutaneous low-molecular-weight heparin. Coronary angiography shortly after admission showed a normal epicardial left coronary system. Echocardiography, however, showed extensive antero-apical left ventricular hypokinesia with an estimated ejection fraction of 35-40%. On day 3, PRA increased to 0 times 89 ng/L per s and ANP to 4 times 1 pmol/L. On day 7 ANP rose further to 6 times 0 pmol/L. Because of her normal angiogram a pharmacological cause for her coronary syndrome was sought. A urine sample collected on admission and examined by fluorescence polarisation immunoassay was positive for the primary cocaine metabolite, benzoylecgonine. She was discharged taking aspirin 75 mg daily and carvedilol 3 times 125 mg at night. 2 months later in October, 1999, repeat echocardiography showed mild residual global left vetricular dysfunction. When assessed in March, 2000, she was pain-free and fasting cholesterol was 4 times 4 mol/L, LDL 2 times 6 mmol/L, triglycerides 1 times 4 mmol/L. When last seen in April, 2001 she had shortness of breath on exertion.