Drug-induced cardiotoxicity due to aminophylline treatment: a case report.

BACKGROUND

Aminophylline, a theophylline compound that contains ethylenediamine, has untoward side effects on many organ systems.

OBJECTIVE

The goal of this case report was to illustrate the occurrence of acute adverse events (ie, chest discomfort and myocardial enzyme elevation) that may be associated with aminophylline treatment.

METHODS

To uncover previous studies/reports on this subject, a literature search (1950-2003) was conducted on MEDLINE, UpToDate, and Doctor's Guide, using the search terms aminophylline toxicity, theophylline toxokinetics, pharmacotoxic myocardial injury, hypersensitivity myocarditis, and diagnosis of myocardial infarction with biomarkers of cardiac injury. A 76-year-old, obese, female patient was admitted to University Hospital (Rion, Greece) for an acute exacerbation of chronic bronchitis. Beginning on day 0 of hospitalization, the patient was treated with aminophylline 750 mg IV, given in a 24hour constant infusion, for persistent wheezing. We monitored the patient's condition using electrocardiography, echocardiography, and blood chemistry analysis.

RESULTS

While undergoing aminophylline treatment, the patient developed vague chest discomfort and myocardial enzyme elevation due to aminophylline-induced cardiotoxicity. Mild wheezing was still present on physical examination on day 2 of hospitalization. The serum creatine kinase (CK) level was slightly increased. On day 6 of hospitalization, the patient's symptoms worsened, with mild epigastric discomfort, tachycardia, fatigue, and tightness in the chest. Blood gas analysis revealed mild hypoxia and hypocapnia. Pulmonary perfusion scan showed a low risk for pulmonary thromboembolism, as indicated by the absence of segmental perfusion defects. Blood chemistry analysis showed increased serum CK (×2.5) and CK isoenzyme (CK-MB) fraction (×8.6) levels. Echocardiography on day 7 showed a slight hypertrophy of the septum, with normal dimensions of the ventricles and a 70% ejection fraction. Aminophylline treatment was permanently discontinued, and the patient's signs and symptoms promptly improved.

CONCLUSIONS

In the case presented here, the exclusion of usual causes of increased serum CK and CK-MB fraction levels, together with the increased serum aminophylline concentration and, most importantly, the rapid alleviation of symptoms and normalization of myocardial enzymes in absolute temporal relationship to the discontinuation of the drug, suggested that aminophylline treatment might be associated with elevated levels of myocardial enzymes. (Curr Ther Res Clin Exp. 2003;64:379-386).