LAUSR

Polypharmacy is very common among older adults and is often associated with adverse drug events and potentially severe drug–drug interactions (DDIs) [1]. Although most DDIs might be prevented or avoided, their lack of recognition is an important cause of morbidity and mortality and might cause a significant burden in terms of health care costs. We describe the first case of a severe QT prolongation in an older patient caused by the concomitant use of two commonly prescribed drugs: trimethoprim/sulfamethoxazole (TMP/SMX) and flecainide. An 88-years-old woman was evaluated at our Day Hospital for unintentional weight loss. Her therapy consisted of acetylsalicylic acid (100 mg/daily) for recurrent transient ischemic attacks. An asymptomatic, rapid, narrow QRS complex tachycardia was found at the EKG. The inefficacy of the carotid sinus massage and verapamil 5 mg iv questioned the diagnosis of paroxysmal supraventricular tachycardia, which is the first arrhythmia to consider in cases of rhythmic narrow QRS complex tachycardia. The suspicion of some other atrial tachycardia (such as atrial flutter) was thus raised. Accordingly, the patient was treated with amiodarone 400 mg per os, but the arrhythmia persisted. Therefore, she was hospitalized. Sinusal rhythm was finally obtained after additional 5 mg iv of verapamil. Prophylaxis with amiodarone (200 mg/daily) was then started, but the evidence of hyperthyroidism at the blood tests led to its replacement with flecainide (50 mg twice a day) and introduction of thiamazole. During the hospitalization, the patient also developed a pneumonia, which was first treated with ceftriaxone and azithromycin and subsequently with piperacillin/tazobactam. Because of persistent mild elevation of the inflammatory markers, a 7-day treatment with TMP/SMX 160/800 mg twice a day was prescribed at the hospital discharge. Six days after hospital discharge, the patient was reevaluated as part of a follow-up visit. The EKG showed a prolonged QTc of 600 ms and forked T waves (Fig. 1). No alteration of either the renal function or electrolyte status was found at blood tests. The patient was immediately admitted to the Cardiology Department. TMP/SMX and flecainide were suspended and propranolol (10 mg a day) was initiated. The QT-interval prolongation reduced over the following days until complete resolution of the EKG abnormality. The QT prolongation was attributed to the concomitant use of TMP/SMX and flecainide. Notched T waves could have raised the suspect that the patient carried a congenital long QT syndrome mutation. However, also in acquired long QT syndrome patients can develop T wave morphologic changes similar to the ones found in type 2 long QT syndrome. Moreover, the normal length of the QT-interval before the assumption of the drugs and its reversal to normality after their discontinuation with a positive dechallenge (Drug Interaction Probability Scale score was 5) suggested a probable relationship with the pharmacological therapy. The patient did not receive any therapy like diuretics or ACE inhibitors, which could have enhanced the interaction and * S. Damanti [email protected]