Long QT syndrome (LQTS) is characterized by inherited or acquired prolonged QT interval on the surface electrocardiogram. This can lead to torsade de pointes ventricular tachycardia (TdP VT) and ventricular fibrillation. In the acquired form of the disease, medications from several classes can cause TdP VT or potentiate the electrocardiographic findings. These include class IA and III antiarrhythmics, antibiotics (macrolides and quinolones), antidepressants (tricyclics and selective serotonin reuptake inhibitors), antipsychotics (haloperidol and phenothiazines), and antiemetics (ondansetron and prochlorperazine). We present four cases of drug-induced LQTS resulting in life-threatening cardiac arrhythmias. Antiarrhythmic medications were the cause in two cases, and the other two cases involved noncardiac medications. All four patients had at least one risk factor for LQTS in addition to the offending drug, including female gender, hypokalemia, hypomagnesemia, and bradycardia. In one patient, amiodarone was administered for treatment of VT, although the correct diagnosis was actually TdP VT. In patients with polymorphic VT or ventricular fibrillation without a significant history of cardiovascular disease, drug-induced LQTS should be high in the differential diagnosis. Prompt diagnosis is key, as amiodarone, while often used to suppress VT, is potentially harmful in the setting of LQTS and TdP VT.
The antiplatelet drug clopidogrel is an oral thienopyridine derivative that has been extensively used for the treatment and secondary prevention of a variety of cardiovascular diseases. Although clopidogrel is well tolerated by most patients, rare but serious hypersensitivity reactions have been documented, including cutaneous reactions and angioedema. An alternative thienopyridine that may be substituted for clopidogrel is ticlopidine; however, deleterious side effects from ticlopidine may occur, including diarrhea, neutropenia, and thrombocytopenia purpura, and cross-reactivity has been documented between these two thienopyridines. In cases of bare-metal stent deployment, cilostazol may be a safe and effective alternative; however, limited therapeutic data are available. In such cases, providers may need to administer a clopidogrel desensitization protocol; three clopidogrel desensitization protocols have been published. We describe a 58-year-old man who developed a generalized diffuse rash along his abdomen within 2 weeks of exposure to clopidogrel after drug-eluting stent placement. Clopidogrel was discontinued, and ticlopidine was begun. The rash resolved within 3 days of clopidogrel discontinuation. Using the Naranjo adverse drug reaction probability scale, we determined that the probability of clopidogrel causing the rash was probable (score of 8). Ticlopidine was subsequently discontinued due to severe diarrhea. Because of the patient's implanted stent and high risk for possible thrombosis, an 8-hour clopidogrel desensitization protocol was devised and successfully used in this patient, who continued to receive clopidogrel over the next year without rash recurrence. Based on our experience and the literature reviewed, administration of a clopidogrel desensitization protocol in patients with a history of isolated cutaneous hypersensitivity reactions, including angioedema, to clopidogrel can be a safe therapeutic alternative to ticlopidine or cilostazol.
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