Cardiac adverse effects of H-1-antihistamines

Non-sedating antihistamines have been a major advance in the treatment of a llergies but since the early 1990's there have been concerns about cardiac toxicity. Life-threatening cardiac arrhythmias were reported, first with as temizole and then with terfenadine. These occurred in situations when serum drug levels were high, such as with overdose or reduced hepatic metabolism due to interactions with other drugs, including ketoconazole or erythromyc in. The reported cardiac arrhythmia is know as << torsades de pointes >>, a polymorphic ventricular tachycardia, which is associated with prolongation of the QT interval on the surface electrocardiogram Concerns that the card iotoxicity may be a class effect of HI-antihistamines are unfounded, as ill ustrated by fexofenadine, the active metabolite of terfenadine. Tefenadine has been shown to increase the QT interval by blocking potassium channels a nd prolonging the cardiac action potential. In contrast, fexofenadine has n one of these cardiac actions. Astemizole and loratadine may also block card iac potassium channels. The incidence of cardiac arrhythmia when using terf enadine or other H-1-antihistamines is very low, and the major concern rela tes to the risks associated with drug interactions. The availability of H-1 -antihistamines without the risk of cardiac adverse effects is a further ad vance in the treatment of patients with allergy.