Abstract
Triptans are effective and well tolerated in the treatment of acute migraine. Chest symptoms are a common adverse effect unrelated to coronary vasoconstriction in most patients. Although the aetiology of chest symptoms remains to be fully defined, pulmonary vasoconstriction is a possible underlying mechanism. Preclinical studies of isolated human blood vessels were used to identify the cerebral selectivity of triptans and ascertain if selectivity vs the pulmonary vasculature predicts a lower rate of chest symptoms. Controlled clinical trials and post-marketing surveillance studies were reviewed to document the incidence of chest symptoms after triptan therapy. In clinical trials, the incidence of chest symptoms at usual therapeutic doses ranged from 1 to 4% depending on the triptan and study design, whereas in post-marketing surveillance studies, up to 41% of patients specifically asked about chest symptoms reported them. A comparative clinical trial showed that almotriptan was associated with lower incidence of chest symptoms than sumatriptan (0.3 vs 2.2%). The intrinsic activity of almotriptan, a second-generation triptan, on human pulmonary arteries and veins was lower than that of sumatriptan. Pre-clinical studies of isolated pulmonary blood vessels may predict the clinical likelihood of chest symptoms; however, additional comparisons are needed.