TRIPTAN AND RISKS

What are the cardiac risks of triptan use in patients without cardiac risk factors? Are there cardiac risks associated with headache preventative medications? This issue of Headache Currents includes a set of articles addressing these questions and reaching some eye-opening conclusions. In these articles, the authors focus on 2 areas of cardiac risk, both of which are routinely encountered in the headache clinic. The first, serotonergic cardiac adverse events including triptan-associated vasospasm, is likely to be familiar to many readers. The second, QT interval prolongation and the risk of torsade de pointes with commonly used headache medications, may be less so.
Part 1 of the series begins by reviewing the evidence for cardiac events associated with triptans in patients with and without coronary artery disease and follows with an overview of serotonin physiology as it relates to migraine and cardiac physiology. The pathophysiology of torsade de pointes is also reviewed. These pathophysiological summaries, while thorough, are concise and serve as excellent resources on the topic for the clinician. Part 1 ends by describing the possible relationship between torsade de pointes and sumatriptan, a novel suggestion.
Concerns about the cardiac safety of triptans are common in clinical practice. One confounding factor is that “triptan sensations” may be similar to cardiac chest pain. How to tell ischemic chest pain from a triptan sensation? As illustrated by a case report in the first article, the answer is not as straightforward as it seems.
In the second article, the authors review medications that are commonly used for prevention of headache and that may potentially cause QTc prolongation. These include tricyclic antidepressants, selective serotonin re-uptake inhibitors, lithium, and others. Less well known are the many drug–drug interactions that can increase the risk of prolonged QTc and thus torsade de pointes, which are also reviewed here in detail. This article highlights the risk of polypharmacy, especially in older adults, and finishes with a summary of risk for cardiac ischemia or arrhythmia as outlined in the prescribing information. This second article also includes excellent tables summarizing this information for quick reference.
Taken together, this pair of articles suggests a need for greater vigilance in screening patients for cardiac risk factors prior to prescribing triptans. As the authors state, “The challenge suggested is to clinically identify those very rare patients at risk for complications associated with serotonin agonists, and in particular triptans, before they are prescribed.” While the literature describing these risks is extensive, there is little information available about how to determine the risk of a medication in a particular patient.
These articles therefore raise thought-provoking questions for clinical practice: Should we be obtaining electrocardiograms prior to starting any medication known to cause QT prolongation? Should we be more cautious about prescribing combinations of these medications? Should we lower our threshold of suspicion for cardiac disease in otherwise healthy older patients? What should we tell our patients about the risks associated with triptan use? And while the evidence that triptans can cause vasospasm in adults without cardiac risk factors is compelling, does the risk of this very rare but potentially devastating adverse effect change our clinical practice? This review highlights the need for further research regarding determination of these risks.