QT prolongation from psychiatric drugs is a real but imperfect risk marker; the arrhythmia itself is unmeasured

The interaction warnings about QT prolongation, which run through the citalopram, pimozide and paroxetine rows of this wave, rest on a marker, not on counted heart rhythm deaths. This review says so.

Significant findings

Beach and colleagues (Psychosomatics, 2013) reviewed the literature on the corrected QT interval and psychiatric medication. "QTc interval prolongation is an established, though imperfect, risk marker for TdP" (torsades de pointes, the dangerous rhythm). "There are no well-controlled studies that assess the risk of TdP associated with psychotropic agents."

What the evidence supports: "There are limited data that selective serotonin reuptake inhibitors (SSRIs) as a class are linked to QTc prolongation; citalopram appears more likely than others to induce this phenomenon. Among antipsychotics, thioridazine remains the agent most associated with QTc prolongation; intravenous haloperidol also appears to carry an increased risk. Of the atypical antipsychotics, ziprasidone appears most likely to prolong the QTc interval."

And the proportion: "The majority of patients in need of psychotropic medications display few risk factors for QTc prolongation and should be considered to be at low risk for TdP. The frequency of cardiac monitoring for patients receiving psychiatric medications should be individually determined, based on the prescribed agent(s) and additional risk factors for TdP."

Worth asking

This is the review to hold beside the labels. The labels say avoid stacking QT drugs; the review says the stacking matters most for people who already have risk factors, such as heart disease, low potassium or magnesium, or a congenital long QT, and that the harm at the end of the chain has never been measured in a controlled study. If you take two drugs from the QT lists, the question is whether you have any of those risk factors and whether anyone has looked at an ECG.