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function.4,5 To our knowledge, there have been 2 reports of severe neurological dysfunction with ranolazine.4,5 One case of an 81-year-old woman with renal dysfunction (creatinine clearance ,30 mL/min/1.73 m2) experienced neurological symptoms including hallucinations, dysarthria, and tremor when starting ranolazine 500 mg twice daily.4 Another case of a 74-year-old man with a strong hepatic CYP3A inhibitor clarithromycin experienced neurological toxicity (confusion, hallucinations, and ataxia) when ranolazine was initiated.5 The possibility of ranolazine’s action on neuronal sodium channels as an underlying mechanism of neurological side effects has been hypothesized.4–6 In our patient without any hepatic or significant renal dysfunction, delirium was noted with a lower dose of ranolazine. It is interesting to note that the mean age of study population in 17 randomized trials of ranolazine was 63 years.7 A younger mean age might have limited the ability of such studies to identify neurological side effects compared with patients age in reported cases of neurotoxicity and delirium (74, 81, and 84 years). Increasing age is a risk factor for delirium and might represent a significant risk factor for neurologic side effects associated with ranolazine. More data on this association should be made available from postmarketing surveillance. It is very important for clinicians to be aware of such neurological adverse effects when using the second-line agent ranolazine, especially in elderly patients receiving higher doses and with coexisting renal or hepatic dysfunction, to prevent misdiagnosis and adverse event–related complications. This case deserves attention because recognizing this rare and important side effect of ranolazine is essential for these patients to attain full recovery and highlights the need for appropriate postmarketing surveillance strategies.