Epilepsy and vascular risk
Epidemiological studies have shown that mortality increases in patients with epilepsy compared to the general population, and this has been associated with an increased risk of cardiovascular or cerebrovascular events. The role played by classic and more speculative vascular risk factors (e.g. oxidative stress) in the development of vascular disease in these subjects has not yet been clearly established. In this context, antiepileptic drugs (AEDs) may have a differential influence on the vascular risk of patients with epilepsy, as enzyme inducers have been linked to the development of early atherosclerosis. The role of AEDs in the pathogenesis of atherosclerosis is not fully understood, but there are several plausible explanations: they can condition an unfavourable lipid profile, they can increase levels of C-reactive protein and homocysteinaemia, as well as clotting factors, and they can increase oxidative stress. Prolonged use of AEDs can be associated with a wide range of chronic adverse effects, and may also play a key role in the pathogenesis of atherosclerosis in patients with epilepsy. Neurologists and epileptologists who prescribe AEDs should be aware of the potentially unfavourable effects, especially in patients at high risk of vascular events. This review examines the pathophysiological mechanisms that may explain increased vascular risk in epilepsy, the evidence regarding accelerated atherosclerosis and its complications, and the potential implications for follow-up and treatment of the disease.
