Neurological diseases are currently a leading cause of mortality and disability worldwide.¹ A relevant proportion of the health impairment secondary to neurological conditions appears to be preventable.² Notably, vascular risk factors appear to be key determinants of neurological diseases, by directly and indirectly affecting the cerebral circulation at multiple levels, from large‑vessel atherosclerosis to microvascular dysfunction resulting in chronic parenchymal damage.³ In the current issue of Polish Archives of Internal Medicine, Szum‑Jakubowska and colleagues⁴ present a cross‑sectional analysis from the Bialystok Polish Longitudinal University Study (PLUS) concerned with the burden of cerebral white matter hyperintensities (WMHs) and its association with vascular risk factors and markers of subclinical atherosclerosis in an unselected population of 735 adults. They were able to find an association between WMH burden and the presence of prediabetes or diabetes, hypertension, overall cardiovascular risk assessed with the Systematic Coronary Risk Evaluation 2 score as well as imaging markers of increased cardiovascular risk, there including carotid intima‑media thickness (IMT) and presence of left ventricular hypertrophy on transthoracic echocardiography.⁴ WMHs are subclinical cerebral alterations that are highly prevalent in the general population. They are defined as areas of signal hyperintensity on T2‑weighted or fluid‑attenuated inversion recovery images on brain magnetic resonance imaging, most commonly located in the deep or periventricular white matter.⁵ WMHs have been associated with definite small‑vessel alteration, local white matter inflammation and likely blood‑brain barrier dysfunction resulting in circumscribed edema.^3,6 Higher burden of WMHs is associated with worse cognitive performance, increased rates of depression, and increased longitudinal risk of stroke and incident dementia.⁶ The authors should be commended for succeeding in gathering such granular unbiased data from a fairly large population. Their results appear consistent with prior literature linking a higher burden of vascular risk factors in general, and of markers of poorly controlled hypertension in particular, with an increased burden of WMHs.⁶ The authors in addition report an increase in WMHs in individuals with higher carotid IMT. Notably, the association between carotid atherosclerosis and WMHs, potentially suggesting an atheroembolic etiology of the latter, has been a subject of intense debate.⁷ However, longitudinal studies assessing the progression of WMHs in unilateral carotid stenosis or among patients with unilateral signs of carotid plaque instability failed to prove a causative role for carotid plaque.⁸ Indeed, in the present work, the association between IMT and WMHs was only found in the subset of patients with no baseline diagnosis of hypertension.⁴ This finding, in combination with the notion that elevated IMT is highly associated with subclinical and incident hypertension⁹ suggest cautious interpretation of the relation between carotid subclinical atherosclerosis and WMHs.

Overall, Szum‑Jakubowska and colleagues⁴ helped shed more light on the complex association between cardiovascular and brain health. They have the chance to longitudinally follow the Bialystok PLUS population to collect hypothesis‑generating data on the impact of preventative measures, especially blood pressure management strategies, on WMH progression rate. We eagerly await future data from this interesting project.