Hypertension and Heart Disease May Contribute to Brain Atrophy in MS

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There were significant associations between the presence of heart disease and higher longitudinal white matter volume and whole brain volume loss.
There were significant associations between the presence of heart disease and higher longitudinal white matter volume and whole brain volume loss.

A study published in the European Journal of Neurology highlights the effect of hypertension and heart disease on accelerated central, whole brain, white matter atrophy in multiple sclerosis (MS).

This 5-year longitudinal study reviewed demographic and clinical data from 194 participants with MS and 43 control participants without neurological disease. The heterogeneous MS population was composed of clinically isolated syndrome (14.9%), relapsing-remitting MS (59.8%) and progressive MS (25.3%). 

The results showed that age-matched comparatives exhibited “significantly smaller T2-[lesion volume] and larger baseline brain volumes” in comparison with their MS counterparts. There were no changes in longitudinal volume across the MS cohorts. Hypertension was pointedly associated with an increase in lateral ventricular volume (24.5% vs 14.1%, P=.05) over the follow-up period. There were significant associations between the presence of heart disease and higher longitudinal white matter volume (-4.2% vs -0.7%, P=.01) and whole brain volume (-3.4% vs -1.6%, P=.01) loss. A history of smoking potentiated cardiovascular or cardiovascular disease risks in participants with MS.

Study limitations included small sample size restrictions on generalizability on MS and cardiovascular comorbidities. 

The authors concluded that results from this longitudinal study highlighted the contribution of hypertension and heart disease on advanced brain atrophy in MS.

Reference

Jakimovski D, Gandhi S, Paunkoski I, et al. Hypertension and heart disease are associated with development of brain atrophy in multiple sclerosis: a 5-year longitudinal study [published online August 13, 2018]. Eur J Neurol. doi:10/1111/ene.13769

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