Blood Pressure, Aging, Vascular Disease, and Their Effects on Brain Volume

In addition to its well-known role in cerebrovascular events, recent epidemiologic studies have shown that hypertension is associated with the development of impaired cognitive function, vascular dementia, and Alzheimer's disease.1 In addition, systolic blood pressure (SBP) has been negatively associated with the volume of total brain matter (TBM) in the elderly,2 as quantified based on brain magnetic resonance images. Similarly, we have shown that nocturnal SBP was a significant indicator of brain atrophy and cognitive function in elderly hypertension.3 In this month's issue, Vlek et al.4 investigated the relationship between BP and the progression of brain atrophy in 331 patients with vascular disease. After a mean follow-up of 4.1 years, they concluded that BP did not influence the rate of change in brain tissue volume.4 Although we recognize that there were no significant associations between BP measures and brain atrophy in this study population, we wonder whether this would be true of other populations. Several points should be taken into account when interpreting the results of this study. First, the mean age was 58 years, and mean clinic BP was 138/80 mm Hg at baseline, meaning that these patients were younger and had lower BP levels than patients in the similar studies published previously. Exposure to long-standing high BP has been suggested to be a risk factor for brain atrophy. In fact, Goldstein et al. revealed that among older subjects (67–80 years old), only those with elevated SBP had smaller TBM volumes. This association was not seen among younger subjects (56–66 years old).2 Second, subjects with heterogeneous vascular diseases were included, such as patients with cerebrovascular disease, coronary heart disease (CHD), abdominal aortic aneurysm, or peripheral arterial disease. This would make it problematic to directly compare the results of this study with those of earlier studies that focused on elderly hypertension. Moreover, patients with CHD accounted for as much as 60% of the population in this study. Insufficient information was provided in the study by Vlek et al. regarding their subject's cardiac function.4 Woo et al. reported regional brain atrophy in patients with systolic dysfunction and NYHA Class III–IV symptoms.5 Although patients with CHD did not show more progression of brain atrophy compared to patients with other localizations of vascular disease, the possibility that decreased cardiac function might confound the relationship between BP and brain atrophy via a disruption of cerebral circulation cannot be excluded. Third, a single clinic BP measure might be not sufficient to detect a significant BP impact on the progression of brain atrophy. Ambulatory BP monitoring has been shown to provide a better predictive value for cardiovascular events than clinic BP measurement. In addition, earlier studies have shown that nocturnal SBP was more strongly associated with brain atrophy than clinic SBP.2,3 Until now, there have been few reports assessing the relationship between BP and brain atrophy using a prospective study design. The data presented in this manuscript would thus make an important contribution, provided they are considered within the context of the study's limitations. The authors declared no conflict of interest.