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Health See other Health Articles Title: Low Diastolic Blood Pressure Linked to Brain Atrophy A new study suggests that low diastolic blood pressure (DBP) and mean arterial pressure (MAP) are associated with more progression of subcortical brain atrophy in patients with manifest arterial disease, irrespective of the course of blood pressure over time. The study also showed that higher baseline DBPs, MAPs, and, to a lesser extent, systolic blood pressures (SBPs) that decline over time are associated with less progression of brain atrophy in these patients. These results were independent of antihypertensive treatment, cardiovascular risk factors, severity of arterial disease, white matter lesions (WMLs), and brain infarcts. "This could imply that BP lowering is beneficial in patients with higher BP levels, but one should be cautious with further BP lowering in patients who already have low BP," write the authors, led by Hadassa M. Jochemsen, MD, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Amsterdam, the Netherlands. The study was published online June 10 in JAMA Neurology. Total Brain Volume The analysis included 663 patients (mean age, 57 years) from the Second Manifestation of ARTerial disease–Magnetic Resonance (SMART-MR) Study. SMART-MR is a prospective cohort study of brain changes on MRI in patients with manifest arterial disease, including coronary artery disease (CAD), cerebrovascular disease, peripheral arterial disease, or abdominal aortic aneurysm. Using information from MRI investigations at baseline and follow-up, researchers calculated total brain volume by summing the volumes of grey matter, white matter, WMLs, and infarcts. They also categorized blood pressure as low, normal, or high and calculated pulse pressure (PP) and MAP. After a mean follow-up of 3.9 years, the analysis showed that lower baseline DBP and MAP, as well as a higher baseline PP, but not SBP, were significantly associated with an increase in ventricular fraction (VF), which indicates more progression of subcortical brain atrophy. The mean difference in change in VF between low and high DBP was 0.07% (95% confidence interval [CI], 0.01% - 0.14%); between low and high MAP, the difference was 0.05% (95% CI, 0.00% - 0.10%); and between low and high PP, it was –0.07% (95% CI, –0.13% to –0.01%). Adjustment for WML volume and brain infarcts at follow-up did not change these results. Baseline SBP, DBP, MAP, and PP were not associated with other measures of brain volume, including changes in brain parenchymal fraction or grey matter fraction. Over time, declining DBP levels were associated with less progression of subcortical atrophy in patients with normal or high baseline DBP. Findings were similar with respect to MAP and, to a lesser extent, SBP. In contrast, declining SBP levels in patients with low baseline SBP was associated with more progression of subcortical brain atrophy; however, this group was very small (n = 8). Adjusting for an increase in the number of antihypertensive drugs during follow-up did not substantially change the results, although the study did not have information on dosages or adherence. Excluding patients with extremely high or low BP ( > 200/110 mmHg and < 100/60 mmHg) also did not change the results, nor did adjustments for measures of arterial disease severity. Vascular Aging According to the authors, low BP, especially low DBP, in high-risk patients could be a risk indicator of early vascular aging, which has been related to an increased risk for ischemic and degenerative brain changes. Because the study found that a higher baseline PP was associated with more progression of subcortical brain atrophy, this might suggest that arterial stiffness or early vascular aging may at least partly explain the low DBP-brain atrophy relation, although adjusting for PP did not change the effect estimates and PP did not modify the relation between DBP and the progression of brain atrophy. Another possible explanation for the findings is that low DBP and MAP are markers of reduced cardiac output, which could be an independent risk factor for brain atrophy. This is supported by the finding that the association of low DBP and MAP with progression of subcortical atrophy was mainly present in patients with CAD. The study authors explain that "lower systemic DBP and MAP levels may be inadequate for healthy cerebral perfusion, which can evolve into a neurodegenerative process, eventually leading to brain atrophy, specifically subcortical brain atrophy because subcortical areas are very vulnerable for impaired perfusion and ischemic damage." It's also possible, they said, that low BP is the consequence of brain atrophy. The authors stressed that because patients with low SBP, DBP, and MAP who experience declining BP over time had similar or even more progression of subcortical atrophy compared with those with increasing BP, decreasing BP further could be harmful. A limitation of the study was that individuals who participated in the follow-up examination were somewhat healthier than those who did not participate and BP measurements were taken on a single day, which may have led to an underestimation of the associations. Also, the results may not apply to persons without arterial disease. The relationship between blood pressure and progression of brain atrophy are "well known," according to Charles DeCarli, MD, Victor and Genevieve Orsi Chair in Alzheimer's Research and professor of neurology, University of California at Davis, Sacramento. The phenomenon was first described almost 20 years ago, he said. Among the first studies to highlight the relationship was a population-based study of 85-year-olds that found patients with low BP levels had an increased risk for brain atrophy, Dr. DeCarli pointed out. (Hypertension. 1998;32:404-409). The authors have disclosed no relevant financial relationships. JAMA Neurol. Published online June 10, 2013. Abstract Post Comment Private Reply Ignore Thread
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