Atlas-derived perfusion correlates of white matter hyperintensities in patients with reduced cardiac output

作者：Jefferson Angela L^*; Holland Christopher M; Tate David F; Csapo Istvan; Poppas Athena; Cohen Ronald A; Guttmann Charles R G

来源：Neurobiology of Aging, 2011, 32(1): 133-139.

DOI：10.1016/j.neurobiolaging.2009.01.011

• Cardiovascular disease
• SPECT
• MRI
• Perfusion
• Cardiac output
• White matter hyperintensities

Reduced cardiac output is associated with increased white matter hyperintensities (WMH) and executive dysfunction in older adults, which may be secondary to relations between systemic and cerebral perfusion. This study preliminarily describes the regional distribution of cerebral WMH in the context of a normal cerebral perfusion atlas and aims to determine if these variables are associated with reduced cardiac output. Thirty-two participants (72 +/- 8 years old, 38% female) with cardiovascular risk factors or disease underwent structural MRI acquisition at 1.5 T using a standard imaging protocol that included FLAIR sequences. WMH distribution was examined in common anatomical space using voxel-based morphometry and as a function of normal cerebral perfusion patterns by overlaying a single photon emission computed tomography (SPECT) atlas. Doppler echocardiogram data was used to dichotomize the participants on the basis of low (n = 9) and normal (n = 23) cardiac output. Global WMH count and volume did not differ between the low and normal cardiac output groups; however, atlas-derived SPECT perfusion values in regions of hyperintensities were reduced in the low versus normal cardiac output group (p<0.001). Our preliminary data suggest that participants with low cardiac output have WMH in regions of relatively reduced perfusion, while normal cardiac output participants have WMH in regions with relatively higher regional perfusion. This spatial perfusion distribution difference for areas of WMH may occur in the context of reduced systemic perfusion, which subsequently impacts cerebral perfusion and contributes to subclinical or clinical microvascular damage.

• 出版日期2011-1