Blood Viscosity in Subcortical Vascular Mild Cognitive Impairment with versus without Cerebral Amyloid Burden

• Published in: Journal of stroke and cerebrovascular diseases 2014-05, Vol.23 (5), p.958-966
• Main Authors: Noh, Hyun J., MD, Seo, Sang W., MD, PhD, Jeong, Yong, MD, PhD, Park, Jeong E., MD, PhD, Kim, Geon H., MD, Noh, Young, MD, Cho, Hanna, MD, Kim, Hee J., MD, Yoon, Cindy W., MD, Ye, Byong S., MD, Werring, David J., PhD, FRCP, Na, Duk L., MD
• Format: Article
• Language: English
• Subjects: Aged; Aged, 80 and over; amyloid; Aniline Compounds; Apolipoprotein E4 - genetics; artherosclerosis; Blood Viscosity; Cardiovascular; Case-Control Studies; Cerebral Amyloid Angiopathy - blood; Cerebral Amyloid Angiopathy - diagnosis; Cerebral Amyloid Angiopathy - genetics; Cognitive Dysfunction - blood; Cognitive Dysfunction - diagnosis; Cognitive Dysfunction - genetics; Dementia, Vascular - blood; Dementia, Vascular - diagnosis; Dementia, Vascular - genetics; Female; Genetic Predisposition to Disease; Hemodynamic; Humans; Magnetic Resonance Imaging; Male; Middle Aged; MRI; Neurology; Neuropsychological Tests; Phenotype; Positron-Emission Tomography; Predictive Value of Tests; Prospective Studies; Radiopharmaceuticals; Risk Factors; Thiazoles; vascular dementia
• ISSN: 1052-3057; 1532-8511
• DOI: 10.1016/j.jstrokecerebrovasdis.2013.08.004

Background Subcortical vascular dementia (SVaD) is a common form of dementia, attributed to ischemic small-vessel disease. Blood viscosity (BV) may contribute to the pathophysiology of SVaD. However, SVaD patients with coexisting amyloid deposition may not show differences in BV because their small-vessel disease may result from amyloid angiopathy independently of BV. We, therefore, hypothesized that BV might show different changes compared with control subjects in subcortical vascular mild cognitive impairment (svMCI) that refers to the prodromal stage of SVaD according to cerebral amyloid burden detected by the [11 C] Pittsburgh compound B (PiB) PET (positron emission tomography), and apolipoprotein 4 (ApoE4) genotype (a known risk factor for vascular and parenchymal amyloid). Methods Our subjects consisted of 33 healthy normal controls (NC), 28 patients with PiB(−) svMCI, and 12 with PiB(+) svMCI. They underwent scanning capillary tube viscometer measuring BV during systolic and diastolic phases. Results Compared with the NC group, the PiB(−) svMCI group showed increased diastolic blood viscosity (DBV) but no difference in systolic blood viscosity (SBV). By contrast, there was no significant difference in SBV and DBV between the NC and PiB(+) svMCI groups. Within the PiB(+) svMCI group, ApoE4(−) subgroup showed increased DBV compared with the ApoE4(+) subgroup. Conclusions Increased DBV is an important contributor to the development of “pure” svMCI (ie, without cerebral amyloid deposition). The relationship between BV and PiB(+) svMCI differed according to ApoE genotype, suggesting that the pathogenesis of PiB(+) svMCI might also be heterogeneous.