Hypertension increases the risk of cerebral microbleed in the territory of posterior cerebral artery: a study of the association of microbleeds categorized on a basis of vascular territories and cardiovascular risk factors.

BACKGROUND: It has been suggested that the etiology of cerebral microbleeds (CMBs) differs according to their location in the brain, with lobar microbleeds being caused by cerebral amyloid angiopathy and deep or infratentorial microbleeds resulting from hypertension and atherosclerosis. We hypothesized that there were associations between cerebral arterial branches, cardiovascular risk factors, and the occurrence of CMBs. We examined these relationships in the current study. METHODS: Three hundred ninety-three patients with CMBs were analyzed in this study. The CMBs were listed according to the various arterial territories, and these were assessed for their relationship with cardiovascular risk factors, markers of small vessel disease, and their presence and location using multiple logistic regression. RESULTS: Systolic blood pressure had a significant association with CMBs in the territory of the posterior cerebral artery and the deep and infratentorial locations. The presence of lacunar infarcts, hemorrhage, and white matter changes were associated with CMBs in nearly all arterial territories. CONCLUSIONS: Hypertension increases the risk of microbleeds in the territory of the posterior cerebral artery and the deep and infratentorial locations. Cerebral amyloid angiopathy may be responsible for the microbleeds in the lobar area of brain.

Multimodality imaging of endothelial progenitor cells with a novel multifunctional probe featuring positive magnetic resonance contrast and near-infrared fluorescence.

The multimodal strategy incorporating T1-weighted magnetic resonance imaging (MRI) and near-infrared (NIR) fluorescence imaging can complement their strengths to provide images with high sensitivity and spatial resolution for noninvasively and dynamically monitoring endothelial progenitor cells (EPCs) in potential EPC-dominated therapies. Here we report the development of a protein-based imaging probe, bCD-PLL-Cy5.5 Conjugate 1, in which the bacterial cytosine deaminase (bCD) protein was modified with poly-l-lysine (PLL) that is labeled with imaging reporters, including T1-weighted MRI contrast chelator and NIR fluorophore. Conjugate 1 showed low cytotoxicity in EPCs isolated from the rabbit peripheral blood. The normalized cell viability was maintained above 90% after incubation for 1 to 5 days. Fluorescence microscopy of live cells indicated rapid cellular uptake of Conjugate 1 into EPCs in 15 minutes, and flow cytometry studies demonstrated the time-dependent internalization of Conjugate 1 with maximum uptake 48 hours after the treatment. MRI of phantoms demonstrated significant reduction of the T1 value of the EPC pellet that was pretreated with 2 µM of Conjugate 1 for 24 hours. Our preliminary data suggest that as a multimodal imaging contrast medium, Conjugate 1 offers a promising imaging probe for tracking the delivery and therapeutic response of EPCs in vivo.