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Cardiac manifestations of neurologic diseases are common in clinical practice. There are numerous anatomic and pathophysiologic links between the normal and abnormal function of both systems. There are a number of brain-heart interactions which affect the care of patients as well as help guide therapeutic development. This is exemplified in the area of vascular neurology where knowledge of the brain-heart connection is essential not only for bedside management but where collaborative efforts between neurology and cardiology are key in developing new strategies for ischemic stroke prevention and treatment, atrial fibrillation, and interventional techniques. This chapter will focus on cardiac manifestations of neurologic disease, with special emphasis on vascular and intensive care neurology, epilepsy, and neurodegenerative and peripheral nervous system diseases., (© 2014 Elsevier B.V. All rights reserved.)

Apolipoprotein E (apoE) is a 34 kDa glycosylated protein with multiple biological properties. In addition to its role in cholesterol transport, apoE has in vitro immunomodulatory properties. Recent data suggest that these immunomodulatory effects of apoE may be biologically relevant, and apoE-deficient mice have altered immune responses after bacterial inoculation and increased susceptibility to endotoxemia induced by lipopolysaccharide (LPS). To better understand the mechanism by which apoE-modulates immune responses, we tested the role of human apoE isoforms in assays of human T cell proliferation, and analyzed the immune responses of apoE-deficient mice. Both the E3 and E4 isoforms of apoE induced similar suppression of human lymphocyte function in assays of T cell proliferation, including mitogenic responses to phytohaemagglutin (PHA), stimulation of the T cell receptor with alphaCD3, and antigen-specific response to tetanus toxoid. ApoE-deficient mice showed no quantitative differences in thymic, splenic, or bone marrow lymphocyte populations, nor were there in vitro abnormalities in splenocyte proliferation after stimulation with alphaCD3 to suggest an inherent T cell defect in apoE-deficient mice. ApoE deficient animals, however, had significantly higher levels of antigen-specific IgM after immunization with tetanus toxoid, and impaired delayed type hypersensitivity responses as compared to control C57-BL/6 mice. These results support a growing body of evidence demonstrating an interplay between lipid metabolism and immune responses, and suggest that apoE plays a biologically relevant role in regulating humoral and cell-mediated immunity.