A healthy
vascular endothelium is critical to health and interference with endothelial
homeostasis disrupts haemostasis, regulation of vascular tone and blood pressure, leukocyte
trafficking, angiogenesis and tissue repair. Endothelial injury and apoptosis leads to
endothelial dysfunction,
which is closely associated with increased generation of reactive
oxygen species, reduced endothelial nitric oxide synthase, increased consumption and
impaired synthesis of nitric oxide. Systemic inflammatory diseases including rhe
umatoid
arthritis and systemic lupus erythematosus are associated with endothelial dysfunction and
increased aortic stiffness, states closely associated with atherogenesis.
Premature
cardiovascular disease is well recognised feature of many rheumatic diseases. The cell and
molecular mechanisms related to this remain poorly understood. Specific diseases display
individual and common attributes that likely influence cardiovascular risk. A key challenge is
the development of the means by which those at highest
risk can be identified. Likewise, the
ability of current therapies to mitigate risk and the identification of novel vasculoprotective
therapies represent important areas of research focus.
Similarly close liaison between
rheumatologists and cardiologists is essential to minimise the cardiovascular impact on
patients and to ensure that patients with rheumatic disease and co-
existent coronary heart
disease receive appropriate therapy.
Identification of safe therapeutic approaches that
combine the targeted im
munosuppression required, along with comprehensive vascular
protection to control the primary disease and prevent secondary complications over the longer
term, remains the ultimate challenge.