Dr. Harald HHW Schmidt
Many cardiovascular diseases (CVD) are associated with inflammation, and inflammatory diseases such as rheumatoid arthritis are associated with cardiovascular risk. Different cells appear to be involved, including macrophages and platelets. Yet, no therapies have emerged so far, with the exception of the possible pleiotropic anti-inflammatory effect of statins. Inflammation and response to statin treatment can now be localised and monitored by PET imaging based either on enhanced glucose uptake into metabolically active macrophages in high-risk plaques, or the new agent 11C-PK11195. For example, FDG-glucose uptake into the carotid is the only predictor of recurrent events after stroke and, in the aorta, allows tracking of inflammation during statin therapy. Plaque heterogeneity includes initial glucose signals that later disappear due to increasing calcification.With respect to treatment, ongoing trials are assessing potential new anti-inflammatory approaches using drugs such as mycophenolate, low dose methotrexate (CIRT), the IL-1 inhibitor canakinumab (CANTOS), as well as different inhibitors of IL-6, TNF-alpha, 5-lipoxygenase, FLAP, CCR2, Nox1 and PLA2. Targets from possibly defective anti-inflammatory pathways have apparently not yet been considered. The timing and duration of such interventions, their efficacy, and potential problems such as increased risk of infection need to be studied.
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