One mechanism offered to explain how infection contributes to the onset and progression of cardiovascular diseases is through increased production of proinflammatory cytokines [1, 3] . However, this explanation does not address how the production of inflammatory cytokines might proceed nor does it identity the cell types which are targets for the LPS stimulation. Platelets may represent one of the first blood borne elements to react to LPS stimulation as changes in platelet reactivity via TLR4 seems to occur prior to sustained changes in circulating levels of cytokines [14] . Alternatively, comparable activation of leukocyte as well as platelet result in formation of cell-derived microvesicles (MV) which may contribute to increased thrombogenic propensity of the blood, pro-inflammatory immune processes and thus cardiovascular risk [15, 16, 17, 18, 19, 20, 21, 22] . Clarifying the interactions of these blood elements (platelets and leukocytes) in the setting of TLR4 activation might provide insight into how infection initiates or facilitates progression of cardiovascular disease.