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Background: Atherosclerosis is a major cardiovascular problem but the responsible molecular mechanisms are still unclear. Toll-like receptors (TLRs) are considered major culprits for the development of atherosclerosis and heart failure. However, evidence for most TLRs beyond TLR2 and TLR4 is lacking. To examine the TLR7 involvement in atherosclerosis we generated toll-like receptor-7-deficient apolipoprotein E-deficient (TLR7-/-ApoE-/-) mice and compare their cardiac and vascular function with ApoE-/- mice.Methods: ApoE-/- mice on a C57BL/6J background were crossed with TLR7-/- mice originally obtained from Shizuo Akira (Osaka University, Japan). Echocardiographic studies were performed in 6 months old anesthetized mice (100mg/kg ketamine i.p.) using a 13 MHz linear transducer (Vivid 7, GE). M-mode measurements of LV end-diastolic diameter (EDD), LV end-systolic diameter (ESD), LV posterior wall thickness at diastole (PWT) and FS (%) = [(EDD-ESD)/EDD] x 100 were made. From transvalvular aortic blood flow we also measured: peak aortic velocity (PAV); stroke distance (ST); mean aortic velocity (MAV); and peak aortic acceleration (PAA). Finally, carotid artery Doppler flow waveforms were recorded and the maximum and mean velocities of the waveforms were measured.Results are presented in Table 1.Conclusions: Overall LV function was not affected in TLR7-/-ApoE-/- mice although an increase in EDD was apparent. No differences were found in PWT and aortic velocities assuming no LV outflow obstruction. Carotid velocity indices were higher in the TLR7-/-ApoE-/- group in agreement with enhanced atherosclerotic lesions in these mice.