Key result
Short-term LPS injection significantly increased maximal aortic valve leaflet thickness at 2 days (128.4 µm vs 67.8 µm; P=0.007) in an atherosclerotic mouse model.
Why the study?
While 12 weeks of LPS administration induces aortic valve thickening in nonatherosclerotic mice, whether earlier effects occur is unknown, prompting investigation of short-term LPS in an atherosclerotic mouse model.
Does short-term LPS administration induce aortic valve thickening in ApoE*3Leiden mice on an atherogenic diet?
Does short-term LPS administration induce aortic valve thickening in ApoE*3Leiden mice on an atherogenic diet?
Absolute Event Rate: 128.4% vs 67.8%
p-value: p=0.007
Short-term systemic inflammation induced by LPS acutely compromises aortic valve structure by increasing thickening and hemorrhage in an atherosclerotic mouse model.
Short-term LPS may accelerate early AV thickening in atherosclerotic models; leaves open causal role in human AV stenosis.
BACKGROUND: Recently, it was shown that 12 weeks of lipopolysaccharide (LPS) administration to nonatherosclerotic mice induced thickening of the aortic heart valve (AV). Whether such effects may also occur even earlier is unknown. As most patients with AV stenosis also have atherosclerosis, we studied the short-term effect of LPS on the AVs in an atherosclerotic mouse model. METHODS: ApoE*3Leiden mice, on an atherogenic diet, were injected intraperitoneally with either LPS or phosphate buffered saline (PBS), and sacrificed 2 or 15 days later. AVs were assessed for size, fibrosis, glycosaminoglycans (GAGs), lipids, calcium deposits, iron deposits and inflammatory cells. RESULTS: LPS injection caused an increase in maximal leaflet thickness at 2 days (128.4 µm) compared to PBS-injected mice (67.8 µm; P = 0.007), whereas at 15 days this was not significantly different. LPS injection did not significantly affect average AV thickness on day 2 (37.8 µm), but did significantly increase average AV thickness at day 15 (41.6 µm; P = 0.038) compared to PBS-injected mice (31.7 and 32.3 µm respectively). LPS injection did not affect AV fibrosis, GAGs and lipid content. Furthermore, no calcium deposits were found. Iron deposits, indicative for valve haemorrhage, were observed in one AV of the PBS-injected group (a day 2 mouse; 9.1%) and in five AVs of the LPS-injected group (both day 2- and 15 mice; 29.4%). No significant differences in inflammatory cell infiltration were observed upon LPS injection. CONCLUSION: Short-term LPS apparently has the potential to increase AV thickening and haemorrhage. These results suggest that systemic inflammation can acutely compromise AV structure.
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Broekhoven et al. (2019) studied Atherosclerosis. Lipopolysaccharide (LPS) vs. Phosphate buffered saline (PBS) was evaluated on Maximal leaflet thickness at 2 days (p=0.007). Short-term LPS injection significantly increased maximal aortic valve leaflet thickness at 2 days (128.4 µm vs 67.8 µm; P=0.007) in an atherosclerotic mouse model.
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