Abstract 1074: Contrast-Enhanced Ultrasound Characterization Of Inflammation And Vasa Vasoral Proliferation Caused By Mural Hemorrhage And Platelet Deposition
Background: Proliferation of the vasa vasorum contributes to growth and destabilization of atherosclerotic lesions. These vessels contribute both to intraplaque hemorrhage and inflammatory cell entry. We hypothesized that plaque hemorrhage, in particular the influx of blood platelets, serves as a self-propagating stimulus for remodeling of the vasa vasorum.
Methods: In 24 rabbits fed a high-fat diet for 2 weeks, 30 μl of either autologous blood (n=8), an equivalent amount of platelets alone (n=8), or saline was injected percutaneously into the media and adventitial layer of a femoral artery using high-frequency (55 MHz) ultrasound guidance. At 48 hours after injection, contrast-enhanced ultrasound (CEU) molecular imaging was performed with microbubbles targeted to ICAM-1 and αv-integrins. CEU perfusion imaging with maximum intensity projection was performed for the injected and contralateral control artery to evaluate mural microvascular density at 1, 2 and 6 weeks.
Results: At 48 hrs, targeted signal enhancement for ICAM-1 and αv-integrins was greater in blood- and platelet-injected vessels compared to controls. Peak microvascular proliferation in response to whole blood or platelets occurred at 2 weeks. At this time point, mural microvascular density was significantly higher for the injected artery compared to the contralateral control artery for whole blood (800±535 vs 208±296 enhancement units [eu], p<0.05) and platelet-treated vessels (853±510 vs 197±188 eu, p<0.05). Mural microvascular density was not increased by saline injection (133±116 vs 260±313 for the control artery, p=0.61). Microvascular density was significantly (p<0.05) greater for both blood and platelet injections compared to saline control injections. At 6 weeks, microvascular density regressed by approximately 50% in both blood- and platelet-treated vessels.
Conclusion: In the presence of hyperlipidemia, intramural hemorrhage triggers an inflammatory response and proliferation of the vasa vasorum. The platelet component of blood appears to play a prominent role in this vascular remodeling. Neovessels formed after mural hemorrhage tend to regress in the absence of additional stimuli.