Why the study?
Coronary adventitial inflammation drives DES-induced coronary hyperconstricting responses, but the role of adventitial lymphatic vessels in this pathogenesis was unknown.
Does cardiac lymphatic vessel dysfunction exacerbate drug-eluting stent-induced coronary hyperconstricting responses in a porcine model?
Comparison
DES vs bare metal stent vs nonstented sites, and DES with vs without lymphatic vessel ligation
Design
In vivo animal experimental study
Follow-up
4 weeks after DES implantation
Authors
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May implicate lymphatic dysfunction in DES vasospasm; hypothesis-generating in porcine model, requires human validation.
Does cardiac lymphatic vessel dysfunction exacerbate drug-eluting stent-induced coronary hyperconstricting responses in a porcine model?
Cardiac lymphatic vessel dysfunction exacerbates DES-induced coronary hyperconstricting responses and adventitial inflammation in a porcine model, suggesting a novel mechanism for DES-related vasomotion abnormalities.
Amamizu et al. (2019) studied this question.
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