Key result
Plasma Urotensin II levels were lower in patients with acute coronary syndrome at admission compared to three-month follow-up, suggesting its down-regulation is related to plaque instability.
Why the study?
Urotensin II is involved in the formation of atherosclerosis, but its role in the stability of atherosclerotic plaques was unknown.
Are dynamic changes in plasma Urotensin II correlated with atherosclerotic plaque stability in patients with ACS and rabbit models?
Observational (n=135)
Are dynamic changes in plasma Urotensin II correlated with atherosclerotic plaque stability in patients with ACS and rabbit models?
Urotensin II expression is down-regulated in ACS and vulnerable plaques, suggesting it may play a role in modulating plaque stability.
May support Urotensin II as plaque stability marker in ACS; hypothesis-generating and requires prospective validation before clinical use.
Urotensin II (UII) is involved in the formation of atherosclerosis, but its role in the stability of atherosclerotic plaques is unknown. The purpose of this study was to observe the dynamic changes in plasma UII and analyze its relationship to the stability of atherosclerotic plaques. One hundred thirty-five consecutive patients with acute coronary syndrome (ACS) were enrolled. The plasma UII levels were measured immediately after admission and during three-month follow-up. A vulnerable plaque model was established using local transfection of a recombinant P53 adenovirus into plaques in rabbits fed with a high-cholesterol diet and subjected to balloon arterial injury. The levels of plasma UII were measured weekly. The changes in plasma UII during the formation of atherosclerotic plaques and before and after plaque transfection were observed. The morphology of the plaques and the expression, distribution, and quantitative expression of UII in the plaques also were observed. Our results showed that the levels of plasma UII in patients with ACS at admission were lower than levels observed at the three-month follow-up. UII dynamic changes and its correlation with plaque stabilities were further verified in rabbits with atherosclerotic vulnerable plaques. The UII levels in rabbits were significantly decreased immediately after the P53 gene transfection, which led to plaque instability and rupture. These results suggested that UII expression was down-regulated in ACS, which may be related to its ability to modulate mechanisms involved in plaque stability and instability.
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Yin et al. (2021) conducted an observational in Acute coronary syndrome (n=135). Plasma Urotensin II levels vs. Three-month follow-up levels was evaluated on Dynamic changes in plasma Urotensin II and correlation with plaque stability. Plasma Urotensin II levels were lower in patients with acute coronary syndrome at admission compared to three-month follow-up, suggesting its down-regulation is related to plaque instability.
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