Effects of renin-angiotensin-aldosterone-system inhibitors on coronary atherosclerotic plaques: The PARADIGM registry.
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Williams Curtis, Han Donghee, Takagi Hidenobu, Fordyce Christopher B, Sellers Stephanie, Blanke Philipp, Lin Fay Y, Shaw Leslee J, Lee Sang-Eun, Andreini Daniele, Al-Mallah Mouaz H, Budoff Matthew J, Cademartiri Filippo, Chinnaiyan Kavitha, Choi Jung Hyun, Conte Edoardo, Marques Hugo, de Araújo Gonçalves Pedro, Gottlieb Ilan, Hadamitzky Martin, Maffei Erica, Pontone Gianluca, Shin Sanghoon, Kim Yong-Jin, Lee Byoung Kwon, Chun Eun Ju, Sung Ji Min, Virmani Renu, Samady Habib, Stone Peter H, Berman Daniel S, Narula Jagat, Bax Jeroen J, Leipsic Jonathon A, Chang Hyuk-Jae
Аннотация
METHODS: We performed a prospective, multinational study consisting of a registry of patients without history of CAD, who underwent serial CCTAs. Patients using RAAS inhibitors were propensity matched to RAAS inhibitor naïve patients based on clinical and CCTA characteristics at baseline. Atherosclerotic plaques in CCTAs were quantitatively analyzed for percent atheroma volume (PAV) according to plaque composition. Interactions between RAAS inhibitor use and baseline PAV on plaque progression were assessed in the unmatched cohort using a multivariate linear regression model.
RESULTS: Of 1248 patients from the registry, 299 RAAS inhibitor taking patients were matched to 299 RAAS inhibitor naïve patients. Over a mean interval of 3.9 years, there was no significant difference in annual progression of total PAV between RAAS inhibitor naïve vs taking patients (0.75 vs 0.79%/year, p = 0.66). With interaction testing in the unmatched cohort, however, RAAS inhibitor use was significantly associated with lower non-calcified plaque progression (Beta coefficient -0.100, adjusted p = 0.038) with higher levels of baseline PAV.
CONCLUSIONS: The use of RAAS inhibitors over a period of nearly 4 years did not significantly impact on total atherosclerotic plaque progression or various plaque components. However, interaction testing to assess the differential effect of RAAS inhibition based on baseline PAV suggested a significant decrease in progression of non-calcified plaque in patients with a higher burden of baseline atherosclerosis, which should be considered hypothesis generating.