Effects of renin-angiotensin-aldosterone-system inhibitors on coronary atherosclerotic plaques: The PARADIGM registry.


Journal

Atherosclerosis
ISSN: 1879-1484
Titre abrégé: Atherosclerosis
Pays: Ireland
ID NLM: 0242543

Informations de publication

Date de publication:
10 2023
Historique:
received: 24 02 2023
revised: 08 09 2023
accepted: 14 09 2023
medline: 23 10 2023
pubmed: 29 9 2023
entrez: 28 9 2023
Statut: ppublish

Résumé

Inhibition of Renin-Angiotensin-Aldosterone-System (RAAS) has been hypothesized to improve endothelial function and reduce plaque inflammation, however, their impact on the progression of coronary atherosclerosis is unclear. We aim to study the effects of RAAS inhibitor on plaque progression and composition assessed by serial coronary CT angiography (CCTA). 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. 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. 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.

Sections du résumé

BACKGROUND AND AIMS
Inhibition of Renin-Angiotensin-Aldosterone-System (RAAS) has been hypothesized to improve endothelial function and reduce plaque inflammation, however, their impact on the progression of coronary atherosclerosis is unclear. We aim to study the effects of RAAS inhibitor on plaque progression and composition assessed by serial coronary CT angiography (CCTA).
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.

Identifiants

pubmed: 37769454
pii: S0021-9150(23)05222-X
doi: 10.1016/j.atherosclerosis.2023.117301
pii:
doi:

Substances chimiques

Aldosterone 4964P6T9RB
Renin EC 3.4.23.15
Angiotensins 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

117301

Informations de copyright

Copyright © 2023. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Curtis Williams (C)

Division of Cardiology, University of British Columbia, Vancouver, British Columbia, Canada.

Donghee Han (D)

Department of Imaging and Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Hidenobu Takagi (H)

Department of Radiology and Centre for Heart Lung Innovation, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada; Dalio Institute of Cardiovascular Imaging, Department of Radiology, NewYork-Presbyterian Hospital and Weill Cornell Medicine, New York, NY, USA.

Christopher B Fordyce (CB)

Division of Cardiology, University of British Columbia, Vancouver, British Columbia, Canada.

Stephanie Sellers (S)

Department of Radiology and Centre for Heart Lung Innovation, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada.

Philipp Blanke (P)

Department of Radiology and Centre for Heart Lung Innovation, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada.

Fay Y Lin (FY)

Dalio Institute of Cardiovascular Imaging, Department of Radiology, NewYork-Presbyterian Hospital and Weill Cornell Medicine, New York, NY, USA.

Leslee J Shaw (LJ)

Dalio Institute of Cardiovascular Imaging, Department of Radiology, NewYork-Presbyterian Hospital and Weill Cornell Medicine, New York, NY, USA.

Sang-Eun Lee (SE)

Division of Cardiology, Department of Internal Medicine, Ewha Womans University Seoul Hospital, Seoul, South Korea; Yonsei-Cedars-Sinai Integrative Cardiovascular Imaging Research Center, Yonsei University College of Medicine, Yonsei University Health System, South Korea.

Daniele Andreini (D)

Centro Cardiologico Monzino, IRCCS Milan, Italy.

Mouaz H Al-Mallah (MH)

Houston Methodist DeBakey Heart & Vascular Center, Houston Methodist Hospital, Houston, TX, USA.

Matthew J Budoff (MJ)

Department of Medicine, Los Angeles Biomedical Research Institute, Torrance, CA, USA.

Filippo Cademartiri (F)

Department of Radiology, Fondazione Monasterio/CNR, Pisa, Italy.

Kavitha Chinnaiyan (K)

Department of Cardiology, William Beaumont Hospital, Royal Oak, MI, USA.

Jung Hyun Choi (JH)

Pusan University Hospital, Busan, South Korea.

Edoardo Conte (E)

Centro Cardiologico Monzino, IRCCS Milan, Italy.

Hugo Marques (H)

UNICA, Unit of Cardiovascular Imaging, Hospital da Luz, Lisboa, Portugal.

Pedro de Araújo Gonçalves (P)

UNICA, Unit of Cardiovascular Imaging, Hospital da Luz, Lisboa, Portugal; Nova Medical School, Lisboa, Portugal.

Ilan Gottlieb (I)

Department of Radiology, Casa de Saude São Jose, Rio de Janeiro, Brazil.

Martin Hadamitzky (M)

Department of Radiology and Nuclear Medicine, German Heart Center Munich, Munich, Germany.

Erica Maffei (E)

Department of Radiology, Fondazione Monasterio/CNR, Pisa, Italy.

Gianluca Pontone (G)

Centro Cardiologico Monzino, IRCCS Milan, Italy.

Sanghoon Shin (S)

Division of Cardiology, Department of Internal Medicine, Ewha Womans University Seoul Hospital, Seoul, South Korea.

Yong-Jin Kim (YJ)

Department of Internal Medicine, Seoul National University College of Medicine, Cardiovascular Center, Seoul National University Hospital, Seoul, South Korea.

Byoung Kwon Lee (BK)

Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.

Eun Ju Chun (EJ)

Icahn School of Medicine at Mount Sinai, Mount Sinai Heart, Zena and Michael A. Wiener Cardiovascular Institute, and Marie-Josée and Henry R. Kravis Center for Cardiovascular Health, New York, NY, USA.

Ji Min Sung (JM)

Yonsei-Cedars-Sinai Integrative Cardiovascular Imaging Research Center, Yonsei University College of Medicine, Yonsei University Health System, South Korea; Department of Cardiology, Heart Lung Center, Leiden University Medical Center, Leiden, the Netherlands.

Renu Virmani (R)

Department of Pathology, CVPath Institute, Gaithersburg, MD, USA.

Habib Samady (H)

Division of Cardiology, Georgia Heart Institute, Gainesville, USA.

Peter H Stone (PH)

Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.

Daniel S Berman (DS)

Department of Imaging and Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Jagat Narula (J)

Icahn School of Medicine at Mount Sinai, Mount Sinai Heart, Zena and Michael A. Wiener Cardiovascular Institute, and Marie-Josée and Henry R. Kravis Center for Cardiovascular Health, New York, NY, USA.

Jeroen J Bax (JJ)

Department of Cardiology, Heart Lung Center, Leiden University Medical Center, Leiden, the Netherlands.

Jonathon A Leipsic (JA)

Department of Radiology and Centre for Heart Lung Innovation, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada. Electronic address: jonathon.leipsic@ubc.ca.

Hyuk-Jae Chang (HJ)

Yonsei-Cedars-Sinai Integrative Cardiovascular Imaging Research Center, Yonsei University College of Medicine, Yonsei University Health System, South Korea; Division of Cardiology, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH