Author + information
- Received October 31, 2019
- Revision received May 19, 2020
- Accepted June 4, 2020
- Published online October 5, 2020.
- Alban Redheuil, MD, PhDa,b,c,∗,
- Anne Blanchard, MD, PhDd,e,f,g,h,∗,
- Helena Pereira, PhDd,e,f,g,
- Zainab Raissouni, MDd,e,g,h,i,
- Aurelien Lorthioir, MDd,e,f,g,j,
- Gilles Soulat, MDd,e,f,g,j,
- Rosa Vargas-Poussou, MScd,e,f,
- Laurence Amar, MD, PhDd,e,f,g,h,
- Jean-Louis Paul, MD, PhDd,e,f,
- Dominique Helley, MD, PhDd,e,f,g,
- Michel Azizi, MD, PhDd,e,f,g,h,
- Nadjia Kachenoura, PhDb,c and
- Elie Mousseaux, MD, PhDd,e,f,g,j,∗ ()
- aDepartment of Radiology, Hôpital Pitié Salpêtrière, Assistance Publique-Hôpitaux de Paris, Paris, France
- bLaboratoire d’Imagerie Biomédicale, National Centre for Scientific Research, French Institute of Health and Medical Research, Sorbonne Université, Paris, France
- cInstitute of Cardiometabolism and Nutrition, Paris, France
- dDepartment of Radiology, Hôpital Européen Georges-Pompidou, Assistance Publique-Hôpitaux de Paris, Paris, France
- eDepartment of Hypertension, Hôpital Européen Georges-Pompidou, Assistance Publique-Hôpitaux de Paris, Paris, France
- fDepartment of Biological & Statistic, Hôpital Européen Georges-Pompidou, Assistance Publique-Hôpitaux de Paris, Paris, France
- gUniversité de Paris, Paris, France
- hDepartment of Cardiology, Center for Clinical Investigation 1418, French Institute of Health and Medical Research, Paris, France
- iDepartment of Cardiology, Tangier Medical School, Abdelmalek Essaâdi University, Tétouan, Morocco
- jParis Cardiovascular Research Center, French Institute of Health and Medical Research, Paris, France
- ↵∗Address for correspondence:
Dr. Elie Mousseaux, Service de Radiologie, Hôpital Européen Georges Pompidou, 20-40 rue Leblanc 75015 Paris, France.
Objectives This study sought to assess the respective effects of aldosterone and blood pressure (BP) levels on myocardial fibrosis in humans.
Background Experimentally, aldosterone promotes left ventricular (LV) hypertrophy, and interstitial myocardial fibrosis in the presence of high salt intake.
Methods The study included 20 patients with primary aldosteronism (PA) (high aldosterone and high BP), 20 patients with essential hypertension (HTN) (average aldosterone and high BP), 20 patients with secondary aldosteronism due to Bartter/Gitelman (BG) syndrome (high aldosterone and normal BP), and 20 healthy subjects (HS) (normal aldosterone and normal BP). Participants in each group were of similar age and sex distributions, and asymptomatic. Cardiac magnetic resonance including cine and T1 mapping was performed blind to the study group to quantify global LV mass index, as well as intracellular mass index and extracellular mass index considered as a measure of myocardial fibrosis in vivo.
Results Median plasma aldosterone concentration was as follows: PA = 709 pmol/l (interquartile range [IQR]: 430 to 918 pmol/l); HTN = 197 pmol/l (IQR: 121 to 345 pmol/l); BG = 297 pmol/l (IQR: 180 to 428 pmol/l); and HS = 105 pmol/l (IQR: 85 to 227 pmol/l). Systolic BP was as follows: PA = 147 ± 15 mm Hg; HTN = 133 ± 19 mm Hg; BG = 116 ± 9 mm Hg; and HS = 117 ± 12 mm Hg. LV end-diastolic volume showed underloading in BG and overloading in patients with PA (63 ± 13 ml/m2 vs. 82 ± 15 ml/m2; p < 0.0001). Intracellular mass index increased with BP across groups (BG: 36 [IQR: 29 to 41]; HS: 40 [IQR: 36 to 46]; HTN: 51 [IQR: 42 to 54]; PA: 50 [IQR: 46 to 67]; p < 0.0001). Extracellular mass index was similar in BG, HS, and HTN (16 [IQR: 12 to 20]; 15 [IQR: 11 to 18]; and 14 [IQR: 12 to 17], respectively) but 30% higher in PA (21 [IQR: 18 to 29]; p < 0.0001) remaining significant after adjustment for mean BP.
Conclusions Only primary pathological aldosterone excess combined with high BP increased both extracellular myocardial matrix and intracellular mass. Secondary aldosterone excess with normal BP did not affect extracellular myocardial matrix. (Study of Myocardial Interstitial Fibrosis in Hyperaldosteronism; NCT02938910).
- extracellular matrix
- cardiac magnetic resonance
- myocardial fibrosis
- myocardial remodeling
- primary hyperaldosteronism
↵∗ Drs. Redheuil and Blanchard contributed equally to this work.
This work was funded by the “Contrat de Recherche Clinique from the Assistance Publique des Hôpitaux de Paris” and the French Ministry of Health (2012-A00615-38). The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Cardiovascular Imaging author instructions page.
- Received October 31, 2019.
- Revision received May 19, 2020.
- Accepted June 4, 2020.
- 2020 American College of Cardiology Foundation
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