Cardiac magnetic resonance imaging of myocardial mass and fibrosis in primary aldosteronism.

Abstract:

BACKGROUND:Primary aldosteronism (PA) is associated with increased cardiovascular morbidity, presumably due to left ventricular (LV) hypertrophy and fibrosis. However, the degree of fibrosis has not been extensively studied. Cardiac magnetic resonance imaging (CMR) contrast enhancement and novel sensitive T1 mapping to estimate increased extracellular volume (ECV) are available to measure the extent of fibrosis. OBJECTIVES:To assess LV mass and fibrosis before and after treatment of PA using CMR with contrast enhancement and T1 mapping. METHODS:Fifteen patients with newly diagnosed PA (PA1) and 24 age- and sex-matched healthy subjects (HS) were studied by CMR with contrast enhancement. Repeated imaging with a new scanner with T1 mapping was performed in 14 of the PA1 and 20 of the HS median 18 months after specific PA treatment and in additional 16 newly diagnosed PA patients (PA2). RESULTS:PA1 had higher baseline LV mass index than HS (69 (53-91) vs 51 (40-72) g/m2; P < 0.001), which decreased significantly after treatment (58 (40-86) g/m2; P < 0.001 vs baseline), more with adrenalectomy (n = 8; -9 g/m2; P = 0.003) than with medical treatment (n = 6; -5 g/m2; P = 0.075). No baseline difference was found in contrast enhancement between PA1 and HS. T1 mapping showed no increase in ECV as a myocardial fibrosis marker in PA. Moreover, ECV was lower in the untreated PA2 than HS 10 min post-contrast, and in both PA groups compared with HS 20 min post-contrast. CONCLUSION:Specific treatment rapidly reduced LV mass in PA. Increased myocardial fibrosis was not found and may not represent a common clinical problem.

journal_name

Endocr Connect

journal_title

Endocrine connections

authors

Grytaas MA,Sellevåg K,Thordarson HB,Husebye ES,Løvås K,Larsen TH

doi

10.1530/EC-18-0039

subject

Has Abstract

pub_date

2018-03-01 00:00:00

pages

413-424

issue

3

issn

2049-3614

pii

EC-18-0039

journal_volume

7

pub_type

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