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

Abstract

BackgroundPrimary 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.ObjectivesTo assess LV mass and fibrosis before and after treatment of PA using CMR with contrast enhancement and T1 mapping.MethodsFifteen 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).ResultsPA1 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.ConclusionSpecific treatment rapidly reduced LV mass in PA. Increased myocardial fibrosis was not found and may not represent a common clinical problem.

Left ventricular remodeling and dysfunction in primary aldosteronism

“…Myocardial fibrosis in PA also can be assessed by cardiac MRI with gadolinium-enhanced imaging or other imaging processing methods evaluating the texture of the myocardium. PA patients have been shown to have a higher fibrosis index, LV stiffness, and noninfarct-related fibrosis compared with healthy volunteers or EH controls, while only one small-sized study has reported conflicting data [82]. Although no difference was found in myocardial fibrosis after treatment in that study [82], it was limited by a small sample size.…”

“…One recent study from Italy reported pathological findings from endomyocardial biopsies in PA patients, and revealed prominent myocardial hypertrophy and fibrosis, with reversible water accumulation in the cytosol and organelles of cardiomyocytes and microvascular smooth muscle cells after adrenalectomy [76]. However, the small sample size limited the clinical and statistical power with regards to proving an increase in myocardial fibrosis due to PA. Clinically, myocardial fibrosis in PA is mostly evaluated by echocardiography and cardiac MRI, in conjunction with serum biomarkers that are elevated during increased myocardial fibrosis, as listed in Table 1 [17,36,39,67,73,[76][77][78][79][80][81][82].…”

CMR-Verified Myocardial Fibrosis is Associated With Subclinical Diastolic Dysfunction in Primary Aldosteronism Patients

“…If the myocardial brosis increases in PA patients, the answer is still controversial [13][14][15][16]26]. Cardiac biopsy samples from four male PA patients exhibited 1.5-fold more brosis than those from EH patients (14% vs. 6%) [16].…”

“…Studies have found that cardiac dysfunction results from brosis of the myocardium in many diseases, such as heart failure [10], hypertrophic cardiomyopathy [11], and diabetic patients [12]. As to if myocardial brosis increases in PA patients, the answer is still controversial [13][14][15][16][17].…”

“…Moreover, adrenalectomy was proven to reverse myocardial brosis in PA patients [17]. However, Gretaas et al [13] reported that increased myocardial brosis was not found and may not represent a common clinical problem in PA.…”