Epicardial Fat Thickness and Primary Aldosteronism

Abstract

Primary aldosteronism (PA) is associated with increased cardiovascular risk and left ventricle (LV) changes. Given its peculiar biomolecular and anatomic properties, excessive epicardial fat, the heart-specific visceral fat depot, can affect LV morphology. Whether epicardial fat can be associated with aldosterone and LV mass (LVM) in patients with PA is unknown. We performed ultrasound measurement of the epicardial fat thickness (EAT) in 79 consecutive newly diagnosed patients with PA, 59 affected by bilateral adrenal hyperplasia (IHA), 20 aldosterone-producing adenoma (APA), and 30 patients with essential hypertension (low renin hypertension) (EH). The 3 groups did not differ by age, sex distribution, body mass index (BMI), waist circumference (WC), or blood pressure values. EAT showed a trend of increase in both APA and IHA groups when compared to patients with EH (8.3±1.8 vs. 7.9±1.3 vs. 7.8±2 mm, respectively). EAT was significantly correlated with indexed LVM in the IHA group (r=0.35, p<005), better than BMI or WC were. Interestingly, EAT was highly associated with plasma aldosterone concentrations (PAC) and PAC/plasma renin activity (PRA) (PAC/PRA) in the APA group (p=0.58, p=0.37, p<0.01, for both), whereas BMI and WC were not. EAT was also correlated with PRA in the IHA group (p=-0.28, p<0.05). Our study indicates a novel and interesting interaction of EAT with PA, independent of obesity, abdominal fat and blood pressure control. EAT can locally affect LVM, at least in patients with IHA. Further studies in larger population will be required to confirm these findings.

Epicardial Fat Thickness in Patients with Autosomal Dominant Polycystic Kidney Disease

“…EAT thickness can be easily and accurately measured with standard ultrasound in a hypertension work-up, as previously shown by our group [36]. We believe that LVMi and EAT are not interchangeable.…”

Critical role of the epicardium in mediating cardiac inflammation and fibrosis in patients with type 2 diabetes

“…It is therefore noteworthy that mineralocorticoid receptor signalling is required for the differentiation of adipocytes and their transition to a proinflammatory biology, whereas natriuretic peptides act in a counterregulatory manner to limit adipogenesis and restrain the proinflammatory transformation of adipose tissue (Figure ) . These interactions may explain why the volume of epicardial adipose tissue is directly and inversely related to circulating levels of aldosterone and natriuretic peptides, respectively . Thus, the imbalance of aldosterone and natriuretic peptide signalling that characterizes diabetes may be directly responsible for the expansion and inflammation of epicardial adipose tissue.…”

“…26 These interactions may explain why the volume of epicardial adipose tissue is directly and inversely related to circulating levels of aldosterone and natriuretic peptides, respectively. 27,28 Thus, the imbalance of aldosterone and natriuretic peptide signalling that characterizes diabetes may be directly responsible for the expansion and inflammation of epicardial adipose tissue.…”

The epicardial adipose inflammatory triad: coronary atherosclerosis, atrial fibrillation, and heart failure with a preserved ejection fraction

“…If additional studies confirm that dysfunctional expansion of epicardial adipocytes contribute to structural and functional derangements of the underlying ventricular myocardium, then epicardial adipose tissue may become an important therapeutic target in the management of patients with HFpEF. Aldosterone can promote the accumulation and inflammation of epicardial fat, and mineralocorticoid receptor antagonists reduce obesity‐related adipose tissue inflammation and may have benefits in obesity‐related HFpEF . Natriuretic peptide receptor signalling has anti‐adipogenic effects and ameliorates adipocyte inflammation, and levels of natriuretic peptides are inversely related to epicardial fat thickness .…”