Endocrinology and Metabolism

Eunhee Choi (Choi E)

1 Article

Clinical Study
Cardiac Dysfunction in Association with Increased Inflammatory Markers in Primary Aldosteronism: Jung Soo Lim, Sungha Park, Sung Il Park, Young Taik Oh, Eunhee Choi, Jang Young Kim, Yumie Rhee; Endocrinol Metab. 2016;31(4):567-576. Published online November 3, 2016; DOI: https://doi.org/10.3803/EnM.2016.31.4.567; Correction in: Endocrinol Metab 2020;35(3):671

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Background

Oxidative stress in primary aldosteronism (PA) is thought to worsen aldosterone-induced damage by activating proinflammatory processes. Therefore, we investigated whether inflammatory markers associated with oxidative stress is increased with negative impacts on heart function as evaluated by echocardiography in patients with PA.

Methods

Thirty-two subjects (mean age, 50.3±11.0 years; 14 males, 18 females) whose aldosterone-renin ratio was more than 30 among patients who visited Severance Hospital since 2010 were enrolled. Interleukin-1β (IL-1β), IL-6, IL-8, monocyte chemoattractant protein 1, tumor necrosis factor α (TNF-α), and matrix metalloproteinase 2 (MMP-2), and MMP-9 were measured. All patients underwent adrenal venous sampling with complete access to both adrenal veins.

Results

Only MMP-2 level was significantly higher in the aldosterone-producing adenoma (APA) group than in the bilateral adrenal hyperplasia (BAH). Patients with APA had significantly higher left ventricular (LV) mass and A velocity, compared to those with BAH. IL-1β was positively correlated with left atrial volume index. Both TNF-α and MMP-2 also had positive linear correlation with A velocity. Furthermore, MMP-9 showed a positive correlation with LV mass, whereas it was negatively correlated with LV end-systolic diameter.

Conclusion

These results suggest the possibility that some of inflammatory markers related to oxidative stress may be involved in developing diastolic dysfunction accompanied by LV hypertrophy in PA. Further investigations are needed to clarify the role of oxidative stress in the course of cardiac remodeling.

Citations

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