Reversal of myocardial fibrosis in patients with unilateral hyperaldosteronism receiving adrenalectomy

Lin, Yen‐Hung; Lee, Hsiu-Hao; Liu, Kao–Lang; Lee, Jen‐Kuang; Shih, Shyang-Rong; Chueh, Shih-Chieh; Lin, Wei-Chou; Lin, Lung‐Chun; Lin, Lian‐Yu; Chung, Shiu-Dong; Wu, Vin‐Cent; Kuo, Chin‐Chi; Ho, Yi‐Lwun; Chen, Ming-Fong; Wu, Kwan‐Dun

doi:10.1016/j.surg.2011.02.006

Cited by 44 publications

(40 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These results also suggest that the elevation of plasma TIMP-1 level may be the result of excessive aldosterone. In our previous studies, myocardial fibrosis improved 1 year after adrenalectomy among patients with APA [20,33]. This current study extended the knowledge that the diastolic dysfunction also improves after adrenalectomy among patients with APA.…”

Section: Discussionsupporting

confidence: 81%

Circulating tissue inhibitor of matrix metalloproteinase-1 is associated with aldosterone-induced diastolic dysfunction

Hung¹,

Chou

et al. 2015

Journal of Hypertension

Self Cite

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 81%

Circulating tissue inhibitor of matrix metalloproteinase-1 is associated with aldosterone-induced diastolic dysfunction

Hung¹,

Chou

et al. 2015

Journal of Hypertension

Self Cite

View full text Add to dashboard Cite

show abstract

“…ACEI, angiotensin-converting enzyme inhibitor; APA, aldosterone-producing adenoma; ARB, angiotensin receptor blocker; ARR, aldosterone-renin ratio; BP, blood pressure; CCB, calcium channel blocker; EH, essential hypertension; MBP, mean blood pressure; PAC, plasma aldosterone concentration; PRA, plasma renin activity. To the best of our knowledge, unlike the reversal of left ventricular geometry [5,7,8] or diastolic function [5], the reversal of myocardial fibrosis after adrenalectomy of APA patients has never been reported before with the exception of our previous preliminary study [33]. This study provides further evidence of the reversibility of increased myocardial fibrosis in APA patients in terms of both serology and image.…”

Section: Discussionsupporting

confidence: 54%

“…However, adrenalectomy remains the treatment of choice of APA patients and whether or not myocardial fibrosis is reversible after adrenalectomy remains unclear. Our team published the preliminary results describing the improvement in myocardial fibrosis (measured by CVIBS) in APA patients receiving adrenalectomy [22]. However, the number of patients was only 11 and serological evidence was still lacking.…”

mentioning

confidence: 99%

Adrenalectomy reverses myocardial fibrosis in patients with primary aldosteronism

Lin

Lee³

et al. 2012

Journal of Hypertension

Self Cite

View full text Add to dashboard Cite

show abstract

“…1,2 In our previous clinical studies, patients with primary aldosteronism (PA), a disease characterized by excessive aldosterone secretion, exhibited increased myocardial fibrosis in serum fibrosis markers, 3 myocardial texture, 3,4 and gadolinium-enhanced cardiac magnetic resonance imaging. 5 Furthermore, in patients with heart failure and diastolic dysfunction, treatment with mineralocorticoid receptor (MR) blockade has been shown to result in improvements in collagen turnover markers 6 and diastolic function.…”

mentioning

confidence: 99%

Aldosterone Induces Tissue Inhibitor of Metalloproteinases-1 Expression and Further Contributes to Collagen Accumulation

et al. 2016

Self Cite

View full text Add to dashboard Cite

Abstract-Aldosterone induces myocardial fibrosis. Tissue inhibitor of metalloproteinases-1 (TIMP-1) is a key factor of myocardial fibrosis. This study tested the hypothesis that aldosterone induces TIMP-1 expression and contributes to the fibrotic process. We prospectively enrolled 54 patients with primary aldosteronism, and measured plasma TIMP-1 and echocardiographic parameters. In the cell study, we investigated the possible molecular mechanism by which aldosterone induces TIMP-1 secretion and the effects on collagen accumulation. In the animal study, we measured serum TIMP-1 levels, cardiac TIMP-1 levels, and cardiac structure in an aldosterone infusion mouse model using implantation of aldosterone pellets. In patients with primary aldosteronism, plasma TIMP-1 was correlated with 24-hour urinary aldosterone, left ventricular mass, and impairment of left ventricular diastolic function. In human cardiac fibroblasts, TIMP-1 protein and mRNA expressions were significantly increased by aldosterone through the glucocorticoid receptor/PI3K/Akt/nuclear factor-κB pathway. TIMP-1 small-interfering RNA significantly reduced aldosterone-induced collagen accumulation, and aldosterone did not alter the levels of collagen1a1 or matrix metalloproteinase-1 mRNA. The aldosterone-induced TIMP-1 expression was inversely related to matrix metalloproteinase-1 activity. Furthermore, in the animal model, the serum and cardiac levels of TIMP-1 were significantly elevated in the mice that received aldosterone infusion. This elevation was blocked by RU-486 but not by eplerenone, suggesting that the effect was through glucocorticoid receptors. In a long-term aldosterone infusion model, serum TIMP-1 was associated with serum aldosterone level, cardiac structure, and fibrosis. In conclusion, aldosterone induced TIMP-1 expression in vivo and in vitro. This increased TIMP-1 expression resulted in enhanced collagen accumulation via the suppression of matrix metalloproteinase-1 activity.

show abstract

Reversal of myocardial fibrosis in patients with unilateral hyperaldosteronism receiving adrenalectomy

Cited by 44 publications

References 45 publications

Circulating tissue inhibitor of matrix metalloproteinase-1 is associated with aldosterone-induced diastolic dysfunction

Circulating tissue inhibitor of matrix metalloproteinase-1 is associated with aldosterone-induced diastolic dysfunction

Adrenalectomy reverses myocardial fibrosis in patients with primary aldosteronism

Aldosterone Induces Tissue Inhibitor of Metalloproteinases-1 Expression and Further Contributes to Collagen Accumulation

Contact Info

Product

Resources

About