Long-term effects of adrenalectomy or spironolactone on blood pressure control and regression of left ventricle hypertrophy in patients with primary aldosteronism

Indra, T.; Holaj, Robert; Štrauch, Branislav; Rosa, Ján; Petrák, Ondřej; Šomlóová, Zuzana; Widimský, Jiří

doi:10.1177/1470320314549220

Cited by 29 publications

(21 citation statements)

References 46 publications

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“…Previous publication in this field have also shown a difference in the cost-benefit between patients receiving adrenalectomy and those only treated with MRA29. There are differential impact of adrenalectomy and MRA in regard to ventricular mass regression, with fewer or no effect of MRA on left ventrical index213031. Our study furthers knowledge in this field by demonstrating a difference in long term-mortality between these two patient groups.…”

Section: Discussionsupporting

confidence: 70%

Long term outcome of Aldosteronism after target treatments

Wang

Chang

et al. 2016

Sci Rep

112

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There exists a great knowledge gap in terms of long-term effects of various surgical and pharmacological treatments on outcomes among primary aldosteronism (PA) patients. Using a validated algorithm, we extracted longitudinal data for all PA patients diagnosed in 1997–2010 and treated in the Taiwan National Health Insurance. We identified 3362 PA patients for whom the mean length of follow-up was 5.75 years. PA has higher major cardiovascular events (MACE) than essential hypertension (23.3% vs 19.3%, p = 0.015). Results from the Cox model suggest a strong effect of adrenalectomy on lowering mortality (HR = 0.23 with residual hypertension and 0.21 with resolved hypertension). While need for receptor antagonist (MRA) MRA after diagnosis suggests that a defined daily dose (DDD) of MRA between 12.5 and 50 mg may alleviate risk of death in a U-shape pattern. A specificity test identified patients who has aldosterone producing adenoma (HR = 0.50, p = 0.005) also confirmed adrenalectomy attenuated all-cause mortality. Adrenalectomy decreases long-term all-cause mortality independently from PA cure from hypertension. Prescription corresponding to a DDD between 12.5 and 50 mg may decrease mortality for patients needing MRA. It calls for more attention on early diagnosis, early treatment and prescription of appropriate dosage of MRA for PA patients.

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Section: Discussionsupporting

confidence: 70%

Long term outcome of Aldosteronism after target treatments

Wang

Chang

et al. 2016

Sci Rep

112

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“…36 In clinical studies, patients with PA who received adrenalectomy have been reported to have a greater decrease in LV mass than in patients who received spironolactone treatment alone. [37][38][39] This also implies that MRs may not be the only pathway of aldosterone-induced myocardial hypertrophy. Taken together with our findings, a GR-mediated profibrotic response in cardiac fibroblasts may be an important pathway for cardiac fibrosis ( Figure 7).…”

Section: Discussionmentioning

confidence: 96%

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

et al. 2016

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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.

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“…MRA, an aldosterone receptor blocker, was effective at reducing blood pressure in PH patients and resulted in a significant decrease in biomarkers of collagen synthesis, left atrial dimension, left ventricular wall thickness and mass. 32,33 In view of this, early detection of PH is necessary because effective targeted treatment could affect hypertension-related outcomes. Considerable evidence has shown that ED is significantly associated with CVD and subsequent all-cause mortality.…”

Section: Discussionmentioning

confidence: 99%

Risk of severe erectile dysfunction in primary hyperaldosteronism: A population-based propensity score matching cohort study

Chang

Chueh

et al. 2019

Surgery

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Background: An elevated plasma aldosterone level has been reported as an independent risk factor for severe erectile dysfunction in men. The aim of this study was to explore whether primary hyperaldosteronism patients experience erectile dysfunction after targeted treatment. Methods: We conducted a population-based cohort study of men with newly identified primary hyperaldosteronism/aldosterone-producing adenoma from January 1, 1997, to December 31, 2009. Men with essential hypertension and normotension were matched to the primary hyperaldosteronism group according to propensity score matching. Results: We identified 1,067 men with primary hyperaldosteronism (mean age, 46.7 ± 12.8 years) and matched them with the same number of men with essential hypertension or normotension. During the mean follow-up interval of 5.4 years, the incident rates of total erectile dysfunction were 5.7, 3.9, and 3.1 per 1,0 0 0 person-years for the primary hyperaldosteronism, essential hypertension, and normotension groups, respectively. Men with primary hyperaldosteronism exhibited a higher risk of erectile dysfunction compared with men with normotension (competing risks hazard ratio, 1.83), and no difference was seen in comparison with men who have essential hypertension. After adrenalectomy, men who have primary hyperaldosteronism had a higher risk of exhibiting severe erectile dysfunction compared with men who have essential hypertension (competing risks hazard ratio, 2.44) or normotension (competing risks hazard ratio, 2.90). Conclusion: Men with primary hyperaldosteronism reported a higher incidence of severe erectile dysfunction than normotension controls despite targeted treatment. The risk of severe erectile dysfunction increased after men who have primary hyperaldosteronism underwent adrenalectomy. This result raises the possibility of severe erectile dysfunction after adrenalectomy and calls for a prospective large-scale study of men who have aldosterone-producing adenoma regarding their erectile function both before and after adrenalectomy.

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Long-term effects of adrenalectomy or spironolactone on blood pressure control and regression of left ventricle hypertrophy in patients with primary aldosteronism

Cited by 29 publications

References 46 publications

Long term outcome of Aldosteronism after target treatments

Long term outcome of Aldosteronism after target treatments

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

Risk of severe erectile dysfunction in primary hyperaldosteronism: A population-based propensity score matching cohort study

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