Effects of Altered Calcium Metabolism on Cardiac Parameters in Primary Aldosteronism.
10.3803/EnM.2018.33.4.485
- Author:
Jung Soo LIM
1
;
Namki HONG
;
Sungha PARK
;
Sung Il PARK
;
Young Taik OH
;
Min Heui YU
;
Pil Yong LIM
;
Yumie RHEE
Author Information
1. Department of Internal Medicine, Institute of Evidence Based Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea.
- Publication Type:Original Article
- Keywords:
Hyperaldosteronism;
Hypocalcemia;
Heart diseases;
Parathyroid hormone
- MeSH:
Adenoma;
Aldosterone;
Calcium*;
Heart Diseases;
Homeostasis;
Humans;
Hyperaldosteronism*;
Hypercalciuria;
Hyperplasia;
Hypocalcemia;
Metabolism*;
Parathyroid Hormone;
Plasma;
Prevalence;
Renin;
Veins
- From:Endocrinology and Metabolism
2018;33(4):485-492
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Increasing evidence supports interplay between aldosterone and parathyroid hormone (PTH), which may aggravate cardiovascular complications in various heart diseases. Negative structural cardiovascular remodeling by primary aldosteronism (PA) is also suspected to be associated with changes in calcium levels. However, to date, few clinical studies have examined how changes in calcium and PTH levels influence cardiovascular outcomes in PA patients. Therefore, we investigated the impact of altered calcium homeostasis caused by excessive aldosterone on cardiovascular parameters in patients with PA. METHODS: Forty-two patients (mean age 48.8±10.9 years; 1:1, male:female) whose plasma aldosterone concentration/plasma renin activity ratio was more than 30 were selected among those who had visited Severance Hospital from 2010 to 2014. All patients underwent adrenal venous sampling with complete access to both adrenal veins. RESULTS: The prevalence of unilateral adrenal adenoma (54.8%) was similar to that of bilateral adrenal hyperplasia. Mean serum corrected calcium level was 8.9±0.3 mg/dL (range, 8.3 to 9.9). The corrected calcium level had a negative linear correlation with left ventricular end-diastolic diameter (LVEDD, ρ=−0.424, P=0.031). Moreover, multivariable regression analysis showed that the corrected calcium level was marginally associated with the LVEDD and corrected QT (QTc) interval (β=−0.366, P=0.068 and β=−0.252, P=0.070, respectively). CONCLUSION: Aldosterone-mediated hypercalciuria and subsequent hypocalcemia may be partly involved in the development of cardiac remodeling as well as a prolonged QTc interval, in subjects with PA, thereby triggering deleterious effects on target organs additively.
