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Role of aldosterone in left ventricular hypertrophy in hypertension
Kiyoshi Matsumura1, Koji Fujii, Hideyuki Oniki
1Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka 812-8582, Japan. matsumk@intmed2.med.kyushu-u.ac.jp
Insights
Aldosterone significantly contributes to left ventricular (LV) hypertrophy in humans, similar to animal models. This hormone plays a key role in hypertensive target organ damage, distinct from angiotensin II.
Area of Science:
- Cardiology
- Endocrinology
- Hypertension Research
Background:
- Aldosterone is known to cause cardiac fibrosis in animal models.
- Limited data exists on aldosterone's role in human left ventricular (LV) hypertrophy.
- This study investigates aldosterone's impact on LV geometry and target organ damage in hypertensive patients.
Purpose of the Study:
- To determine the role of aldosterone in LV geometry.
- To investigate other target organ damage in hypertensive patients.
- To compare LV hypertrophy in primary aldosteronism, renovascular hypertension, and essential hypertension.
Main Methods:
- Included 25 patients with primary aldosteronism, 29 with renovascular hypertension, and 29 with essential hypertension (EHT).
- Conducted echocardiographic examinations and 24-h ambulatory blood pressure monitoring.
- Analyzed LV mass index adjusted for age, sex, BP, pulse rate, BMI, and hypertension duration.
Main Results:
- Mean 24-h BP was comparable across all groups.
- LV mass index was significantly increased in primary aldosteronism and renovascular hypertension compared to EHT.
- LV hypertrophy was particularly pronounced in primary aldosteronism, while proteinuria and retinopathy were more severe in renovascular hypertension.
Conclusions:
- Aldosterone appears to induce LV hypertrophy in humans, mirroring findings in experimental animals.
- Angiotensin II and aldosterone may have differential roles in causing hypertensive target organ damage.
- Primary aldosteronism is strongly associated with exaggerated LV hypertrophy.
Background:
Aldosterone induces cardiac fibrosis in experimental animal models, but only limited information is available on the association between aldosterone and left ventricular (LV) hypertrophy in human beings. The aim of the present study was to determine the role of aldosterone in LV geometry and to investigate other types of target organ damage in hypertensive patients.
Methods:
A total of 25 patients with primary aldosteronism caused by Conn's adenoma, 29 patients with renovascular hypertension, and 29 patients with essential hypertension (EHT) were included in the present study. Echocardiographic examinations and 24-h ambulatory blood pressure (BP) monitoring were conducted in all subjects.
Results:
The mean 24-h systolic and diastolic BP in primary aldosteronism and renovascular hypertension were found to be comparable to those in EHT. However, LV mass index adjusted by age, sex, mean 24-h systolic BP, mean 24-h pulse rate, body mass index, and duration of hypertension was significantly increased in the patients with primary aldosteronism and renovascular hypertension compared with values in patients with EHT (150.2 +/- 7.7, 142.3 +/- 7.2, and 115.2 +/- 7.2 g/m(2), respectively). Hypertensive organ damages, such as proteinuria and hypertensive retinopathy, were more pronounced in the patients with renovascular hypertension; however, LV hypertrophy was especially exaggerated in patients with primary aldosteronism.
Conclusions:
These results indicate that aldosterone may induce LV hypertrophy in human beings as well as in experimental animals, and that angiotensin II and aldosterone may differentially participate in causing hypertensive target organ damage.
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