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Updated: Aug 4, 2026

Ultrasonic Assessment of Myocardial Microstructure
Published on: January 14, 2014
Comparison of changes in cardiac structure after treatment in secondary hypertension
Y Yoshitomi1, T Nishikimi, H Abe
1Division of Hypertension and Kidney Disease, National Cardiovascular Center, Osaka, Japan.
Insights
Aldosterone and high blood pressure contribute to left ventricular hypertrophy in secondary hypertension. While high blood pressure is key in renovascular hypertension, aldosterone excess and volume expansion play roles in primary aldosteronism.
Area of Science:
- Cardiology
- Endocrinology
- Hypertension Research
Background:
- The relationship between hormonal influences, blood pressure, and left ventricular hypertrophy (LVH) in secondary hypertension is not fully understood.
- Aldosterone and the renin-angiotensin system are implicated in cardiovascular remodeling.
Purpose of the Study:
- To investigate the distinct roles of aldosterone and the renin-angiotensin system in cardiac structure, specifically left ventricular hypertrophy, in patients with secondary hypertension.
- To compare the impact of primary aldosteronism and unilateral renovascular hypertension on LVH.
Main Methods:
- Echocardiography was performed on 16 patients with primary aldosteronism and 11 with unilateral renovascular hypertension before and after treatment.
- Blood pressure and hormonal levels were monitored. Patients underwent surgical or interventional treatment to normalize blood pressure.
Main Results:
- Both groups achieved normalized blood pressure post-treatment, with no significant pre-treatment differences in LVH.
- Left ventricular mass index significantly decreased in both groups after treatment.
- In primary aldosteronism, changes in left ventricular internal dimension correlated with LVH changes (r=.58). In renovascular hypertension, blood pressure changes correlated with LVH changes (r=.77).
Conclusions:
- High blood pressure significantly contributes to LVH in unilateral renovascular hypertension.
- Expanded plasma volume from aldosterone excess and hypertension are key factors in LVH development in primary aldosteronism.
- Different mechanisms modulate LVH development in distinct types of secondary hypertension.
Abstract:
To investigate the role of aldosterone and the renin-angiotensin system in cardiac structure, we performed echocardiography in patients with secondary hypertension. The relation between blood pressure or hormonal influences and left ventricular hypertrophy has not been well established in secondary hypertension. Sixteen patients with primary aldosteronism and 11 with unilateral renovascular hypertension who had completely normalized blood pressure after operation or percutaneous transluminal angioplasty were evaluated by echocardiography before and after surgery or other interventional treatment. Blood pressure was not statistically different between the groups before treatment and was normalized after treatment in both groups. Left ventricular hypertrophy was mild in both groups before treatment, and its degree was not statistically different between the groups. At the end of the follow-up period, all parameters of primary aldosteronism and left ventricular mass index in patients with unilateral renovascular hypertension were significantly reduced. In patients with primary aldosteronism, changes in end-diastolic left ventricular internal dimension correlated positively with changes in left ventricular mass index (r=.58,P<.01). In patients with unilateral renovascular hypertension, changes in mean blood pressure and left ventricular mass index were significantly correlated (r=.77,P<.01). The expanded plasma volume induced by an excess of aldosterone and high blood pressure may play an important role in the increase of left ventricular mass in primary aldosteronism. In unilateral renovascular hypertension, high blood pressure mainly contributes significantly to increased left ventricular mass. Therefore, different factors may modulate the development of left ventricular hypertrophy in patients with secondary hypertension.
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