Abstract

Background: Although aldosterone has been demonstrated to induce left ventricular (LV) hypertrophy not only in primary aldosteronism but also in primary hypertension (HT), it can be affected by multiple factors, including age, and the effect of aldosterone on LV function is controversial. This study was to investigate the relationship of aldosterone to changes in LV geometry and function in young adults with never-treated HT. Methods: Seventy-five consecutive patients (age, 29.8 ± 6.3 years) with never-treated HT and 45 normal controls were enrolled. Echocardiographic values and LV global longitudinal strain (LVGLS) were obtained. Serum aldosterone concentration (SAC) and serum procollagen type III amino-terminal peptide (PIIINP) level were obtained in HT patients. Results: HT patients had higher LV mass index, higher relative wall thickness (RWT), and worse LV function than normal controls. LVGLS and e’ velocity were worse in HT patients with normal geometry than in normal controls. SAC was well correlated with LV mass index, RWT, e’ velocity, LVGLS, and PIIINP (all p < 0.05). LV geometry pattern was most related to SAC among clinical parameters (p = 0.019). LVGLS was most related to LV geometry and diastolic blood pressure. In contrast, e’ velocity was most related to PIIINP. Conclusion: Our findings may indicate that in young patients with never-treated HT, aldosterone significantly contributes to changes in LV geometry and functional impairment through its pro-hypertrophic and myocardial fibrosis effects beyond blood pressure.

Highlights

  • Elevation in blood pressure (BP) increases the afterload and left ventricular (LV) wall stress, resulting in subendocardial damage and myocardial fibrosis, which lead to LV remodeling with increased LV mass in systemic arterial hypertension (HT)

  • (4) LV global longitudinal strain (LVGLS) was most related to LV geometry and diastolic BP (DBP), whereas e’ velocity was most related to procollagen type III amino-terminal peptide (PIIINP) and LV geometry

  • Excess plasma aldosterone in patients with primary aldosteronism is frequently associated with an increase in LV mass beyond levels needed to compensate for the BP-related hemodynamic load in this condition [19,20]

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Summary

Introduction

Elevation in blood pressure (BP) increases the afterload and left ventricular (LV) wall stress, resulting in subendocardial damage and myocardial fibrosis, which lead to LV remodeling with increased LV mass in systemic arterial hypertension (HT). Many factors beyond BP level contribute to the HT-related changes in LV remodeling, including excess plasma aldosterone levels, which have been reported to increase myocardial mass and collagen content in HT patients [4,5]. Results: HT patients had higher LV mass index, higher relative wall thickness (RWT), and worse LV function than normal controls. Conclusion: Our findings may indicate that in young patients with never-treated HT, aldosterone significantly contributes to changes in LV geometry and functional impairment through its pro-hypertrophic and myocardial fibrosis effects beyond blood pressure

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