Elevated plasma aldosterone-to-renin ratio as a potential risk marker of adverse left ventricular remodeling: a cross-sectional study.

BACKGROUND: Recent evidence has suggested that primary aldosteronism (PA) is the predominant cause of secondary hypertension and is linked to adverse left ventricular (LV) remodeling. However, few studies have investigated the potential associations of aldosterone-to-renin ratio (ARR), an important parameter for PA screening, with the risk of adverse LV remodeling in the Chinese population. This study aimed to investigate the associations of ARR, plasma aldosterone concentration (PAC), and plasma renin concentration (PRC) with adverse LV remodeling in a population from Guangxi, China.

METHODS: The analyzed data were primarily obtained from the First Affiliated Hospital of Guangxi Medical University and the First People's Hospital of Yulin City during the period from September 2022 to March 2024. A total of 724 participants (mean age: 56.4 ± 14.3 years, 71% with hypertension) who underwent aldosterone-renin testing and echocardiography were included in the study. Data on demographics, clinical history, and medications, including calcium channel blockers and mineralocorticoid receptor antagonists (MRAs), were collected. We applied a generalized linear model (GLM) and a multivariable logistic regression model to estimate the relationships between ARR, PAC, and PRC with the risk of adverse LV remodeling and left ventricular hypertrophy (LVH) and further explored the dose-response relationship.

RESULTS: Of the 724 participants included in this study, GLM revealed that ARR was associated with greater left atrium size, left ventricular end-diastolic diameter, left ventricular mass, and left ventricular mass index. In adjusted multivariable regression analyses, one standard deviation (SD) of ARR emerged as a significant predictor of LVH occurrence [OR = 1.531 (95%CI, 1.041-2.251), p = 0.030], and compared with the first tertile of ARR, the third tertile of ARR had a 2.106-fold higher risk of LVH (p-trend <0.05), especially in participants without mineralocorticoid receptor antagonists (MRA). Furthermore, a significant dose-response relationship was observed between ARR and LVH risk (p overall <0.001, p non-linear = 0.079; p overall tests the overall association, while p non-linear tests for a non-linear trend between ARR and LVH risk).

CONCLUSION: Elevated ARR is associated with an increased risk of adverse LV remodeling, and the presence of LVH may even occur at ARR levels below the clinical standard range, suggesting that ARR could serve as an early indicator of cardiac structural changes. Our results revealed that earlier targeted intervention with MRAs may be beneficial. However, this hypothesis requires confirmation in prospective and interventional studies, particularly those assessing the clinical and cost-effectiveness of early MR blockade. Our study provided a foundation for further exploration of this approach.