Primary aldosteronism (PA) is a common cause of secondary hypertension and is associated with worse cardiovascular outcomes. The elevated aldosterone in PA leads to left ventricular (LV) remodeling and dysfunction. In recent decades, clinical studies have demonstrated worse LV remodeling including increased LV mass and cardiac fibrosis in patients with PA compared to patients with essential hypertension. Several mechanisms may explain the process of aldosterone-induced LV remodeling, including directly profibrotic and hypertrophic effects of aldosterone on myocardium, increased reactive oxygen species and profibrotic molecules, dysregulation of extracellular matrix metabolism, endothelium dysfunction and circulatory macrophages activation. LV remodeling causes LV diastolic and systolic dysfunction, which may consequently lead to clinical complications such as heart failure, atrial fibrillation, ischemic heart disease, and other vascular events. Adequate treatment with adrenalectomy or medical therapy can improve LV remodeling and dysfunction in PA patients. In this review, we discuss the mechanisms of aldosterone-induced LV remodeling and provide an up-to-date review of clinical research about LV remodeling-related heart structural changes, cardiac dysfunction, and their clinical impacts on patients with PA.

Objective: The presence of autonomous cortisol secretion (ACS) in patients with primary aldosteronism (PA) is common and potentially associated with poor outcomes. The aim of this study was to investigate the association between ACS and vascular remodeling in PA patients. Design and methods: We prospectively enrolled 436 PA patients from October 2006 to November 2019. ACS (defined as a cortisol level >1.8 μg/dL after a 1 mg dexamethasone suppression test) was detected in 23% of the PA patients. Propensity score matching (PSM) with age, sex, systolic and diastolic blood pressure was performed. The brachial-ankle pulse wave velocity (baPWV) was examined at baseline and 1 year after targeted treatment. Small arteries of periadrenal fat in 46 patients were stained with Picro Sirus red to quantify the severity of vascular fibrosis. Results: After PSM, the PA patients with ACS had a significantly higher prevalence of diabetes mellitus, higher plasma aldosterone concentration and higher aldosterone-to-renin ratio. The baseline mean baPWV was also significantly higher in the PA patients with ACS. After multivariable regression analysis, the presence of ACS was a significant predictor of worse baseline mean baPWV (β: 235.745, 95% CI: 59.602–411.888, P = 0.010). In addition, the PA patients with ACS had worse vascular fibrosis (fibrosis area: 25.6 ± 8.4%) compared to those without ACS (fibrosis area: 19.8 ± 7.7%, P = 0.020). After 1 year of PA treatment, baPWV significantly improved in both groups. Conclusion: The presence of ACS in PA patients is associated with worse arterial stiffness and vascular remodeling.

Background: Hereditary transthyretin amyloid cardiomyopathy (hATTR‐CM) is a progressive and fatal disease. Recent evidence indicates that bone scintigraphy may serve as a tool to monitor the effectiveness of hATTR‐CM treatment. The objective of this study was to examine how eplontersen therapy influences the semiquantitative uptake of technetium‐99m‐pyrophosphate in individuals diagnosed with hATTR‐CM. Methods and Results: We retrospectively analyzed a prospective cohort from the NEURO‐TTRansform trial, including patients with hATTR‐CM receiving eplontersen (45 mg/4 weeks). A control group comprised patients with hATTR‐CM who had not received eplontersen, inotersen, tafamidis, or patisiran. Technetium‐99m‐pyrophosphate single‐photon emission computed tomography/computed tomography was conducted at baseline and during follow‐up. Thirteen patients with hATTR‐CM were enrolled, with 6 receiving eplontersen and 7 serving as the control group. The median follow‐up time was 544 days. The eplontersen group exhibited a significant decrease in volumetric heart and lung ratio (3.774 to 2.979, P =0.028), whereas the control group showed no significant change (4.079 to 3.915, P =0.237). Patients receiving eplontersen demonstrated a significantly greater reduction in volumetric heart and lung ratio compared with the control group (−20.7% versus −3.4%, P =0.007). Conclusions: The volumetric heart and lung ratio used to quantify technetium‐99m‐pyrophosphate uptake showed a significant reduction subsequent to eplontersen treatment in individuals diagnosed with hATTR‐CM. These findings suggest the potential efficacy of eplontersen in treating hATTR‐CM and highlight the value of technetium‐99m‐pyrophosphate single‐photon emission computed tomography/computed tomography as a tool for monitoring therapeutic effectiveness.

Background: The saline suppression test (SST) and the captopril challenge test (CCT) have traditionally been used to confirm or exclude primary aldosteronism (PA). New guidelines recommend using these tests to predict the likelihood of unilateral PA. This study evaluated the diagnostic accuracy, consistency, and clinical implications of these tests. Methods: We conducted a retrospective study of 531 patients with high-probability features of PA who underwent both SST and CCT to evaluate their accuracy and ability to predict unilateral PA. Adrenal lateralization and surgical treatment decisions were guided by individualized clinical judgment rather than strictly relying on SST/CCT results. Results: The rate of PA diagnosis ranged from 47.8% to 97.2% based on SST and CCT criteria. Discordance rates between SST and CCT ranged from 10.9% to 51.6%. In analyses restricted to only patients with clinically overt PA, where suppression testing is not considered necessary, the positivity rates of the SST and CCT were still suboptimal and test discordance persisted. Among patients with lateralizing PA, 6.6% to 27.9% had either a negative SST or CCT interpretation, and among those who achieved Primary Aldosteronism Surgical Outcome-defined biochemical cure after unilateral adrenalectomy, 4.1% to 39.8% had either a negative SST or CCT, and up to 5.1% had false-negative results on both tests. Conclusions: Well-established aldosterone suppression tests for PA demonstrated substantial inconsistency, false-negative interpretations, and the inability to reliably predict lateralization outcomes in PA. Aldosterone suppression testing, using SST and CCT, lack accuracy for the diagnosis and subtyping of PA in high-risk patients.