Subclinical atherosclerosis due to increase of plasma aldosterone concentrations in essential hypertensive individuals

Concistrè, Antonio; Petramala, Luigi; Bisogni, Valeria; Mezzadri, Martina; Olmati, Federica; Saracino, Vincenza; Oliviero, Gaia; Bonvicini, Maria; Tonnarini, Gianfranco; Iannucci, Gino; Letizia, Claudio

doi:10.1097/hjh.0000000000002170

Cited by 12 publications

(6 citation statements)

References 44 publications

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“…A recent meta-analysis comparing PA and EH showed that patients with APA may have lower long-term mortality than EH patients due to the better recovery of adrenalectomy ( 39 ). Besides well-recognized risk factors like hyperaldosteronism ( 27 ), our results also showed that female gender was a potential determinants of subclinical changes. Gender differences of TOD in hypertension have been also described, but contradictory results are available in the literature.…”

Section: Discussionsupporting

confidence: 64%

“…Consistent with previous studies (4,23), our study showed that compared to matched EH controls, PA patients exhibited more renal damage indicated by reduced eGFR and greater prevalence of microalbuminuria, as well as more cardiac damage indicated by an increased prevalence of LVH. On the one hand, there is accumulating evidence including our previous researches, which support that many detrimental effects of aldosterone excess are involved in causing pre-clinical TOD in the PA patients; they include inflammation, oxidative stress, endothelial dysfunctions, and vascular calcification (7,(24)(25)(26)(27). On the other hand, a majority of patients with MetS, a cluster of risk factors, tend to develop structural and functional abnormalities of target organs, which precede cardiovascular complications (28,29).…”

Section: Discussionmentioning

confidence: 92%

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Associations Between Metabolic Profiles and Target-Organ Damage in Chinese Individuals With Primary Aldosteronism

et al. 2020

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Purpose: Patients with primary aldosteronism (PA) have an increased risk of target-organ damage (TOD), but whether metabolic syndrome (MetS) is more prevalent and contributes to TOD in PA patients remains unresolved. We aimed to evaluate the associations between MetS profiles and TOD in Chinese PA individuals. Methods: Metabolic parameters and pre-clinical TOD including left ventricular hypertrophy, estimated glomerular filtration, and microalbuminuria; insulin sensitivity or resistance; and islet β-cell function were assessed by the homeostasis models (HOMA-IR, HOMA-β) and the other surrogate indexes [composite insulin sensitivity index (ISI), modified β-cell function index (MBCI)] determined from the oral glucose tolerance test were compared in PA vs. matched essential hypertension (EH) patients. Results: A total of 109 PA patients and 109 essential hypertension (EH) controls individually matched for sex, age, and office systolic blood pressure and duration of hypertension were studied. The prevalence of MetS and its individual components in PA was significantly lower than in EH [MetS: 28 (25.6%) vs. 54 (49.5%), P < 0.001]. PA patients had a higher composite ISI but a lower HOMA-IR, HOMA-β, and MBCI than EH controls (all P < 0.05). Concerning TOD, PA patients had significantly higher prevalence of microalbuminuria and left ventricular hypertrophy (LVH), and lower levels of estimated glomerular filtration (eGFR) than EH controls (all P < 0.05). On multivariate logistic regression analysis, female gender and elevated plasma aldosterone levels were significantly associated with TOD in PA. However, there were no significant associations between MetS and its individual components and TOD in PA patients. Conclusions: PA patients had a lower MetS prevalence but exhibited more severe TOD than matched EH controls. The study highlights the deleterious effects of aldosterone excess on the development of TOD, whereas MetS or its individual components might be less influential in PA.

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Section: Discussionsupporting

confidence: 64%

Section: Discussionmentioning

confidence: 92%

Associations Between Metabolic Profiles and Target-Organ Damage in Chinese Individuals With Primary Aldosteronism

et al. 2020

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“…In order to better resemble the human cardiovascular disease and to speed up plaque progression, we treated ApoE-KO mice with aldosterone at a dose of 6 µg/kg/day. Such concentration is able to raise serum aldosterone levels to a range which promotes atherosclerosis, without inducing hypertension (27,30,40). Aldosterone promotes rapid lipid accumulation in the aortic arch section of ApoE-KO mice, as shown in Figure 2A.…”

Section: Characterization Of Atherosclerotic Plaques In Apoe-ko Micementioning

confidence: 95%

Altered Tregs Differentiation and Impaired Autophagy Correlate to Atherosclerotic Disease

et al. 2020

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Atherosclerosis is a progressive vascular disease representing the primary cause of morbidity and mortality in developed countries. Formerly, atherosclerosis was considered as a mere passive accumulation of lipids in blood vessels. However, it is now clear that atherosclerosis is a complex and multifactorial disease, in which the involvement of immune cells and inflammation play a key role. A variety of studies have shown that autophagy-a cellular catalytic mechanism able to remove injured cytoplasmic components in response to cellular stress-may be proatherogenic. So far, in this context, its role has been investigated in smooth muscle cells, macrophages, and endothelial cells, while the function of this catabolic protective process in lymphocyte functionality has been overlooked. The few studies carried out so far, however, suggested that autophagy modulation in lymphocyte subsets may be functionally related to plaque formation and development. Therefore, in this research, we aimed at better clarifying the role of lymphocyte subsets, mainly regulatory T cells (Tregs), in human atherosclerotic plaques and in animal models of atherosclerosis investigating the contribution of autophagy on immune cell homeostasis. Here, we investigate basal autophagy in a mouse model of atherosclerosis, apolipoprotein E (ApoE)-knockout (KO) mice, and we analyze the role of autophagy in driving Tregs polarization. We observed defective maturation of Tregs from ApoE-KO mice in response to tumor growth factor-β (TGFβ). TGFβ is a well-known autophagy inducer, and Tregs maturation defects in ApoE-KO mice seem to be related to autophagy impairment. In this work, we propose that autophagy underlies Tregs maturation, advocating that the study of this process in atherosclerosis may open new therapeutic strategies.

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“…127 A summary of preclinical and clinical studies investigating the association between aldosterone and cerebrovascular disease is available in the Supplemental Material. [3][4][5]68,124,[128][129][130][131][132][133][134][135][136][137][138][139][140][141][142][143][144]…”

Section: Aldosterone and Brainmentioning

confidence: 99%

Aldosterone as a Mediator of Cardiovascular Damage

et al. 2022

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Besides the physiological regulation of water, sodium, and potassium homeostasis, aldosterone modulates several physiological and pathological processes in the cardiovascular system. At the vascular level, aldosterone excess stimulates endothelial dysfunction and infiltration of inflammatory cells, enhances the development of the atherosclerotic plaque, and favors plaque instability, arterial stiffness, and calcification. At the cardiac level, aldosterone increases cardiac inflammation, fibrosis, and myocardial hypertrophy. As a clinical consequence, high aldosterone levels are associated with enhanced risk of cardiovascular events and mortality, especially when aldosterone secretion is inappropriate for renin levels and sodium intake, as in primary aldosteronism. Several clinical trials showed that mineralocorticoid receptor antagonists reduce cardiovascular mortality in patients with heart failure and reduced ejection fraction, but inconclusive results were reported for other cardiovascular conditions, such as heart failure with preserved ejection fraction, myocardial infarction, and atrial fibrillation. In patients with primary aldosteronism, adrenalectomy or treatment with mineralocorticoid receptor antagonists significantly mitigate adverse aldosterone effects, reducing the risk of cardiovascular events, mortality, and incident atrial fibrillation. In this review, we will summarize the major preclinical and clinical studies investigating the cardiovascular damage mediated by aldosterone and the protective effect of mineralocorticoid receptor antagonists for the reduction of cardiovascular risk in patients with cardiovascular diseases and primary aldosteronism.

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Subclinical atherosclerosis due to increase of plasma aldosterone concentrations in essential hypertensive individuals

Cited by 12 publications

References 44 publications

Associations Between Metabolic Profiles and Target-Organ Damage in Chinese Individuals With Primary Aldosteronism

Associations Between Metabolic Profiles and Target-Organ Damage in Chinese Individuals With Primary Aldosteronism

Altered Tregs Differentiation and Impaired Autophagy Correlate to Atherosclerotic Disease

Aldosterone as a Mediator of Cardiovascular Damage

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