P rimary aldosteronism (PA) is a common curable cause of high blood pressure (BP).1 PA is of peculiar interest because the excess aldosterone secretion is held to be autonomous from angiotensin II, which allows elucidating the cardiovascular effects of excess aldosterone without the confounding effects of excess angiotensin II. Moreover, as the excess of aldosterone is cured with adrenalectomy in practically all patients, 2 causation between aldosterone excess and the cardiovascular changes could be inferred. However, whether surgery or pharmacological blockade of the mineralocorticoid receptor (MR) warrant cure of high BP and regression of cardiovascular damage, and of cardiac remodeling, at long term remains unclear because limited data exist. 3,4 The adaption of the left ventricle (LV) to the increased afterload of patients with high BP involves development of hypertrophy (LVH), which predicts cardiovascular events and death, 5 and when regressed improved prognosis. 6 In the complex interplay of hemodynamic, genetic, and endocrine-paracrine factors that underlie development of LVH aldosterone plays a pivotal role. [7][8][9] In the setting of a high sodium intake, this major effector of the system causes LVH, transcription of collagen type I and III genes, 10 and promotes fibroblasts proliferation, oxidative stress, and inflammation, 11 in part, by potentiating the effects of angiotensin II on AT-1 receptors.12-15 These actions, alongside the effects of the steroid on pre-and after-load, are held to cause inflammation and fibrosis, which contribute to worsening prognosis of patients with hyperaldosteronism, 8,16 and can explain the survival benefit conferred by MR antagonists to optimally treated patients with LV systolic dysfunction. 17,18 Compared with BP-matched primary (essential) hypertensive patients, those with PA have an excess LVH and a LV mass inappropriately high for the degree of LV workload and BP elevation. [2][3][4]9,[19][20][21][22][23][24][25][26][27][28] Cardiac fibrosis with ensuing altered LV diastolic dysfunction can lead to left atrium dilatation and increased risk of atrial fibrillation (AF) 7,8,29 ; whether these changes regress with specific treatment for PA remains uncertain. 3,4,19,20,26 We, therefore, set out to prospectively investigate the long-term effects of correction of hyperaldosteronism on BP, LV mass, and cardiovascular events in a large cohort of patients with PA.Abstract-Primary aldosteronism (PA), a common cause of high blood pressure (BP), induces left ventricular (LV) hypertrophy and an excess rate of cardiovascular events. Whether its treatment provides long-term cure of hypertension and regression of cardiovascular damage remains uncertain. To the aim of assessing the effect of treatment of PA on BP and LV changes, we prospectively recruited 323 patients in a long-term follow-up study entailing serial echocardiography evaluations. Of them, 180 had PA and were assigned to either adrenalectomy (n=110) or medical therapy (n=70)

The oxidative modification hypothesis of atherosclerosis, which assigns to oxidized low-density lipoproteins (LDLs) a crucial role in atherosclerosis initiation and progression, is still debated. This review examines the role played by oxidized LDLs in atherogenesis taking into account data derived by studies based on molecular and clinical approaches. Experimental data carried out in cellular lines and animal models of atherosclerosis support the proatherogenic role of oxidized LDLs: (a) through chemotactic and proliferating actions on monocytes/macrophages, inciting their transformation into foam cells; (b) through stimulation of smooth muscle cells (SMCs) recruitment and proliferation in the tunica intima; (c) through eliciting endothelial cells, SMCs, and macrophages apoptosis with ensuing necrotic core development. Moreover, most of the experimental data on atherosclerosis-prone animals benefiting from antioxidant treatment points towards a link between oxidative stress and atherosclerosis. The evidence coming from cohort studies demonstrating an association between oxidized LDLs and cardiovascular events, notwithstanding some discrepancies, seems to point towards a role of oxidized LDLs in atherosclerotic plaque development and destabilization. Finally, the results of randomized clinical trials employing antioxidants completed up to date, despite demonstrating no benefits in healthy populations, suggest a benefit in high-risk patients. In conclusion, available data seem to validate the oxidative modification hypothesis of atherosclerosis, although additional proofs are still needed.

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