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)
Abstract-Hyperaldosteronism has been causally linked to myocardial interstitial fibrosis experimentally, but it remains unclear if this link also applies to humans. Thus, we investigated the effects of excess aldosterone due to primary aldosteronism (PA) on collagen deposition in the heart. We used echocardiography to estimate left ventricular (LV) wall thickness and dimensions and for videodensitometric analysis of myocardial texture in 17 consecutive patients with PA and 10 patients with primary (essential) hypertension who were matched for demographics, casual blood pressure, and known duration of hypertension. The groups differed in serum K ϩ , ECG PQ interval duration, plasma renin activity, and aldosterone levels (all PՅ0.002) but not for casual blood pressure values, demographics, and duration of hypertension. Compared with hypertensive patients, PA patients showed a higher LV mass index (53.7Ϯ1.8 versus 45.5Ϯ2.0 g/m 2.7 ; Pϭ0.008) and lower values of the cyclic variation index of the myocardial mean gray level of septum (CVI s ; Ϫ12.02Ϯ5.84% versus 6.06Ϯ3.08%; Pϭ0.012) and posterior wall (Ϫ11.13Ϯ6.42% versus 8.63Ϯ9.62%; Pϭ0.012). A regression analysis showed that CVI s was predicted by the PQ duration, supine plasma renin activity, plasma aldosterone, and age, which collectively accounted for Ϸ36% of CVI s variance. PA is associated with alterations of myocardial textures that suggest increased collagen deposition and that can explain both the dependence of LV diastolic filling from presystole and the prolongation of the PQ interval. Key Words: hypertension, endocrine Ⅲ aldosterone Ⅲ myocardial Ⅲ hypertrophy Ⅲ fibrosis Ⅲ echocardiography L eft ventricular hypertrophy (LVH) is commonly associated with arterial hypertension and represents an important independent predictor of cardiovascular events, 1 including congestive heart failure. Extracellular matrix and collagen deposition are invariable findings of LVH and lead to cardiac fibrosis (CF), which occurs particularly in the perivascular areas and correlates directly with the severity of LVH. 2 CF is a major cause of cardiac dysfunction because an excessive deposition of collagen may be responsible for abnormal tissue stiffness and diastolic dysfunction. The latter is an early marker of heart involvement in hypertension (for review, see Agabiti-Rosei and Muiesan 3 ) and is associated with CF more closely than with LVH. 4,5 Fibroblasts constitute the vast majority (Ͼ90%) of nonmyocyte cells in the heart; they can increase the production of extracellular matrix on exposure to a variety of injuries, including pressure overload. The latter seems to be only one of the determinants of CF, because it was experimentally shown, both in vitro and in vivo, that CF in both ventricles was linked to activation of the renin-angiotensin-aldosterone system 6 and that it could be prevented by nonantihypertensive dosages of spironolactone. 7 Thus, angiotensin II and aldosterone play important roles in the heart (for review, see Swynghedauw 8 ). Angiotensin II induces cardi...
The Allergic Rhinitis and its Impact on Asthma (ARIA) initiative commenced during a World Health Organization workshop in 1999. The initial goals were (1) to propose a new allergic rhinitis classification, (2) to promote the concept of multi-morbidity in asthma and rhinitis and (3) to develop guidelines with all stakeholders that could be used globally for all countries and populations. ARIA—disseminated and implemented in over 70 countries globally—is now focusing on the implementation of emerging technologies for individualized and predictive medicine. MASK [MACVIA (Contre les Maladies Chroniques pour un Vieillissement Actif)-ARIA Sentinel NetworK] uses mobile technology to develop care pathways for the management of rhinitis and asthma by a multi-disciplinary group and by patients themselves. An app (Android and iOS) is available in 20 countries and 15 languages. It uses a visual analogue scale to assess symptom control and work productivity as well as a clinical decision support system. It is associated with an inter-operable tablet for physicians and other health care professionals. The scaling up strategy uses the recommendations of the European Innovation Partnership on Active and Healthy Ageing. The aim of the novel ARIA approach is to provide an active and healthy life to rhinitis sufferers, whatever their age, sex or socio-economic status, in order to reduce health and social inequalities incurred by the disease.
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