{'fraction_non_alphanumeric': 0.025049203793165147, 'fraction_numerical': 0.003041689032027196, 'mean_word_length': 5.530373831775701, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 1, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Excess Arterial Damage in Hyperaldosteronism.

After the publication of the seminal report by Brunner et al in the New England Journal of Medicine, followed by other reports, that high-renin arterial hypertension was associated with poorer outcomes, a high renin level was regarded as the villain contributing to vascular damage and cardiovascular events. It was, therefore, argued that if high-renin hypertension was bad, low renin should be harmless, or even benign. In the following years, with the development of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, alongside marketing pressure to promote prescription of these agents in arterial hypertension and other cardiovascular diseases, the other major mediator of the system—aldosterone—was practically forgotten. It took some decades and multiple randomized clinical trials, such as the RALES (Randomized Aldactone Evaluation Study), EPHESUS (Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study), and EMPHASIS (Eplerenone in Mild Patients Hospitalization and Survival Study in Heart Failure), to re-establish the role of this hormone in cardiovascular diseases. Primary aldosteronism (PA; the paradigm of low-renin hypertension with high aldosterone) was considered to be practically devoid of cardiovascular damage, that is, a benign form of hypertension for a long time. Therefore, this common cause of arterial hypertension received scant attention until Dr Suzuki et al in Japan, and our group in Italy, independently showed that PA carried a higher risk of left ventricular (LV) hypertrophy as compared to blood pressure (BP)-matched patients with essential hypertension (EH). Additionally, it was found that this higher risk was associated with changes of LV texture (which suggested fibrosis and alterations of diastolic filling) particularly in patients with PA with the most florid clinical phenotypes, which is usually caused by an aldosterone-producing adenoma. These studies were followed by numerous others that examined hypertension-mediated organ damage as surrogate of cardiovascular events in PA.3 Retrospective studies also documented a markedly increased rate of cardiovascular events in PA as compared to patients with EH. Additionally, longterm prospective data from the PAPY study (PA Prevalence in Hypertensives) showed a markedly increased rate of atrial fibrillation in medically treated patients with PA compared with that in adrenalectomized aldosterone-producing adenoma patients. Excess vascular damage has also been reported in PA. Endothelial dysfunction, microalbuminuria, and excess vascular remodeling of resistance arteries that predict a poor response to surgery have been documented in patients with PA. Moreover, stiffening of large arteries has been found to regress after an adrenalectomy, suggesting that it is causally related to hyperaldosteronism and hypertension. The feasibility of a noninvasive assessment of the arterial pulse contour, first described by the O’Rourke’s group in 1989, has been documented in multiple studies. These studies also confirmed the relevance of measuring pulse wave velocity (PWV) to improve risk stratification in different cohorts of patients, including those with PA. The finding that the arterial pulse pressure might consist of a forward and a backward component, which was claimed to predict long-term cardiovascular mortality, is a relatively novel development. This has opened the way for a more in-depth analysis of the components of the pulse pressure wave. During systole, the LV ejection of blood into the ascending aorta generates a forward moving pressure, as well as a pressure wave propagating into the arterial tree with a definite velocity, that is, the PWV. This wave is partially reflected when it travels along sites of abrupt impedance change, such as branching points or regions with increased stiffness. In healthy subjects, the reflected pressure wave merges with the forward wave in the ascending aorta in the early diastolic phase, contributing to coronary artery BP and thus to myocardial perfusion. As the aorta stiffness increases with age or disease status, as in hypertension, the PWV augments; therefore, the reflected wave increases late systolic pressure, thus broadening the pulse pressure and adversely affecting myocardial perfusion, and the LV systolic and diastolic function. A study by Hung et al in this issue of Hypertension, opened a new window of investigation in the field of vascular damage in PA. The results of the study showed the effect of hyperaldosteronism not only on arterial stiffness, measured by heart-carotid PWV, but also on 2 additional wave reflection parameters, that is, pulse wave amplitude moving forward from the heart to the periphery (Pf) and backward from the periphery to the heart (Pb). The authors measured these parameters in a cross-sectional comparison of 67 patients with PA, mostly aldosterone-producing adenoma, and 132 patients with EH. In a longitudinal study, they also examined Pb and Pf at baseline The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association. From the Clinica dell’Ipertensione Arteriosa, Department of Medicine, DIMED, University of Padua, Italy. Correspondence to Gian Paolo Rossi, Clinica dell’Ipertensione Arteriosa, Department of Medicine, DIMED University Hospital, Via Giustiniani, 2, Padua 35126, Italy. Email gianpaolo.rossi@unipd.it Excess Arterial Damage in Hyperaldosteronism Further Evidence From Pressure Wave Analysis