LAUSR

In this issue of the Journal Wei et al. focus on a topic of great interest such as the association between oxidative stress (OS) markers and alterations of left ventricular (LV) geometry and function in patients with essential hypertension. Before addressing in detail the results of this study some more general considerations on available evidence on such issue and related topics may warrant some considerations. Left ventricular hypertrophy (LVH), diagnosed by electrocardiography or more accurately by echocardiography, is the hallmark of subclinical hypertensive heart disease in relation to its high frequency in the general hypertensive population and its unfavorable clinical and prognostic implications. Increasing evidence has accumulated over time on the value of LVH in predicting the risk of morbid and fatal events, regardless of conventional cardiovascular (CV) risk factors and clinical settings. Indeed, LVH reflects the cumulative burden of several haemodynamic and non-haemodynamic factors operating in systemic hypertension. The mechanisms underlying the alterations in LV structure and geometry remain so far incompletely understood. The classical view identified in the increased LV wall stress secondary to chronic blod pressure (BP) overload the most important stimulus for the development of LV remodeling and LVH. This interpretation is, however, challenged by numerous studies which have shown that BP load, even when accurately defined by ambulatory BP monitoring (ABPM) or home recordings, accounts for only 20%–40% of the observed variance of LV mass (LVM). A large amount of research have progressively revealed that beyond the BP several growth factors, cytokines, neuro-hormones and increased OS interacting with ethnic/ genetic predisposition contribute to the pathogenesis of LVH. Thus, the old notion that BP overload is invariably accompanied by concentric LVH has also been challenged by the evidence that patients with hypertension have different abnormal LV geometric patterns. In the early 90s, a group of Italian researchers proposed to classify LV structural/geometric changes into three echocardiographic abnormal patterns: concentric remodeling (normal LVM and increased relative wall thickness, RWT), eccentric hypertrophy (increased LVM and normal RWT), concentric hypertrophy (increased LVM and RWT). These patterns have been shown to differ from each other in many respects such as office and ambulatory BP, levels, systemic hemodynamic, LV diastolic function, left atrial size and function, extra-cardiac organ damage, comorbidities and, more importantly, prognostic implications. Even though concentric LVH has been reported in some studies to be associated with the highest risk is uncertain whether abnormal LV geometric patterns, defined by combining LVM and RWT, carry prognostic information beyond that provided by LVM alone. An updated classification of LVH based on four sub-types (i.e., eccentric nondilated and dilated LVH, concentric nondilated and dilated LVH) has been suggested by the investigators of the Dallas Heart Study to overcome the limitations of the old classification criticized for not taking into account the absolute values of LV wall thickness and internal dimensions, considering only their ratio. Both the Dallas Heart Study and Losartan Intervention for Endpoint Reduction (LIFE) echocardiographic sub-study documented a marginal impact of eccentric nondilated LVH on LV function and CV prognosis supporting the view that the new classification of LV geometry may improve the clinical/prognostic evaluation of hypertensive patients with increased LVM index. In this complex research scenario, encompassing pathophysiological, clinical and prognostic aspects of the hypertensive heart disease, the study by Wei et al. offers a new interesting piece of information. The authors report the findings of a cross-sectional investigation aimed at assessing the relationship of superoxide dismutase (SOD) [Corrected added on 08 Dec 2022, after first online publication: Article category has been changed to Commentary] Received: 20 November 2022 Accepted: 21 November 2022