Concentric or eccentric hypertrophy: how clinically relevant is the difference?

Different combinations of volume and pressure overloads cause different left ventricular (LV) geometric adaptations. Whereas this cause-effect relationship is obvious for valve disease, because clear-cut types of overloads are easily recognizable, in systemic hypertension the type of cardiac load is less evident but at least as important for LV adaptation. Human arterial hypertension encompasses a large range of interactions between volume and pressure overloads, therefore producing a very large spectrum of possible LV adaptations. Based on the assumption that LV geometry is more useful than simple assessment of brachial blood pressure to identify the predominant type of overload, for convenience (and somewhat arbitrarily), we use generated cutoff points to define different LV geometric patterns according to the predominance of one hemodynamic load over the other one.1 When considering together the prevalence of concentric remodeling and concentric LV hypertrophy,1 we can easily conclude that pressure overload is the fundamental abnormality in arterial hypertension, although this is, in most circumstances, associated with some volume component. Thus, under chronic antihypertensive treatments that reduce pressure overload, a consistent reduction of concentric LV geometry can be expected when reduction of LV hypertrophy occurs. Whether modifications of LV geometry from concentric to eccentric are beneficial beyond the reduction of LV mass has been debated; however, the conclusion has been, in general, that concentric LV hypertrophy is also characterized by greater LV mass than eccentric LV hypertrophy; therefore, these 2 features (ie, concentric geometry and LV hypertrophy) are so interrelated that they cannot to be easily discriminated.2,3 In contrast to this argument, in the presence of normal LV mass, Verdecchia et al4 demonstrated that concentric LV remodeling (ie, with normal LV mass) reflecting a nearly pure pressure overload1 was associated with poor prognosis. However, even in this study,4 although the measurements were in the range of arbitrarily defined normal LV mass, hypertensive patients with concentric LV remodeling exhibited higher values of LV mass than hypertensive patients with normal LV geometry, making it difficult to discriminate the type of LV geometry from the magnitude of LV mass. Another argument of this issue is now proposed by Muiesan et al,5 who convincingly demonstrated that the normalization of the relation between chamber size and wall thickness has a favorable prognostic value that adds to the recognized positive effect of reducing LV mass. This finding stimulates 2 considerations. In the Muiesan study,5 and in other studies on LV geometry and prognosis, LV hypertrophy has been assessed by traditional normalization of LV mass for body surface area, a method that increases the proportion of patients with concentric LV remodeling and apparently “normal LV mass,” caused by the exaggerating effect of body fat included in the computation of body surface area.6,7 Normalization for height6 reduces the proportion of overweight/obese subjects in the concentric LV remodeling cluster and increases the proportion of subjects with recognized concentric LV hypertrophy.8 Thus, the favorable change from concentric to normal (eccentric) LV geometry found by Muiesan et al5 probably included a number of patients initially classified in the group with concentric LV remodeling. These patients were not considered among those in whom regression of LV hypertrophy could have occurred because of their initial classification in the group without LV hypertrophy (by body surface area index). Thus, the effect of regression of LV concentric geometry independent of regression of LV hypertrophy could have been attenuated by using normalization for height,6 which increases the proportion of individuals with concentric LV hypertrophy and reduces the prevalence of concentric LV remodeling.8 Even taking the potential body size adjustment limitations into account, the Muiesan study5 clearly indicates that when cardiovascular disease has not yet occurred, the natural prognostically adverse LV geometric pattern in hypertensive patients is concentric (ie, because of pressure overload). This finding is in line with an impressive series of experimental and clinical data. Physiologically, there is little adaptive advantage in the concentric LV geometry. The perception that concentric LV geometry in pressure overload is a compensatory mechanism to reduce wall stress to maintain systolic performance should be probably revised, because LV function may be normally maintained even in the presence of elevated wall stress.9,10 A scenario alternative to the stress-correction theory is that cardiomyocyte hypertrophy and structural disarray are produced by pressure-overload neurohormonal activation, causing abnormal contractility and distensibility, which is at least The opinions expressed in this editorial are not necessarily those of the editors or of the American Hearth Association. From the Department of Clinical and Experimental Medicine, Federico II University Hospital, Naples, Italy. Correspondence to Dr Giovanni de Simone, Department of Clinical and Experimental Medicine, Federico II University Hospital, School of Medicine, v.S. Pansini 5-80131, Naples, Italy. E-mail [email protected] (Hypertension 2004;43:714-715.) © 2004 American Heart Association, Inc.