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Left ventricular hypertrophy, arterial stiffness and blood pressure

exploring the Bermuda Triangle

Weber, Thomasa; Protogerou, Athanaseb

doi: 10.1097/HJH.0000000000001973

aCardiology Department, Klinikum Wels-Grieskirchen, Wels, Austria

bCardiovascular Prevention and Research Unit, Department of Pathophysiology, Medical School, National and Kapodistrian University of Athens, Athens, Greece

Correspondence to Associate Professor Thomas Weber, MD, FESC, Cardiology Department, Klinikum Wels-Grieskirchen, Grieskirchnerstrasse 42, 4600 Wels, Austria. E-mail:

Left ventricular (LV) mass is directly linked to LV afterload, defined as the hydraulic load imposed by the systemic circulation. The latter is easily approximated in everyday clinical practice with brachial blood pressure (BP). Left ventricular hypertrophy (LVH) is an important marker of hypertension-mediated organ damage [1] and an intermediate step from hypertension to heart failure [2]. LVH regression is accomplished with brachial BP lowering [3], and has favorable prognostic cardiovascular (CV) implications, independently and beyond brachial BP reduction [4]. Therefore, LVH, because of high BP, is not only a strong mediator of heart disease, but also a potent surrogate biomarker of cardiovascular death, useful to guide effective BP-lowering strategies.

Rather than considering LV afterload merely as BP waveform's extremes (i.e. SBP and DBP), and merely at the peripheral circulation (brachial artery), the contemporary view of cardiovascular haemodynamics takes pulsatile phenomena and central (aortic) haemodynamics into consideration. Brachial and central pulse pressures as well as wave reflections are closely related to LV late systolic afterload, remodelling and LVH, diastolic dysfunction, exercise capacity, and, in the long-term, the risk of new-onset heart failure [5]. In this scenario, arterial – in particular aortic – stiffness, expressed as pulse wave velocity (PWV), seems to be a major player. Aortic stiffening, although not a direct measure of ventricular afterload, is highly informative of arterial wall properties, reflecting large artery damage in hypertension [1], and has important prognostic implications [6]. Moreover, PWV also is closely associated with BP and its changes [7], although BP-independent reduction of carotid–femoral PWV (cfPWV) under long-lasting antihypertensive therapy has been suggested [8]. Reduction in cfPWV also has prognostic implications, independent from BP, at least in patients with end-stage renal disease undergoing dialysis [9]. However, recent data suggest that arterial stiffening may precede rather than antedate the development of arterial hypertension [10] and that increased aortic stiffness is a major cause of reduced response to BP-lowering drug treatment [11].

Against this quite complicated background (as summarized in Fig. 1), in this issue of the Journal van der Waaij et al.[12] investigated the mutual treatment induced changes in LV mass (indexed for body height), PWV, and brachial BP in a meta-analysis, including 14 randomized controlled trials and 9 prospective observational studies, with a follow-up ranging from 3 months to 4.8 years. Notably, PWV could be cfPWV, brachial–ankle (baPWV), or local aortic PWV, calculated from aortic distensibility or compliance. Only in 13 of the studies included, changes in BP, LVMI, and PWV were available simultaneously. At study level, changes in brachial SBP seemingly correlated with reductions in both PWV and LVMI. In pooled analysis, however, the changes in BP were neither significantly related to the changes in LVMI nor to the changes in PWV. However, the authors observed a moderate (r = 0.61), statistically significant positive relationship between the changes in PWV and the changes in LVMI. A subanalysis, performed for each method of PWV separately, displayed a trend towards a direct relationship between changes in cfPWV and SBP changes, a trend towards an inverse (!) relationship between changes in calculated aortic PWV and SBP changes, and no relationship between changes in baPWV and SBP changes. In some contrast, the relationship between changes in LVMI and PWV was closest for calculated aortic PWV, and only weak for cfPWV. However, all of these subanalysis are limited by a small number of included studies, and all of them failed to reach statistical significance.



Overall, the authors should be congratulated having performed a pioneering study on the relationships between BP, and cardiac as well as arterial damage in hypertension. However, because of the limited number of well performed studies available for the meta-analysis, several issues remain ambiguous. First of all, why was reduction in LVMI not related to BP reduction? Previous studies have also shown similar results; probably taking out-of-office BP measurements and central BP measurements into account, might lead to different results, as both are closely related to LVM than office brachial BP [13,14]. Secondly, why was reduction in PWV not related to BP reduction? Particularly, based on the subanalysis showing opposite relationships between cfPWV and calculated aortic PWV with BP changes, pooling data from both methods can be debated. Thirdly, as also discussed by the authors, which is the most likely chain of events in this pathophysiological array? The parallel reduction of both LVMI and PWV by BP reduction or the reduction of arterial stiffness because of to BP decrease, and consecutively the reduction in LVMI through reduction in LV afterload?

As attempted to summarize in the Fig. 1, the above observations and questions might be related to the reciprocal and quite complex associations between these three parameters creating a rather confusing triangle. Obviously, these pathophysiological links cannot be addressed with observational studies. We assume that the results would have differed if the authors could have taken the time course of events into account. There was a large span of follow-up durations, and it is likely that improvement in aortic stiffness may follow a different (faster) time course, as compared with improvement in LV structure [1]. This is particularly true as arterial stiffness measurement by PWV, but not LVH, is per se BP-dependent. In other words, PWV rapid reduction reflects the passive effect of distending BP on arterial stiffness. However, and without any doubt, the present study highlights the critical role of arterial stiffness in the reduction of cardiovascular risk through one more pathway, that is, the reduction of LVH. As stated by the authors, further well designed studies might elucidate this obscure ‘Bermuda Triangle’.

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Conflicts of interest

There are no conflicts of interest.

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