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NDT Advance Access originally published online on October 12, 2005
Nephrology Dialysis Transplantation 2005 20(12):2610-2612; doi:10.1093/ndt/gfi190
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Editorial Comment

The role of non-haemodynamic factors of the genesis of LVH

Roland E. Schmieder

Department of Nephrology and Hypertensiology, University of Erlangen-Nuremberg, Germany

Correspondence and offprint requests to: Prof. Dr. Roland E. Schmieder, Medizinische Klinik 4/Nephrology–Hypertensiology, Universität Erlangen-Nürnberg, Krankenhausstraße 12, 91054 Erlangen, Germany. Email: roland.schmieder@rzmail.uni-erlangen.de

Keywords: left ventricular hypertrophy; non-haemodynamic factors

The first 10% of the full text of this article appears below.

"Things are never so simple as they look"

Left ventricular hypertrophy (LVH) is a common finding in arterial hypertension. In mild hypertension, the prevalence of LVH is 20% and in severe hypertension 50% [1]. Evidence of LVH either by electrocardiography or echocardiography clearly increases the risk for myocardial infarction, cardiac sudden death, congestive heart failure and stroke. Most intriguingly, the cumulative incidence of cardiovascular events increases progressively with increasing left ventricular mass, without evidence of any threshold [2]. In other words, hypertensive patients with left ventricular mass in the upper normal range already have increased risk for cardiovascular events [2].

Although the pathogenesis of cardiac hypertrophy in hypertension is not yet completely understood, several haemodynamic and non-haemodynamic factors are of pathogenetic relevance [3]. . . . [Full Text of this Article]


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