Literature DB >> 11212058

Left ventricular hypertrophy is associated with an attenuated endothelium-dependent vasodilation in hypertensive men.

J Millgård1, A Hägg, T Kahan, J Landelius, K Malmqvist, M Sarabi, L Lind.   

Abstract

To investigate the relationship between left ventricular hypertrophy (LVH) and endothelium-dependent vasodilation (EDV), 30 untreated hypertensive patients, 18 treated hypertensives (53 +/- 7 years, all males) and 26 age-and sex-matched healthy normotensive controls, underwent evaluation of EDV and endothelium-independent vasodilation (EIDV) in the forearm, by means of local intra-arterial infusions of methacholine (MCh, evaluating EDV) and sodium nitroprusside (SNP, evaluating EIDV). Forearm blood flow was measured by venous occlusion plethysmography and LVH was measured by echocardiography. The reduction in forearm vascular resistance during MCh infusion (4 microg/min) was significantly smaller in the hypertensive patients with LVH when compared to those without LVH, both in the untreated (-61 +/- 12%, n = 19 vs -72 +/- 4%, n = 11, p < 0.01) and in the treated group (-60 +/- 15%, n = 11 vs -75 +/- 5%, n = 7, p < 0.01). Thereby, EDV was significantly impaired only in the hypertensive patients with LVH when compared to controls (-77 +/- 7% at MCh 4 microg/min, p < 0.001). EIDV was not significantly different between patients with and without LVH and controls. In conclusion, the presence of LVH was related to endothelial dysfunction, both in untreated and treated hypertensive patients, suggesting either a role for endothelial function in the development of LVH, or that a dysfunctional endothelium and LVH are coexisting markers of a more severe hypertensive disease.

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Year:  2000        PMID: 11212058     DOI: 10.1080/080370500300000879

Source DB:  PubMed          Journal:  Blood Press        ISSN: 0803-7051            Impact factor:   2.835


  6 in total

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2.  Endothelial dysfunction is associated with left ventricular mass (assessed using MRI) in an adult population (MESA).

Authors:  J Yeboah; J R Crouse; D A Bluemke; J A C Lima; J F Polak; G L Burke; D M Herrington
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3.  Endothelial Nogo-B regulates sphingolipid biosynthesis to promote pathological cardiac hypertrophy during chronic pressure overload.

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6.  Comorbid CAD and ventricular hypertrophy compromise the perfusion of myocardial tissue at subcritical stenosis of epicardial coronaries.

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  6 in total

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