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Volume 16, Issue 2, Pages 114-120 (February 2010)


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Endothelial Function and Arterial Compliance are not Impaired in Subjects With Heart Failure of Non-Ischemic Origin

Ashish Shah, MD1, Eugenia Gkaliagkousi, MD, PhD1, James M. Ritter, BM, DPHIL1, Albert Ferro, MB, PhD1Corresponding Author Informationemail address

Received 11 May 2009; received in revised form 4 October 2009; accepted 8 October 2009. published online 16 November 2009.

Abstract 

Background

Patients with heart failure and underlying ischemic heart disease (IHD) exhibit both endothelial dysfunction and increased arterial stiffness. We investigated whether this is also the case in heart failure of nonischemic etiology.

Methods and Results

Eleven patients with heart failure and IHD, 12 patients with heart failure from angiographically verified idiopathic nonischemic dilated cardiomyopathy (DCM), and 16 healthy subjects of similar age and sex were compared. Endothelium-dependent and independent function were evaluated by ultrasonic measurement of flow-mediated dilatation (FMD) and glyceryl trinitrate (GTN)-induced dilatation of the brachial artery respectively. Vascular compliance was assessed by carotid-femoral pulse wave velocity (PWV) and augmentation index (AIx). Heart failure severity was similar in IHD and DCM patients. FMD was impaired in the subjects with IHD as compared with control subjects (4.8 ± 0.3 vs. 8.0 ± 3.6 %, P < .01), but not in those with DCM. GTN-induced vasodilatation was not different in patients and controls. PWV was also increased in IHD patients compared with controls (12.1 ± 3.6 vs. 8.0 ± 1.6 m/s, P < .01), but not in DCM patients. AIx was similar in patients and controls.

Conclusion

Heart failure of nonischemic etiology is not associated with abnormalities of endothelium-mediated dilatation or of arterial compliance. The findings of our study now need to be confirmed in larger studies.

1 Department of Clinical Pharmacology, Cardiovascular Division, School of Medicine, King's College London, London, UK

Corresponding Author InformationReprint requests: Professor Albert Ferro, King's College London, 3.07 Franklin-Wilkins Building, 150 Stamford Street, London SE1 9NH, UK. Tel +44 20 7848 4283; Fax +44 20 7848 3743.

 A.S. was supported by a doctoral studentship from Pfizer plc; E.G. was supported by the Greek Foundation for State Scholarships.

PII: S1071-9164(09)01129-4

doi:10.1016/j.cardfail.2009.10.019


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