© 2004 European Society of Cardiology
Impaired endothelium-dependent and -independent vasodilation in elderly patients with chronic heart failure
Department of Therapeutics and Pharmacology, Whitla Medical Building, Queen's University 97 Lisburn Road, Belfast BT9 7BL, UK
* Corresponding author. Tel.: +44-28-90-335770; Fax: +44-28-90-438346 E-mail address: g.mcveigh{at}qub.ac.uk
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Abstract |
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Background: Impaired endothelium-dependent and independent vasodilator responses in chronic heart failure (CHF) have been well described. Previous studies involved younger patients and omitted medications prior to study.
Aims: We explored if new therapeutic interventions would restore vasodilator responses in typical patients with chronic heart failure.
Methods and results: 24 patients and 15 controls were recruited, patients were maintained on their usual medications. Forearm blood flow responses were measured by venous occlusion plethysmography in response to incremental doses of sodium nitroprusside (SNP) (6, 9 and 12 nmol/min), acetylcholine (ACH) (120, 180 and 240 nmol/min), angiotensin II (AII) (1, 10 and 100 nmol/min) and Ng-Nitro-L-arginine methyl ester (L-NAME) (1, 2 and 4 nmol/min) infused into the non-dominant brachial artery. FBF responses to SNP were impaired in patients compared with controls (13.7(9.9,17.4) vs. 24.8(18.6,30.9)) arbitrary units, P<0.001). Similarly FBF responses to ACH were reduced in patients compared with controls (7.5(4.2,10.9) vs. 24.8(16.4,33.2)) arbitrary units, P<0.001. Decreased FBF was noted in response to AII and L-NAME but was significant only for AII and did not differ between groups.
Conclusions: In elderly patients with CHF, endothelium-dependent and independent vasodilator responses were blunted compared with controls. Defects in nitric oxide bioavailability and smooth muscle responsiveness are not reversed by modern medical management of the heart failure syndrome.
Key Words: Heart failure • Endothelium • Nitric oxide • Acetylcholine
Received June 26, 2003; Revised January 28, 2004; Accepted February 5, 2004
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