Impaired bradykinin response to ischaemia and exercise in patients with mild congestive heart failure during angiotensin-converting enzyme treatment. Relationships with endothelial function, coagulation and inflammation
Détails
ID Serval
serval:BIB_C7F37528CB5A
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Impaired bradykinin response to ischaemia and exercise in patients with mild congestive heart failure during angiotensin-converting enzyme treatment. Relationships with endothelial function, coagulation and inflammation
Périodique
British Journal of Haematology
ISSN
0007-1048 (Print)
Statut éditorial
Publié
Date de publication
07/2005
Volume
130
Numéro
1
Pages
113-20
Notes
Journal Article --- Old month value: Jul
Résumé
Inflammation and endothelial dysfunction play important roles in the pathophysiology of congestive heart failure (CHF), and the peptide bradykinin, generated during inflammation, may act as a defence mechanism by inducing vasodilation. Plasma bradykinin levels are increased in experimental heart failure but low in patients with advanced chronic CHF despite treatment with angiotensin-converting enzyme (ACE) inhibitors. It is not currently known how bradykinin behaves in less severe phases of CHF controlled by long-term ACE inhibitor treatment. We studied 10 male patients with clinically stable chronic CHF [New York Heart Association (NYHA) class II] on long-term ACE inhibitor treatment and 10 normal sex- and age-matched control subjects. High performance liquid chromatography/radioimmunoassay methods were used to evaluate plasma levels of bradykinin in relation to an array of parameters of endothelial function, coagulation and inflammation before and after stimuli of forearm arterial occlusion and physical exercise. CHF patients had higher levels of bradykinin (P = 0.008), activated factor XII (P = 0.049), interleukin-6 (P = 0.050) and tumour necrosis factor receptor II (sTNFRII) (P = 0.026) than controls. Arterial occlusion and exercise significantly increased bradykinin and von Willebrand factor levels in controls but not in CHF patients. The increase in brachial artery diameter after arterial occlusion was less in CHF patients (P = 0.036) and inversely related to baseline plasma levels of bradykinin (r = -0.855, P = 0.002) and sTNFRII (r = -0.780, P = 0.008). NYHA class II CHF patients during long-term treatment with ACE inhibitors have increased bradykinin levels and signs of inflammation. They are unable to respond adequately to stimuli of ischaemia and physical exercise which both require vasodilation.
Mots-clé
Adult
Angiotensin-Converting Enzyme Inhibitors/*therapeutic use
Biological Markers/blood
Blood Coagulation Factors/analysis
Brachial Artery/ultrasonography
Bradykinin/*blood
Case-Control Studies
Endothelium, Vascular/physiopathology
*Exercise
Factor XIIa/analysis
Heart Failure, Congestive/*blood/*drug therapy/physiopathology
Humans
Interleukin-6/blood
Ischemia/physiopathology
Lisinopril/*therapeutic use
Male
Middle Aged
Receptors, Tumor Necrosis Factor, Type II/blood
Tissue Plasminogen Activator/analysis
Vasodilation
von Willebrand Factor/analysis
Pubmed
Web of science
Open Access
Oui
Création de la notice
05/03/2008 17:39
Dernière modification de la notice
20/08/2019 16:43