Document Detail


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.
MedLine Citation:
PMID:  15982353     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Massimo Cugno; Piergiuseppe Agostoni; Daniela Mari; Pier Luigi Meroni; Luisa Gregorini; Maurizio Bussotti; Gian Battista Anguissola; Francesco Donatelli; Jürg Nussberger
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  British journal of haematology     Volume:  130     ISSN:  0007-1048     ISO Abbreviation:  Br. J. Haematol.     Publication Date:  2005 Jul 
Date Detail:
Created Date:  2005-06-28     Completed Date:  2005-09-30     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0372544     Medline TA:  Br J Haematol     Country:  England    
Other Details:
Languages:  eng     Pagination:  113-20     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, University of Milan, Milan, Italy. massimo.cugno@unimi.it
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MeSH Terms
Descriptor/Qualifier:
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 / 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
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; 0/Biological Markers; 0/Blood Coagulation Factors; 0/Interleukin-6; 0/Receptors, Tumor Necrosis Factor, Type II; 0/von Willebrand Factor; 58-82-2/Bradykinin; 83915-83-7/Lisinopril; EC 3.4.21.38/Factor XIIa; EC 3.4.21.68/Tissue Plasminogen Activator

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