PMID- 15982353 OWN - NLM STAT- MEDLINE DCOM- 20050930 LR - 20161124 IS - 0007-1048 (Print) IS - 0007-1048 (Linking) VI - 130 IP - 1 DP - 2005 Jul TI - 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. PG - 113-20 AB - 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. FAU - Cugno, Massimo AU - Cugno M AD - Department of Internal Medicine, University of Milan, Milan, Italy. massimo.cugno@unimi.it FAU - Agostoni, Piergiuseppe AU - Agostoni P FAU - Mari, Daniela AU - Mari D FAU - Meroni, Pier Luigi AU - Meroni PL FAU - Gregorini, Luisa AU - Gregorini L FAU - Bussotti, Maurizio AU - Bussotti M FAU - Anguissola, Gian Battista AU - Anguissola GB FAU - Donatelli, Francesco AU - Donatelli F FAU - Nussberger, Jurg AU - Nussberger J LA - eng PT - Journal Article PL - England TA - Br J Haematol JT - British journal of haematology JID - 0372544 RN - 0 (Angiotensin-Converting Enzyme Inhibitors) RN - 0 (Biomarkers) RN - 0 (Blood Coagulation Factors) RN - 0 (Interleukin-6) RN - 0 (Receptors, Tumor Necrosis Factor, Type II) RN - 0 (von Willebrand Factor) RN - E7199S1YWR (Lisinopril) RN - EC 3.4.21.38 (Factor XIIa) RN - EC 3.4.21.68 (Tissue Plasminogen Activator) RN - S8TIM42R2W (Bradykinin) SB - IM MH - Adult MH - Angiotensin-Converting Enzyme Inhibitors/*therapeutic use MH - Biomarkers/blood MH - Blood Coagulation Factors/analysis MH - Brachial Artery/diagnostic imaging MH - Bradykinin/*blood MH - Case-Control Studies MH - Endothelium, Vascular/physiopathology MH - *Exercise MH - Factor XIIa/analysis MH - Heart Failure/*blood/*drug therapy/physiopathology MH - Humans MH - Interleukin-6/blood MH - Ischemia/physiopathology MH - Lisinopril/*therapeutic use MH - Male MH - Middle Aged MH - Receptors, Tumor Necrosis Factor, Type II/blood MH - Tissue Plasminogen Activator/analysis MH - Ultrasonography MH - Vasodilation MH - von Willebrand Factor/analysis EDAT- 2005/06/29 09:00 MHDA- 2005/10/01 09:00 CRDT- 2005/06/29 09:00 PHST- 2005/06/29 09:00 [pubmed] PHST- 2005/10/01 09:00 [medline] PHST- 2005/06/29 09:00 [entrez] AID - BJH5569 [pii] AID - 10.1111/j.1365-2141.2005.05569.x [doi] PST - ppublish SO - Br J Haematol. 2005 Jul;130(1):113-20. doi: 10.1111/j.1365-2141.2005.05569.x.