title: Heart failure determines the myocardial inflammatory response to injury.
abstract: OBJECTIVE
  Systemic complications after cardiac surgery are common in heart failure patients. However, the pathophysiological mechanisms, such as a different local inflammatory response of failing hearts, remain in question. This study examines whether failing hearts respond differently to cardioplegic arrest and reperfusion compared with non-failing hearts (controls).
  
  
  RESULTS
  The inflammatory response was evaluated in samples collected simultaneously from the radial artery and coronary sinus, and myocardial tissue in 62 patients undergoing cardiac surgery. No myocardial release of inflammatory mediators was observed upon reperfusion in controls (n = 19). In contrast, in patients with heart failure, reperfusion was characterized by a myocardial release of several cytokines. Myocardial interleukin-6 was 115% increased in non-ischaemic heart failure (n = 18, P = 0.002) as compared with a 117% increase in patients with ischaemic heart failure (n = 25, P = 0.01). Furthermore, a myocardial release of monocyte chemoattractant protein-1 was observed in both patient groups: a 109% (P = 0.001) and 114% (P = 0.01) increase in patients with non-ischaemic heart failure and ischaemic heart failure, respectively. Post-operative myocardial damage, expression of inflammatory mediators, and p65-nuclear factor-κB activity were similar in all patient groups. Inflammatory cell content was increased in early ischaemic myocardial tissue in both heart failure groups compared with controls.
  
  
  CONCLUSIONS
  Heart failure patients show a clear myocardial inflammatory response upon reperfusion, probably explained by degranulation of infiltrated inflammatory cells. Results in controls indicate that they better withstand cardioplegic arrest and reperfusion without an explicit myocardial inflammatory response.
authors.affiliation: Department of Cardiothoracic Surgery, Leiden University Medical Center, 2300 RC Leiden, The Netherlands. k.a.kortekaas@lumc.nl
authors.forename: Kirsten A
authors.initials: KA
authors.lastname: Kortekaas
authors.forename: Jan H
authors.initials: JH
authors.lastname: Lindeman
authors.forename: Michel I
authors.initials: MI
authors.lastname: Versteegh
authors.forename: Els
authors.initials: E
authors.lastname: van Beelen
authors.forename: Robert
authors.initials: R
authors.lastname: Kleemann
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Klautz
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000097:blood*; D006333:Heart Failure / Q000097:blood* / Q000150:complications / Q000601:surgery; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000097:blood* / Q000209:etiology / Q000473:pathology; D015850:Interleukin-6 / Q000097:blood*; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000097:blood* / Q000150:complications / Q000601:surgery; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D011183:Postoperative Complications; D011446:Prospective Studies
chemical_list: D018932:Chemokine CCL2; D015850:Interleukin-6