title: Hibernation and congestive heart failure.
abstract: The most common cause of heart failure is coronary artery disease, and whilst intensive treatment of acute coronary syndromes and myocardial infarction continue to reduce the mortality associated with these conditions, many survivors develop heart failure. In general, heart failure secondary to ischaemic heart disease results from: (i) irreversible myocyte loss due to infarction with scar formation; (ii) chronic left ventricular dysfunction which may recover after revascularisation (hibernating myocardium); (iii) changes in remote myocardium (adverse remodelling). A number of studies suggest that patients with post-ischaemic heart failure may derive symptomatic and prognostic benefit from coronary revascularisation and most of this benefit is thought to derive from functional improvement of hibernating myocardium. Although the mechanisms of hibernation remain poorly understood, studies with positron emission tomography have shown that blood flow to hibernating myocardium is usually within or only slightly below the normal range whilst the coronary vasodilator reserve is always severely reduced and the concept that stunning and hibernation may be causally related has gained support in recent years. There is increasing consensus amongst clinicians regarding the importance of identifying and treating hibernating myocardium in patients with coronary artery disease and heart failure, and a randomised study comparing optimum medical treatment to optimum medical treatment with complete revascularisation has just commenced in the United Kingdom (HEART-UK) and will provide guidance regarding diagnosis and treatment of these patients.
authors.affiliation: Department of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK.
authors.forename: David P
authors.initials: DP
authors.lastname: Dutka
authors.forename: Paolo G
authors.initials: PG
authors.lastname: Camici
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D003324:Coronary Artery Disease / Q000188:drug therapy / Q000503:physiopathology; D003326:Coronary Circulation / Q000502:physiology; D006333:Heart Failure / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology*; D006801:Humans; D015994:Incidence; D009200:Myocardial Contraction / Q000502:physiology; D017682:Myocardial Stunning / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology*; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors