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Hibernation and Heart Failure P G Camici 141 MINI-SYMPOSIUM Heart: first published as 10.1136/hrt.2003.016626 on 16 January 2004. Downloaded from Hibernation and heart failure P G Camici ............................................................................................................................... Heart 2004;90:141–143. doi: 10.1136/hrt.2003.023119 eart failure accounts for approximately 20% of all in the infarcted and hibernating segments. The changes in hospital admissions among people over 65, and in the ventricular geometry, local wall strain, and filling pres- past 10 years the hospitalisation rate has increased by sures combine to increase the metabolic requirements of H 1 almost 160%. Although different large randomised trials such myocardium which, while ‘‘remote’’ from the site of carried out during the past two decades have demonstrated a infarction, adopts a ‘‘crucial’’ role in maintaining cardiac significant reduction in mortality for heart failure patients output. These segments undergo compensatory hypertro- treated medically, symptomatic heart failure continues to phy, but in the long term adverse ‘‘remodelling’’ and have a one year mortality close to 45%.23 ventricular dilatation occurs leading to heart failure.1 In an effort to improve the early recognition of heart failure, the American College of Cardiology and the American Based on available studies, it is logical to assume that the Heart Association have recently proposed a new approach to beneficial effect of coronary revascularisation in heart fail- the classification of heart failure based on four progressive ure derives primarily from recovery of contractile function stages.4 This new categorisation emphasises the evolution in hibernating segments which, in turn, may attenuate 8 and progression of heart failure and is quite different from remodelling. the traditional New York Heart Association (NYHA) classi- fication whose primary objective was to describe functional VENTRICULAR DYSFUNCTION IN HIBERNATING limitations. Although this recent classification underscores MYOCARDIUM AND ITS INCIDENCE the risk factors and structural abnormalities, which are The dysfunction associated with hibernating myocardium necessary for the development of heart failure, patients are can be limited to a discrete portion of the left ventricle, with considered independent of the origin of their condition and preserved global ejection fraction, or may be generalised and no major emphasis is placed on the aetiology. result in global impairment of ventricular function and heart failure. The severity of functional impairment can vary from hypokinesia to akinesia or dyskinesia.5 HEART FAILURE IN PATIENTS WITH CORONARY The prevalence of hibernating myocardium can be esti- ARTERY DISEASE mated from the frequency of functional recovery of regional In over two thirds of cases heart failure is secondary to wall motion abnormalities after revascularisation. In a http://heart.bmj.com/ coronary artery disease. The increasingly successful treatment prospective study of 252 patients without previous infarction and reduced mortality of acute coronary syndromes has who were referred for coronary angiography, evidence of increased the prevalence of chronic heart failure in patients 5 hibernating myocardium was present in up to one third of all with coronary artery disease. Evidence from non-rando- patients and 85% of the asynergic myocardial segments were mised studies suggests that in patients with post-ischaemic found to improve their function after revascularisation.9 In heart failure, coronary revascularisation can lead to sympto- 5 patients with previous infarction, areas of hibernating tissue matic and prognostic benefits. To understand the reasons for may be intermixed with scar in up to 50% of the cases, even the beneficial effects of revascularisation, it is necessary to in the presence of Q waves on the ECG.10 The incidence and on September 30, 2021 by guest. Protected copyright. review the underlying mechanisms of heart failure in degree of functional recovery following coronary revascular- patients with coronary artery disease. This is generally the isation depends on a number of factors such as patient result of three factors: selection, techniques for myocardial protection, the occur- N Permanent myocyte loss due to infarction with scar formation— rence of perioperative myocardial infarction, and adequacy of The size of the infarct can be reduced by prompt revascularisation. From the available literature regional thrombolysis with rapid ‘‘door to needle’’ times and functional recovery varies widely from 24–82% of all 5 primary percutaneous interventions, but a degree of segments. It follows that at least a quarter of all the patients necrosis is usually inevitable, even if clinically silent. with proven coronary artery disease have some degree of hibernating myocardium. N Chronic dysfunction in viable myocardium subtended by stenosed coronary arteries which recovers after revascularisation (hibernat- ing myocardium)—This represents the myocardium where IDENTIFICATION OF PATIENTS WITH HIBERNATING the ischaemic insult is insufficient to induce necrosis, MYOCARDIUM although the myocardium remains jeopardised, prone to In principle, hibernating myocardium should be suspected in repeated episodes of ischaemia, and exhibits notably all patients with coronary artery disease and chronic left reduced contraction. The concept of myocardial hiberna- ventricular dysfunction of any degree ranging from regional tion arose from the observation that sustained improve- dysfunction to ischaemic cardiomyopathy. Other causes of ment in left ventricular function may occur after coronary left ventricular dysfunction, such as ethanol abuse and tachycardiomyopathy, that can be associated with coronary artery bypass grafting6 and that transient improvement in chronically dysfunctional segments may occur in response to inotropic stimulation.7 ................................................................ N Changes in the remote myocardium (adverse remodelling)—The Abbreviations: MBF, myocardial blood flow; NYHA, New York Heart workload of myocardium remote from the site of infarc- Association; PET, positron emission tomography; SPECT, single photon tion is increased to compensate for the loss of contraction emission computed tomography www.heartjnl.com 142 Mini-symposium artery disease, should be excluded. If the demonstration of CORONARY FLOW RESERVE AND HIBERNATION coronary artery disease is the condition sine qua non for the The coronary flow reserve is the ratio of MBF during near Heart: first published as 10.1136/hrt.2003.016626 on 16 January 2004. Downloaded from definition of hibernation, the presence and severity of left maximal vasodilatation (pharmacologically induced) to rest- ventricular dysfunction is not necessarily commensurate to ing blood flow and is an index of the functional significance the extent and severity of coronary artery disease. In many of coronary stenoses. In patients with coronary artery disease, patients the recruitment and development of coronary flow reserve decreases in proportion to the degree of stenosis collaterals can result in the preservation of normal left severity and is abolished (that is, hyperaemic flow = resting ventricular function despite the presence of sometimes severe flow) for stenoses > 80% of the luminal diameter.13 Under coronary artery disease.11 these circumstances, any increase in cardiac workload above Myocardial hibernation implies the concept of tissue baseline conditions cannot be met by an adequate increase in viability, which can be diagnosed by imaging modalities that MBF, leading to ischaemia. Therefore, in patients with severe detect either the presence of contraction reserve or the coronary artery disease the limited flow reserve leads to the persistence of metabolic activity within chronically dysfunc- development of myocardial ischaemia, which is often tional myocardial regions (see Kim and Shah on page 137). asymptomatic, even for small increases of oxygen demand such as those associated with ordinary daily activities. Regardless of the blood flow level under baseline conditions, PATHOPHYSIOLOGY OF MYOCARDIAL these patients will develop ischaemia when oxygen demand HIBERNATION is increased (demand ischaemia). Ischaemia is invariably The debate on whether resting myocardial blood flow (MBF) associated with the development of post-ischaemic contrac- to hibernating myocardium is reduced or not has attracted a tile dysfunction that persists following reperfusion, despite lot of interest and, undoubtedly, has stimulated new research the restoration of normal or near normal coronary blood on heart failure in patients with coronary artery disease. flow. In the mid 1970s this phenomenon, later known as Although the debate is not yet over, some of the initial myocardial stunning, was initially described by Heyndrickx paradigms have been proven incorrect while new pathophy- and colleagues14 as a sustained, but eventually completely siological concepts have emerged. reversible, post-ischaemic contractile dysfunction in a con- The initial hypothesis that hibernation is caused by a scious healthy dog model subjected to a 15 minute coronary down regulation of myocardial function, secondary to a occlusion. reduction of resting blood flow beyond a flow limiting Two decades later it was shown that patients with coronary 6 stenosis, was supported by a series of studies in which artery disease and absence of contractile dysfunction at semiquantitative measurements
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