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PubMed1993

The hibernating myocardium in ischaemia and congestive heart failure.

Hibernating myocardium refers to the presence of persistent myocardial and left ventricular dysfunction at rest due to reduced coronary blood flow that can be partially or completely restored to normal by myocardial revascularization. An increasing amount of data show it is most likely a downgrading of cardiac function so that blood flow and myocardial function are once again in a state of equilibrium. It has been demonstrated to occur in patients with unstable angina, chronic stable angina, acute myocardial infarction and in left ventricular dysfunction and/or congestive heart failure. Salvage of this viable myocardium by successful revascularization improves left ventricular dysfunction and probably also patient survival. Therefore, diagnosis of hibernating myocardium is important because it does not render left ventricular dysfunction a necessary contraindication to revascularization, nor does it leave the patient with chronic heart failure a candidate only for cardiac transplantation. Instead, these patients should have complete revascularization by coronary bypass surgery/percutaneous transluminal coronary angioplasty as soon as possible.

Angina Pectoris↗
PubMed1999

The role of neurohormonal antagonists in hibernating myocardium.

Hibernating myocardium is characterized by chronic reduction of myocardial blood flow due to obstructive coronary artery disease, causing reversible left ventricular dysfunction and flow-metabolism mismatch. The condition is unstable and increasing demand may lead to further left ventricular dysfunction or necrosis causing death or worsening heart failure. Recognition of the condition is difficult and requires complex cardiac imaging protocols. Treatment protocols are also poorly defined. This review addresses both the diagnostic and therapeutic aspects of hibernating myocardium.

Chronic Disease↗
PubMed1998

Gated metabolic positron emission tomography (GAPET) of the myocardium: 18F-FDG-PET to optimize recognition of myocardial hibernation.

The aim of this study was to test the feasibility of the direct measurement of global and regional metabolic wall thickening with 18F-FDG-gated positron emission tomography (PET) in patients with coronary artery disease (CAD). Based on non-invasive (ECG, echocardiography) and invasive [cineventriculography (CVG), coronary angiography] investigations, 12 patients with CAD underwent gated metabolic PET studies with 18F-FDG. Myocardial wall thickening and wall motion analysis from short-axis horizontal and vertical long-axis slices were studied. PET-derived global ejection fraction correlated with CVG-derived global ejection fraction (r = 0.75). Forty-eight of 72 segments investigated were normal (66.7%); 24 of 72 segments were abnormal (33.3%), of which 10 (41.7%) were considered to be hibernating. Four segments were classified as partially fibrotic (16.7%) and 10 (41.7%) as entirely scar-like. Gated PET (8 gates, tail drop corrected) allows quantification of global and regional ejection fraction to detect metabolic wall thickening in left ventricular segments with dyskinesia on CVG due to critical CAD stenoses. By improving data analysis methods, our approach may enhance the detection of viable, hibernating myocardium before revascularization.

Coronary Disease↗
PubMed2002

Echocardiographic and magnetic resonance methods for diagnosing hibernating myocardium.

Hibernating myocardium refers to regions of impaired left ventricular function at rest due to coronary artery disease that is reversible with revascularization. The accurate identification and assessment of myocardial viability is a critical aspect of the management of the patient with coronary artery disease and left ventricular dysfunction. Several non-invasive methods exist to assist the clinician in distinguishing those patients with significant regions of hibernating myocardium from those who have non-viable scar. This is important not only to identify those patients who would most benefit from percutaneous intervention or surgery, but also to spare the latter group from the morbidity and mortality associated with a revascularization procedure that would provide little benefit. While nuclear medicine imaging is the most widely used means for evaluating myocardial viability, alternative modalities have emerged and have gained increasing acceptance in recent years. This article will review the echocardiographic and magnetic resonance imaging (MRI) methods that are currently available or under investigation to assess myocardial viability. These techniques include rest and stress echocardiography, myocardial contrast echocardiography, stress MRI, contrast-enhanced MRI and magnetic resonance spectroscopy (MRS).

Cardiotonic Agents↗
PubMed1999

Electromechanical characterization of myocardial hibernation in a pig model.

BACKGROUND: This study attempted to assess in-vivo electromechanical changes following gradual coronary artery occlusion in a pig ameroid constrictor model using a novel three-dimensional left ventricular mapping system. METHODS AND RESULTS: We measured unipolar and bipolar voltage potentials and local endocardial shortening in the ischemic lateral and non-ischemic anterior zones in animals at rest (n = 9) 5 weeks after the implantation of ameroid constrictors around the left circumflex artery. Echocardiography was used to assess regional contractility (percentage myocardial thickening), and an echo-contrast perfusion study was performed using acoustic densitometry methods. The ischemic lateral zone showed reduced myocardial perfusion at rest (peak intensity; 3.4 +/- 1.7 versus 20.7 +/- 14.8, P = 0.005), impaired mechanical function (percentage wall thickening 22 +/- 19% versus 40 +/- 11%, P = 0.03; local endocardial shortening 2.9 +/- 5.5% versus 11.7 +/- 2.1%, P = 0.002), and preserved electrical activity (unipolar voltage 12.4 +/- 4.7 versus 14.4 +/- 1.9 mV, P = 0.25; bipolar voltage 4.1 +/- 1.1 versus 3.8 +/- 1.5 mV, P = 0.62), compared with the anterior region. CONCLUSIONS: Gradual coronary artery occlusion resulting in regional reduced perfusion and function at rest (i.e. hibernating myocardium) is characterized by preserved electrical activity. An electromechanical left ventricular mapping procedure such as the one described here may be of diagnostic value for identifying the hibernating myocardium.

Animals↗
PubMed2001

Clinical pathophysiology of hibernating myocardium.

Our current knowledge of the pathophysiology of chronic hibernating myocardium is mainly based on results from clinical studies, because of the absence of appropriate and validated animal models. These clinical observations have given rise to two major controversies: the role of reduced blood flow and that of histological changes in the hibernating segments. In this review, these two subjects will be briefly discussed, and put into the perspective of findings emerging from recently developed animal models.

Animals↗
PubMed2005

Detection of hibernate myocardium by 99mTc sestamibi gated SPECT during low-dose dobutamine infusion plus nitrate in patients with first acute myocardial infarction.

AIM: To investigate the role of Tc-MIBI gated SPECT imaging following the administration of low-dose dobutamine plus nitrate (LDD+nitrate) in the assessment of left ventricular function and the perfusion of hibernate myocardial tissue. METHODS: The study group comprised 29 patients diagnosed as having acute myocardial infarction. In the first month post-infarction, Tc-MIBI gated SPECT imaging was performed in all patients at rest-dobutamine stress and LDD+nitrate. Ejection fraction, end diastolic volume (EDV), end systolic volume (ESV), stroke volume, volume, extent score, and reversibility score values were calculated. RESULTS: The findings of Tc-MIBI gated SPECT imaging following the administration of LDD+nitrate and the rest Tc-MIBI gated SPECT findings revealed that while the levels of ejection fraction (P=0.004) and reversibility score (P=0.000) increased significantly, there was a significant decrease in EDV (P=0.001), ESV (P=0.001), volume (P=0.017), stroke volume (P=0.257) and extent score (P=0.039) values. CONCLUSION: The use of Tc-MIBI gated SPECT concomitantly with the administration of LDD+nitrate is useful in the determination of myocardial hibernation in patients with left ventricular failure following acute myocardial infarction.

Adult↗
PubMedDate not supplied

Diastolic hibernation masquerading as constrictive pericarditis.

BACKGROUND: Hibernating myocardium has traditionally been characterized in terms of systolic dysfunction. METHODS: We describe a case in which a 75-year-old patient with significant coronary artery disease was operated upon for classic constrictive pericarditis. RESULTS: At sternotomy, there was no evidence of pericarditis, but marked diastolic without systolic dysfunction remained. After successful coronary revascularization, the patient immediately exhibited dramatic improvement of diastolic performance. Ex vivo evaluation of myocardial contractile function revealed normal myocardial adrenergic responsiveness, indicating a reversible impairment of contractility. CONCLUSION: Diastolic hibernation may therefore represent a unique form of surgically correctable restrictive cardiomyopathy.

Aged↗
PubMed2004

Atypical cause of hibernating myocardium due to complex cardiovascular lesions associated with Takayasu's arteritis.

Myocardial hibernation is recognised as chronic hypoperfusion of the myocardium and its functional recovery after surgical revascularisation has been described. A case of surgery for complex lesions including severe aortic valve regurgitation, coronary ostial stenosis, and aortic calcification (porcelain aorta) caused by Takayasu's arteritis is presented. The onset of left ventricular functional improvement after aortic valve replacement and coronary revascularisation were indicative of preoperative atypical myocardial hibernation caused by aortic valve disease and coronary artery disease associated with Takayasu's arteritis.

Aortic Diseases↗
PubMed1991

Stunned and hibernating myocardium.

Myocardium that is not functioning may be dead (infarct or scar), viable but stunned (postischemic ventricular dysfunction), viable but hibernating (chronic low flow state), or acutely ischemic. Stunned myocardium has clearly been documented (a) in experimental studies of brief coronary artery occlusion followed by reperfusion, and (b) in myocardial infarct models in which early reperfusion salvages viable tissue. Recent clinical studies have confirmed the existence of stunned myocardium in humans. Evidence supporting the concept of hibernating myocardium comes from clinical studies in which patients with chronic low flow ischemia exhibit improvement in left ventricular function (sometimes immediately) following revascularization.

Animals↗
PubMed1999

Concept and evaluation of hibernating myocardium.

Hibernating myocardium is a state of persistently impaired myocardial and left ventricular function at rest due to reduced coronary blood flows. It can be defined as an exquisitely regulated tissue successfully adapting its activity to prevailing circumstances. It has been documented in patients with angina (chronic stable and/or unstable), acute myocardial infarction, heart failure and/or severe left ventricular dysfunction, and anomalous left coronary artery from the pulmonary artery. The diagnosis of hibernating myocardium involves (a) documenting left ventricular dysfunction at rest and (b) documenting that there is viable myocardium in the area of dysfunction. Tests commonly used for the latter are dobutamine echocardiography, 201Tl isotope studies, and positron image tomography. Revascularization, either by surgery or by interventional catheter techniques, has been shown to improve or normalize the abnormal left ventricular function at rest.

Adaptation, Physiological↗
PubMed2001

Short-term hibernation in adult cardiomyocytes is PO(2) dependent and Ca(2+) mediated.

The mechanism of myocardial hibernation, the reversible downregulation of contractile activity on reduction of coronary flow with unchanged cardiac energetics, is presently not understood. The oxygen consumption (VO(2)), shortening fraction (DeltaL), energy status [phosphocreatine (PCr), ATP, and adenosine and lactate release], and free intracellular Ca(2+) concentration ([Ca(2+)](i)) were measured in isolated rat cardiomyocytes at precisely controlled ambient PO(2) (Oxystat). When PO(2) was reduced from 25 to 6 mmHg, VO(2) decreased by 50%, while DeltaL was downregulated from 11.2 +/- 4.1 to 7.6 +/- 4.0%, and energy status was unchanged in the steady state (observation time 12 min). Only transiently PCr decreased, and lactate and adenosine release increased. Further reduction of PO(2) (to 3 mmHg) reduced VO(2) by 80%, decreased PCr by 35%, moderately increased adenosine and lactate release, and progressively reduced DeltaL by 50% (to 5.6 +/- 3.3%). All parameters fully recovered during reoxygenation. PO(2)-dependent downregulation of DeltaL was accompanied by a progressive reduction in systolic [Ca(2+)](i) (from 512 +/- 110 to 357 +/- 91 nmol/l at 6 mmHg and to 251 +/- 69 nmol/l at 3 mmHg), whereas diastolic free [Ca(2+)](i) remained unchanged. Therefore, the mechanism of the reversible, PO(2)-dependent downregulation of contractile activity (myocardial hibernation) involves a substantial reduction of systolic calcium.

Adenosine Triphosphate↗
PubMed2001

Acute hibernation decreases myocardial pyruvate carboxylation and citrate release.

In the well-perfused heart, pyruvate carboxylation accounts for 3-6% of the citric acid cycle (CAC) flux, and CAC carbon is lost via citrate release. We investigated the effects of an acute reduction in coronary flow on these processes and on the tissue content of CAC intermediates. Measurements were made in an open-chest anesthetized swine model. Left anterior descending coronary artery blood flow was controlled by a extracorporeal perfusion circuit, and flow was decreased by 40% for 80 min to induce myocardial hibernation (n = 8). An intracoronary infusion of [U-(13)C(3)]lactate and [U-(13)C(3)]pyruvate was given to measure the entry of pyruvate into the CAC through pyruvate carboxylation from the (13)C-labeled isotopomers of CAC intermediates. Compared with normal coronary flow, myocardial hibernation resulted in parallel decreases of 65% and 79% in pyruvate carboxylation and net citrate release by the myocardium, respectively, and maintenance of the CAC intermediate content. Elevation of the arterial pyruvate concentration by 1 mM had no effect. Thus a 40% decrease in coronary blood flow resulted in a concomitant decrease in pyruvate carboxylation and citrate release as well as maintenance of the CAC intermediates.

Acute Disease↗
PubMedDate not supplied

Serial prognostic capabilities of electrocardiographic indices of infarcted and hibernating myocardium in predicting short- and long-term outcome following coronary artery bypass surgery.

The present study was performed to test the hypothesis that patients with a large amount of ischemic (hibernating) myocardium are most likely to develop a perioperative myocardial infarction undergoing coronary artery bypass grafting (CABG). Furthermore, we evaluated the Selvester QRS scoring system as a postoperative prognostic tool. A relationship between a high amount of hibernating myocardium determined by ventriculographic and electrocardiographic investigations and an increased risk of perioperative myocardial infarction was found. The Selvester QRS scoring system used in diagnosing and prognosing after acute myocardial infarction was proven valid in predicting prognosis after CABG as well.

Adult↗
PubMed2000

Altered adrenergic receptor density in myocardial hibernation in humans: A possible mechanism of depressed myocardial function.

BACKGROUND: Alterations in adrenergic receptor densities can potentially contribute to myocardial dysfunction. Their relevance to myocardial hibernation in humans is unknown. METHODS AND RESULTS: Accordingly, 22 transmural myocardial biopsies were obtained in 11 patients with ischemic ventricular dysfunction during bypass surgery, guided by transesophageal echocardiography. Patients underwent dobutamine echocardiography (DE) and rest scintigraphic studies before revascularization and DE at 3 to 4 months. alpha- and ss-receptor density (ARD and BRD) and extent of fibrosis were quantified from the myocardial biopsies. Of the 22 segments, 16 had abnormal rest function and 6 were normal. Severely hypokinetic or akinetic segments showed a 2.4-fold increase in ARD with a concomitant 50% decrease in BRD compared with normal segments. An increase in ARD, a decrease in BRD to a lesser extent, and thus an increase in ARD/BRD ratio were seen in dysfunctional segments with contractile reserve compared with normal segments and were most pronounced in those without contractile reserve (P:<0.001). Similar findings were observed if recovery of function or scintigraphic uptake was analyzed as a marker for viability. No significant relation between either ARD or BRD and percent myocardial fibrosis was noted (r=0.37 and -0.39, respectively). CONCLUSIONS: Thus, graded and reciprocal changes in alpha- and ss-adrenergic receptor densities occur in viable, hibernating myocardium and may account in part for the observed depression in resting myocardial function and preserved contractile reserve in this entity.

Aged↗
PubMed2000

Hibernation in noncontracting mammalian cardiomyocytes.

BACKGROUND: -The aim of the present study was to establish whether isolated neonatal mammalian cardiomyocytes were capable of downregulating energy-using processes other than contraction while maintaining metabolic stability when oxygen availability was reduced. METHODS AND RESULTS: Metabolic response of cardiomyocytes was investigated under moderate (5 to 6 micromol/L) and severe (2 to 3 micromol/L) forms of hypoxia. Cells exposed to oxygen concentrations of 5 to 6 micromol/L exhibited rates of oxygen consumption, which were decreased to 64% of normoxic rates. Rates of cellular energy usage were decreased because this reduced rate of oxygen consumption was not associated with either decreased intracellular ATP and phosphocreatine concentrations or a compensatory switch to glycolysis. When cells were exposed to oxygen concentrations of 2 to 3 micromol/L, rates of oxygen consumption decreased to 9% of normoxic rates. This decreased rate of oxygen consumption was associated with energetic stress, because a significant switch to glycolysis occurred and intracellular phosphocreatine concentrations were decreased by 40%. Rates of cellular energy usage were further decreased as indicated by stable intracellular ATP concentrations. CONCLUSIONS: -Our results suggest that isolated cardiomyocytes are capable of downregulating energy-consuming processes other than contraction when oxygen supply is decreased. Regions of myocardial tissue are also capable of downregulating metabolic activity during ischemia by shutting down contractile activity (myocardial hibernation). We suggest that metabolic downregulation associated with myocardial hibernation may not be exclusively due to reduced rates of contractile activity. Other energy-using processes (eg, protein synthesis, mRNA synthesis, ion channel activity, and proton leak) may also be shut down.

Adenosine Triphosphate↗
PubMed2000

Spatial heterogeneity in fasting and insulin-stimulated (18)F-2-deoxyglucose uptake in pigs with hibernating myocardium.

BACKGROUND: Previous studies of hibernating myocardium in the fasting state have shown regionally increased (18)F-2-deoxyglucose (FDG) uptake with a marked transmural gradient. We hypothesized that this adaptation to chronic ischemia might be associated with altered maximal FDG uptake. METHODS AND RESULTS: Pigs were instrumented with a 1.5-mm proximal left anterior descending artery (LAD) stenosis. Studies were conducted 106+/-4 days later on anesthetized animals with complete LAD occlusion and anteroapical dysfunction. In fasting animals (n=9), FDG uptake in dysfunctional LAD regions was 2-fold higher than in normally perfused myocardium (7.9+/-1.2 versus 4. 0+/-0.5 micromol x min(-1) x 100 g(-1), P<0.05), with a pronounced transmural gradient (endocardial/epicardial ratio 2.56+/-0.19 versus 1.25+/-0.03, P<0.05). Euglycemic, hyperinsulinemic clamp (insulin clamp, n=8) produced a 5- to 9-fold increase in FDG uptake, but there was no longer a regional difference in accumulation (LAD, 37. 8+/-4.2 versus normal, 36.4+/-5.1 micromol x min(-1) x 100 g(-1), P=NS) and the transmural distribution was uniform. FDG uptake in the fasting state varied inversely with coronary flow during vasodilation. In contrast, during insulin clamp there was no relation between FDG uptake and vasodilated flow, resulting in a reduced spatial heterogeneity in individual samples (relative dispersion=SD/mean; fasting, 52+/-5% versus insulin, 24+/-2%, P<0.05). CONCLUSIONS: In the fasting state, FDG uptake in pigs with hibernating myocardium was heterogeneous and was increased in dysfunctional regions with a marked transmural gradient and high spatial heterogeneity. In contrast, FDG uptake was more homogeneously distributed during insulin clamp with (1) uptake in dysfunctional myocardium similar to remote normal regions, (2) uniform transmural distribution, and (3) reduced spatial heterogeneity.

Animals↗
PubMed1991

Myocardial perfusion-contraction matching. Implications for coronary heart disease and hibernation.

Experimental studies demonstrate that short-term regional perfusion-contraction matching, in which the energy demands of regional myocardial contraction are reduced to match the diminished myocardial substrate supply, occurs during states of low coronary blood flow under resting conditions and during exercise-induced ischemia. This phenomenon is rapidly reversible and appears to occur in several clinical settings. Sustained perfusion-contraction matching is observed in states of partial experimental ischemia of intermediate duration lasting several hours. This condition might be called short-term hibernation and resembles clinical conditions such as unstable angina pectoris or myocardial infarction with some residual perfusion in which the contractile defect can be improved by reperfusion provided the ischemia is not severe enough to cause transmural necrosis. Such experimental and clinical observations may or may not relate to the setting of regional dysfunction at rest in patients with chronic coronary heart disease, in whom manifestations of acute ischemia may be absent but improvement of wall motion abnormalities occurs after CABG or balloon angioplasty. This condition may constitute the hypothetical state of chronic myocardial hibernation, for which tentative evidence exists from metabolic and perfusion studies using PET. Whether such a condition of prolonged perfusion-contraction matching might be associated with adaptive processes that could allow its persistence for long periods without manifest ischemia remains to be investigated.

Animals↗