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PubMed1981

The effects of cold-stress. Hibernation, and prolonged inactivity on bone dynamics in the golden hamster, Mesocricetus auratus.

The effects of cold-stress and hibernation on bone dynamics in the femurs of hamsters were investigated using histometric analyses. Control animals were maintained at 27 degrees C for 90 days; experimental animals were kept at 5 degrees C and hibernated for 7, 15, 21, 50, or 90 days. Histometric analyses of cross sections indicated that bone diameter and cortical thickness at the femoral midshaft increased after 83 days of extreme cold and 7 days of hibernation but decreased significantly after 69 days of cold stress and 21 days of hibernation. Osteoporosis was evident although the number of osteons per unit area of bone increased during hibernation. An initial decrease in the number of non-Haversian longitudinal vessels per unit area of bone was seen in experimental animals which was apparently related to a corresponding reduction in cortical thickness. Lacunar area increased in these animals, suggesting that osteocytic osteolysis may be a significant mechanism for calcium regulation during hibernation.

Animals↗
PubMed2000

Myocardial hibernation--adaptation to ischemia.

The concept of myocardial hibernation implies a downregulation of contractile function as an adaptation to a reduction in myocardial blood flow that serves to maintain myocardial integrity and viability during persistent ischemia. Unequivocal evidence for this concept exists in scenarios of myocardial ischemia that last for several hours; the recovery of energy and substrate metabolism, the potential for recruitment of inotropic reserve at the expense of metabolic recovery, and lack of necrosis are established criteria of short-term hibernation. Furthermore, experimental studies have demonstrated regional myocardial dysfunction at reduced resting blood flow that recovered upon reperfusion, which is consistent with chronic hibernation. In patients, the importance of reduced baseline blood flow vs. that of superimposed repetitive stunning is somewhat controversial; however, in most studies blood flow is reduced, and the myocardium must be ischemic often enough to have persistent dysfunction. Morphologically, hibernating myocardium displays features of dedifferentiation with loss of cardiomyocytes and myofibrils and of degeneration with increased interstitial fibrosis. The mechanisms of short-term hibernation, apart from reduced calcium responsiveness, are not clear at present. With the identification of the underlying mechanism(s) of hibernation, it can potentially be recruited and reinforced pharmacologically to delay impending myocardial infarction.

Acute Disease↗
PubMed2002

Immunocytochemical evidence for inducible nitric oxide synthase and cyclooxygenase-2 expression with nitrotyrosine formation in human hibernating myocardium.

BACKGROUND: Myocardial hibernation may result from repetitive episodes of transient ischaemia leading to prolonged dysfunction. Inducible nitric oxide synthase (iNOS) expression has been demonstrated in animals following brief, non-lethal ischaemia-reperfusion injury. We therefore, hypothesised that in human hibernating myocardium: 1). iNOS would be present; 2). the reaction of nitric oxide and superoxide would form the strong oxidant peroxynitrite; 3) that this process would be accompanied by the expression of cyclooxygenase-2 (Cox-2) which interacts with NOS and whose products could further affect myocardial function. METHOD AND RESULTS: In sixteen patients with coronary artery disease (CAD), left ventricular biopsies were obtained from chronically dysfunctional segments subtended by a stenotic artery (> 75 %) and shown to be viable by (18)F-fluorodeoxyglucose positron emission tomography. Comparison was made with myocardial biopsies (n = 8) from normally contracting myocardium in patients undergoing coronary surgery, from unused transplant donors and at post-mortem. Regional wall motion score improved in all patients 6 months post-revascularisation (from 2.7 +/- 0.7 to 1.5 +/- 0.5; p < 0.001), confirming hibernation. Immunocytochemistry localized reactivity to iNOS, Cox-2 and nitrotyrosine (a marker of peroxynitrite formation) to cardiomyocytes from hibernating segments. No difference in reactivity to endothelial NOS was seen between hibernating and control cardiomyocytes. CONCLUSION: Cox-2 and iNOS are co-expressed in hibernating myocardium with nitrotyrosine suggesting nitric oxide production and peroxynitrite formation. We propose that this is secondary to ischaemia-reperfusion and that the products of these enzymes may have consequences for myocardial contractile function and survival.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Adrenal activity in the female lizard Lacerta vivipara Jacquin during artificial hibernation.

The variations of interrenal activity were investigated in captive female Lacerta vivipara submitted to artificial hibernation (4 months at 6 degrees) and compared to data obtained in nonhibernating females. Plasma corticosterone levels reached 25 ng/ml during the prehibernal period. During the first day following the transfer to cold conditions, an initial significant peak of plasma corticosterone was observed (up to 63 ng/ml). A second, more gradual, but also significant increase was observed thereafter and levels remained maximum during the two first months of artificial hibernation (75 ng/ml). The circulating levels of corticosterone then decreased gradually. At the time of transfer to warm conditions, a third significant peak of corticosterone was observed (up to 82 ng/ml). The minimal values (15 ng/ml) previously described during vitellogenesis were reached within 1 week. High corticosterone levels appeared to be actually related to the "hibernation state" since they were also observed in hibernating males and not in nonhibernating females. In order to explain the pattern of plasma corticosterone, variations of adrenal sensitivity to synthetic ACTH 1-39 were examined in vitro, using a perifusion system technique. Surprisingly, ACTH-induced stimulation of corticosterone and aldosterone release was significantly reduced during hibernation, whatever the temperature of the perifusion bath (30 or 6 degrees). Nevertheless, a fourfold increase in the half-life of injected tritiated corticosterone was observed during hibernation which likely contributes to maintain high levels of corticosterone despite a low production rate of the hormone.

Adrenal Glands↗
PubMed2004

Identification of hibernating myocardium by acoustic microscopy.

Hibernating myocardium is viable myocardium that recovers after revascularization. The observation of loss of contractile proteins (myofibrils) and accumulation of glycogen in hibernating cardiomyocytes provide the basis for diagnosing hibernating myocardium. In this pilot study, acoustic microscopy was used to identify the cellular structure of normal vs. hibernating myocardium. Sections cut at 5-microm of archival paraffin blocks on glass slides were used for this study. Acoustic microscopy of normal cardiomyocytes showed intracellular linear echoes suggestive of myofibrils, and cardiomyocytes of hibernating myocardium revealed absence of myofibrils and dense intracellular echoes that corresponded to glycogen accumulation on optical microscopy. This modality of visualization allows a definitive diagnosis of hibernating myocardium.

Glycogen↗
PubMed2001

Adult rabbit cardiomyocytes undergo hibernation-like dedifferentiation when co-cultured with cardiac fibroblasts.

OBJECTIVES: Little is known about the causal factors which induce the typical structural changes accompanying cardiomyocyte dedifferentiation in vivo such as in chronic hibernating myocardium. For identifying important factors involved in cardiomyocyte dedifferentiation, as seen in chronic hibernation, an in vitro model mimicking those morphological changes, would be extremely helpful. METHODS: Adult rabbit cardiomyocytes were co-cultured with cardiac fibroblasts. The typical changes induced by this culturing paradigm were investigated using morphometry, electron microscopy and immunocytochemical analysis of several structural proteins, which were used as dedifferentiation markers, i.e., titin, desmin, cardiotin and alpha-smooth muscle actin. RESULTS: Close apposition of fibroblasts with adult rabbit cardiomyocytes induced hibernation-like dedifferentiation, similar to the typical changes seen in chronic hibernation in vivo. Both changes in ultrastructure and in the protein expression pattern of dedifferentiation markers as seen in chronic hibernating myocardium were seen in the co-cultured cardiomyocytes. CONCLUSION: Hibernation-like changes can be induced by co-culturing adult rabbit cardiomyocytes with fibroblasts. This cellular model can be a valuable tool in identifying and characterizing the pathways involved in the dedifferentiation phenotype in vivo, and already suggests that many of the structural changes accompanying dedifferentiation are not per se dependent on a decreased oxygen availability.

Actins↗
PubMed2002

Biochemical mechanisms of hibernation and stunning in the human heart.

BACKGROUND: Myocardial hibernation and stunning are characterized by depressed cardiac function in the presence of reduced or normal coronary blood flow. The underlying biochemical mechanisms are widely unknown and only limited data are available in human hearts. METHODS AND RESULTS: Left ventricular transmural myocardial biopsies were obtained from normal and dysfunctional segments of patients undergoing coronary bypass surgery. Segments were classified as hibernating (n=10) or stunned (n=9) using contrast ventriculography and echocardiography, single photon emission computed tomography (SPECT), and positron emission tomography (PET). In each patient, biopsies from normal myocardial segments were used as controls (n=19). Compared to control myocardium, levels of cAMP (3'-5'cyclic adenosine monophosphate, in fmol/mg wet weight, means+/-S.E.M.) were higher in hibernating (673+/-76 versus 518+/-47, P<0.05) but unchanged in stunned myocardium (513+/-73 versus 466+/-97, P>0.05). Protein expression of phospholamban, sarcoendoplasmic Ca(2+)-ATPase 2a, calsequestrin, the inhibitory subunit of troponin, as well as the activation of p38 MAP kinase were not different when compared to controls. However, heat shock protein 72 (Hsp72) was increased 55% in stunned (2.89+/-0.58 versus 1.86+/-0.32, P<0.05) but not in hibernating myocardium (1.68+/-0.34 versus 1.67+/-0.29, P>0.05). CONCLUSIONS: The data from the present study suggest different pathophysiological mechanisms for myocardial hibernation and stunning. Alterations in the homeostasis of cAMP might be a compensatory mechanism in myocardial hibernation, whereas expression of Hsp72 appears to be cardioprotective in human myocardial stunning. Future studies should further elucidate these mechanisms and their potential impact on future therapeutic interventions.

Aged↗
PubMed2001

Stability of hibernating myocardium in pigs with a chronic left anterior descending coronary artery stenosis: absence of progressive fibrosis in the setting of stable reductions in flow, function and coronary flow reserve.

OBJECTIVES: This study was performed to determine whether hibernating myocardium is adaptive or is destined to undergo progressive irreversible injury. BACKGROUND: Previous studies have suggested that hibernating myocardium eventually results in progressive dysfunction. Since serial studies cannot be performed in humans, the temporal progression of physiologic and structural adaptations was evaluated in pigs with hibernating myocardium. METHODS: Pigs were instrumented with a left anterior descending coronary artery (LAD) stenosis (1.5 mm) and underwent physiologic studies three to five months later to quantify regional function, perfusion and 18F-2-deoxyglucose (FDG) uptake. Viability was confirmed by histology and contractile reserve. RESULTS: Hibernating myocardium was characterized by severe regional dysfunction (centerline score, -1.9+/-0.1), reduced resting subendocardial flow (LAD: 0.85+/-0.03 vs. normal: 1.02+/-0.03 ml/min/g, p < 0.01), critically reduced subendocardial flow reserve (adenosine flow: 1.04+/-0.09 ml/min/g, p = NS vs. rest; epinephrine flow: 0.88+/-0.07 ml/min/g, p = NS vs. rest) and increased FDG uptake (0.022+/-0.002 vs. 0.014+/-0.001 ml/g/min, p < 0.01). Physiologic parameters were not different among animals studied at three (93+/-1 days, n = 27), four (118+/-2 days, n = 26) or five months (150+/-6 days, n = 9). Pathology revealed a small increase in LAD connective tissue (6.4+/-0.4% vs. 4.0+/-0.2%, p < 0.001), with no change over this time frame. CONCLUSIONS: Thus, physiologic and structural features of hibernating myocardium remain constant for at least two months. The absence of functional deterioration or progressive fibrosis suggests that hibernation is adaptive rather than an unstable physiology destined to progress to irreversible injury. The stability of this model appears ideally suited for interventions targeted to improve flow and function in chronically dysfunctional myocardium.

Animals↗
PubMed1998

Prolonged myocardial hibernation exacerbates cardiomyocyte degeneration and impairs recovery of function after revascularization.

OBJECTIVES: We sought to define the effects of time on contractile function, morphology and functional recovery after coronary revascularization in patients with dysfunctional but viable (hibernating) myocardium. BACKGROUND: Functional recovery after coronary artery bypass graft surgery in patients with chronic myocardial hibernation is incomplete or delayed. The proposed cause is a progressive temporal degeneration of cardiomyocytes. METHODS: In 32 patients with multivessel coronary disease, regional wall motion analysis was performed in hypoperfused but metabolically active areas before and 6 months after bypass surgery. During bypass surgery, transmural biopsy samples were obtained from the center of the hypokinetic zone for light and electron microscopic analyses. The proposed duration of myocardial hibernation was retrospectively assessed. RESULTS: Patients with a subacute hibernating condition (<50 days) demonstrated a higher preoperative ejection fraction (EF, 50+/-8%), and a better preserved wall motion (WM) in the supraapical wall (-1.4+/-0.4) than did patients with intermediate-term (>50 days, EF 37+/-9%, p < 0.05; WM -2.4+/-1.5, p = 0.08) or chronic (>6 months, EF 40+/-14%, WM -2.7+/-0.9, p < 0.005) ischemia. Structural degeneration correlated with the duration of ischemia (r = 0.56, p < 0.05). Postoperative recovery of function was enhanced in patients with a short history of hibernation compared with patients with an intermediate-term or chronic condition (EF 60+/-10% vs. 40+/-10%, p < 0.001, and vs. 47+/-14%, p < 0.05). CONCLUSIONS: Hibernating myocardium exhibits time-dependent deterioration due to progressive structural degeneration with enhanced fibrosis. Early revascularization should be attempted to salvage the jeopardized tissue and improve postoperative outcome.

Aged↗
PubMed2003

The non-invasive assessment of hibernating myocardium in ischaemic cardiomyopathy--a myriad of techniques.

Heart failure is placing an ever-increasing burden on society. Many subjects with heart failure and underlying coronary artery disease have a significant amount of akinetic but viable myocardium that is able to contract should myocardial perfusion improve (hibernating myocardium). Non-randomised studies have shown prognostic benefit in subjects with hibernating myocardium undergoing revascularisation. Several non-invasive techniques have been developed to assess the presence or absence of hibernating myocardium. This review will examine the epidemiology and underlying pathogenesis of hibernating myocardium; evaluate the non-invasive techniques for diagnosing hibernating myocardium, and look at therapeutic intervention in subjects with hibernating myocardium.

Cardiomyopathy, Dilated↗
PubMed2003

Hibernation and congestive heart failure.

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.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Myocardial adaptation during acute hibernation: mechanisms of phosphocreatine recovery.

OBJECTIVES: Acute hibernation, defined as a prolonged period of moderately reduced oxygen supply and stable haemodynamic function, results in metabolic adaptation characterised primarily by an increase in phosphocreatine. The mechanism of this increase in phosphocreatine is unknown, but has been postulated to result from either an increase in adenosine triphosphate (ATP) production or a decrease in ATP utilisation under conditions of constant myocardial oxygen consumption (MVO2). These experiments were performed to test the hypotheses that (1) acute hibernation could be modelled in an isolated perfused rat heart exhibiting metabolic adaptation; and (2) recovery of phosphocreatine could be explained by alterations in relative creatine kinase flux during hibernation. METHODS: Nuclear magnetic resonance techniques were used in an isolated, perfused rat heart model of acute hibernation to determine the changes in metabolites and creatine kinase kinetics. A flow reduction from 12.5 to 5.4 ml.min-1 was employed for two hours, followed by reperfusion. RESULTS: Reduction of flow resulted in a stable 44% reduction in rate-pressure product. Phosphocreatine had a significant decrease of 9% within the first 15 minutes of ischaemia, but recovered to control values by the end of ischaemia. ATP and [ADP], although unchanged in the early phase of ischaemia, were progressively reduced during the later phase of ischaemia. Intracellular pH fell from 6.99(0.04) to 6.92(0.03) after 15 minutes of ischaemia with little recovery. Saturation transfer measurements showed stability of the forward flux in the creatine kinase reaction during ischaemia, but a progressive reduction in the calculated reverse flux. CONCLUSIONS: These data show that acute hibernation can be modelled in an isolated perfused heart, exhibiting recovery of phosphocreatine despite progressive reductions in ATP. Metabolic changes during acute hibernation have a phasic response characterised by an early ischaemic phase and a later adaptive phase. There is a time related change in measured creatine kinase flux, consistent with a differential change in either ATP production via an increase in MB creatine kinase isoenzyme or a shift in the activity of mitochondrial v cytosolic creatine kinase, a reduction in ATP utilisation via increased efficiency of ATP utilisation at the myofibril, or a changing contribution of glycolytically produced ATP.

Adenosine Diphosphate↗
PubMed1995

Characterization of hibernating and stunned myocardium.

Both the hibernating and the stunned myocardium are characterized by reversible contractile dysfunction. In hibernating myocardium, perfusion is still reduced, whereas in stunned myocardium blood flow is fully or almost fully restored. Both the hibernating and the stunned myocardium retain an inotropic reserve. In hibernating myocardium the increase in contractile function is at the expense of metabolic recovery, whereas in the stunned myocardium no metabolic deterioration occurs during inotropic stimulation. Therefore, inotropic stimulation in combination with metabolic imaging may help not only to identify viable, dysfunctional myocardium but also to distinguish hibernating and stunned myocardium. The therapy of hibernating myocardium is to restore blood flow to the hypoperfused tissue. Myocardial stunning per se requires no therapy at all, since, by definition, blood flow is normal and contractile function will recover spontaneously. If, however, myocardial stunning is severe, and it involves large parts of the LV and thus impairs global LV function, it can be reversed with inotropic agents and procedures. In the experimental setting, anti-oxidant agents, calcium antagonists and ACE inhibitors attenuate stunning, but most effectively when administered before ischaemia.

Animals↗
PubMed1997

Characterization of hibernating and stunned myocardium.

Both the hibernating and the stunned myocardium are characterized by reversible contractile dysfunction. In hibernating myocardium ischaemia is still ongoing, whereas in stunned myocardium blood flow is fully or almost fully restored. Both the hibernating and the stunned myocardium retain an inotropic reserve. In hibernating myocardium the increase in contractile function is at the expense of metabolic recovery whereas in stunned myocardium no metabolic deterioration occurs during inotropic stimulation. Therefore, inotropic stimulation in combination with metabolic imaging may help not only to identify viable, dysfunctional myocardium but also to distinguish between hibernating and stunned myocardium. The therapy of hibernating myocardium is to restore blood flow to the hypoperfused tissue. Myocardial stunning per se requires no therapy at all, since by definition blood flow is normal and contractile function will recover spontaneously. If, however, myocardial stunning is severe, involves large parts of the left ventricle and thus impairs global left ventricular function, it can be reversed with inotropic agents and procedures. In the experimental setting, anti-oxidant agents, calcium antagonists and ACE inhibitors attenuate stunning, most effectively when administered before ischaemia.

Animals↗
PubMed2005

Evidence of myocardial hibernation in the septic heart.

OBJECTIVE: Myocardial hibernation is an adaptive response to ischemia and hypoxia. Hibernating cardiomyocytes are reversibly hypocontractile and demonstrate characteristic metabolic and ultrastructural changes. These include a switch in primary substrate utilization from fatty acids to glucose, up-regulation of the myocardial specific glucose transporters (GLUT1 and GLUT4), and glycogen deposition within and between cardiomyocytes. We hypothesized that myocardial hibernation may underlie sepsis-associated myocardial depression. DESIGN: Prospective observational study aimed at identifying the characteristic changes of hibernation in the septic heart. SETTING: University hospital-based laboratory. SUBJECTS: Forty-three C57Bl6 male mice. INTERVENTIONS: Mice underwent cecal ligation and double puncture, sham operation, or no operation and were evaluated 48 hrs after the procedure. MEASUREMENTS AND MAIN RESULTS: Using novel, clinically relevant technology such as magnetic resonance imaging, positron emission tomography, and single photon emission computed tomography imaging, we found septic mice to have diminished cardiac performance, increased myocardial glucose uptake, increased steady-state levels of myocardial GLUT4, and increased deposits of glycogen, recapitulating the changes during hibernation. Importantly, these changes occurred in the setting of preserved arterial oxygen tension and myocardial perfusion. CONCLUSIONS: Sepsis-associated cardiac dysfunction may reflect hibernation. Furthermore, such down-regulation of cellular function may underlie sepsis-induced dysfunction in other organ systems.

Animals↗
PubMed2002

Direct epicardial mapping can differentiate hibernating from scarred myocardium: a validation study with 18F-FDG-PET.

AIM: This study investigated the value of epicardial mapping immediately before CABG in the differentiation of hibernating from scarred myocardium in correlation to the noninvasive gold standard (18)F-FDG PET. METHODS AND RESULTS: In 35 patients with CAD, myocardial perfusion ((99m)Tc-Tetrofosmin-SPECT), viability ((18)F-FDG-PET), and function (LVangiography) were assessed before CABG. 102 bipolar epicardial electrograms per patient (n = 3570 electrograms) were recorded simultaneously with a ventricular jacket array. Based on the scintigraphic and LV angiographic data at the site of each electrode with good myocardial contact (n = 1963), segments (n = 492, 14.1 +/- 5.6 per patient; mean +/- SD) were classified into three groups: hibernating (n = 139), scarred (n = 104), and control (n = 249). Regional mean bipolar voltage values were calculated for Receiver Operating Characteristic (ROC) analysis. Mean bipolar voltage was significantly lower in scarred when compared to hibernating myocardium. ROC curve analysis (area under the curve of 0.92 +/- 0.47, mean +/- SE) for mean bipolar voltage to discriminate between hibernating and scarred myocardium revealed a sensitivity of 94% with a specificity of 83% at a cut-off value of 8.75 mV. CONCLUSION: Hibernating myocardium can be differentiated correctly from scarred myocardium by direct epicardial mapping. In the future, hibernating myocardium may be detectable by body surface mapping techniques using inverse solutions.

Aged↗
PubMed1999

Efficacy of coronary angioplasty for the treatment of hibernating myocardium.

OBJECTIVES: To determine the efficacy of coronary angioplasty as the sole method of revascularisation in patients with coronary artery disease and chronically dysfunctional but viable myocardium (hibernating myocardium), and to assess the effect of restenosis on functional outcome. DESIGN AND PATIENTS: 24 consecutive patients with hibernating myocardium were studied. Positron emission tomography was used to assess myocardial viability, blood flow, and flow reserve. One patient refused angioplasty, one had bypass surgery, and one died while waiting for an elective procedure. The procedure failed in three patients. The remaining 18 patients had repeat echocardiography, 15 had repeat coronary angiography, and nine had repeat assessments of blood flow and flow reserve at mean (SD) 17 (2) weeks after angioplasty. In three patients restenosis was documented. RESULTS: The wall motion score index in the revascularised territories improved from 1.71 (0.37) to 1.34 (0.47) (p = 0.008). Thirty of 51 dysfunctional segments improved in territories without restenosis compared with three of 14 in restenosed territories (p = 0.001). Hibernating and normal segments had comparable flows (0.82 (0.26) v 0.89 (0.24) ml/min/g; NS) while flow reserve was lower in hibernating segments (1.55 (0.68) v 2.07 (1.08); p = 0.03). In segments without restenosis flow reserve improved from 2.03 (1.25) to 2.33 (1.4) (p = 0.03). Sensitivity, specificity, and positive and negative predictive accuracy of the viability study were 97%, 77%, 82%, and 96%, respectively. After excluding patients with restenosis, specificity and positive predictive accuracy improved to 90% and 93%. CONCLUSIONS: Angioplasty improves function in hibernating myocardium, and restenosis prevents recovery; hibernating myocardium is characterised by an impairment of flow reserve; restenosis affects the diagnostic accuracy of viability studies.

Adult↗
PubMed1992

Metabolic responses of hibernating and infarcted myocardium to revascularization. A follow-up study of regional perfusion, function, and metabolism.

BACKGROUND: The presence of persistent myocardial uptake of 18F-deoxyglucose (FDG) within hypoperfused, dysfunctional segments has been shown to predict the recovery of regional contractile function after revascularization. The spectrum of metabolic responses of such hibernating tissue to revascularization is less clear. METHODS AND RESULTS: Sixteen patients with previous infarction were studied before and after revascularization by myocardial perfusion imaging using 82Rb positron emission tomography, digitized two-dimensional echocardiography, and imaging of postexercise FDG uptake. Hibernation was identified in 35 of 85 segments showing perfusion and wall motion disturbances before intervention. At follow-up (4.9 +/- 2.6 months after revascularization), hibernating segments were characterized by reduction of wall motion score (p less than 0.001), improvement of perfusion (p less than 0.001), and reduction of FDG activity (p less than 0.001). Of the 35 hibernating segments, however, 10 still had abnormal elevation of FDG uptake (greater than 2 SD above normal) without differing from other hibernating segments with respect to postoperative perfusion or wall motion score. Segments with persistently abnormal metabolism were characterized before intervention by more severe malperfusion (p less than 0.01) and greater FDG activity (p less than 0.01). CONCLUSIONS: Although wall motion and perfusion improve with revascularization of hibernating tissue, myocardial metabolism remains abnormal in a significant proportion of segments. These segments are characterized by more extensive perfusion and metabolic changes before revascularization.

Deoxyglucose↗