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PubMed1994

Spontaneous delayed recovery of perfusion and contraction after the first 5 weeks after anterior infarction. Evidence for the presence of hibernating myocardium in the infarcted area.

BACKGROUND: In patients with ventricular dysfunction caused by stunning or hibernation, it is not clear when complete recovery of the salvaged myocardium occurs after acute myocardial infarction. The purpose of this study was to determine whether a delayed recovery of perfusion and contraction continues even after the subacute phase. METHODS AND RESULTS: We prospectively studied 71 consecutive male patients with first uncomplicated Q-wave anterior infarction. Resting regional blood flow distribution and contraction were assessed quantitatively 5 weeks and 7 months after the acute phase by serial sestamibi tomography and two-dimensional echocardiography. Coronary angiography also was performed in 52 patients. Overall, at 7 months there was an improvement in the perfusion defect severity (1019 +/- 811 versus 1365 +/- 821 at 5 weeks, P < .001) as well as in the extent of abnormal wall motion (28 +/- 19% versus 32 +/- 15%, P < .001) and left ventricular ejection fraction (53 +/- 14% versus 50 +/- 13%, P < .01). Among the 68 of 71 patients showing resting perfusion defects at 5 weeks, two groups were identified: 47 (group 1) who showed a significant (beyond the reproducibility limits) 7-month reduction of the resting perfusion defect, and 21 patients (group 2) in whom the perfusion defect remained unchanged. Ejection fraction and the extent of abnormal wall motion significantly (P < .01) improved in group 1 but not in group 2. Despite the presence of a comparable perfusion defect size between the two groups at 5 weeks after infarction, group 1 already showed a better regional and global ventricular function (P < .05). No significant differences were found between the two groups regarding age, medical therapy, the extent of underlying coronary disease, thrombolysis in the acute phase, Thrombolysis in Myocardial Infarction grade of the infarct-related vessel, and presence of collaterals on angiography. CONCLUSIONS: After anterior Q-wave infarction, the recovery of perfusion and wall motion may continue well after the subacute phase. Several patients exhibit relative hypoperfusion in viable tissue as late as 5 weeks after infarction, and a significant improvement of perfusion in the infarcted area commonly is observed between 5 weeks and 7 months. This delayed improvement of perfusion is associated with a delayed improvement of contractile function in the infarcted area after the first 5 weeks, which may continue for up to 7 months, suggesting the presence of hibernating myocardium in the infarcted area. Despite similar perfusion defect sizes, the level of regional function can be different at 5 weeks, and measurements taken around this time may not accurately estimate the eventual recovery of function.

Adult↗
PubMed1996

Myocardial blood flow, glucose uptake, and recruitment of inotropic reserve in chronic left ventricular ischemic dysfunction. Implications for the pathophysiology of chronic myocardial hibernation.

BACKGROUND: Previous work has documented that dysfunctional noninfarcted collateral-dependent myocardium, a condition typical of myocardial hibernation, exhibited almost normal resting perfusion. The present study was designed to test whether these observations could be extended to unselected patients with chronic dysfunction and a previous infarction. METHODS AND RESULTS: Dynamic positron emission tomographic imaging with [13N]ammonia and [18F]fluorodeoxyglucose (FDG) to assess myocardial perfusion and glucose uptake was performed in 39 patients with chronic anterior wall dysfunction undergoing coronary revascularization. Left ventricular function was evaluated by echocardiography before (at rest and during low-dose dobutamine infusion) and 5 months after revascularization. At follow-up, wall motion was improved in 24 patients and unchanged in 15 patients. Before revascularization, absolute myocardial blood flow was higher (84 +/- 27 versus 60 +/- 26 mL.min-1 x 100 g-1, P = .007) in reversibly compared with persistently dysfunctional segments. In segments with reversible dysfunction, values of myocardial blood flow were similar to those in the remote segments of the same patients or in anterior segments of normal volunteers. During glucose clamp, FDG uptake was higher (69 +/- 17% versus 49 +/- 18%, P < .01) but myocardial glucose uptake was not different (38 +/- 20 versus 29 +/- 19 mumol.min-1.100 g-1, P = NS) in reversibly compared with persistently dysfunctional segments. A flow-metabolism mismatch was present in 18 of 24 reversibly injured but absent in 10 of 15 persistently dysfunctional segments. With dobutamine, wall motion improved in 17 of 24 reversibly dysfunctional segments and did not change in 13 of 15 segments with persistent dysfunction. CONCLUSIONS: This study indicates that chronic but reversible ischemic dysfunction is associated with almost normal resting myocardial perfusion, with maintained FDG uptake, and with recruitable inotropic reserve. These data support the contention that chronic hibernation is not the consequence of a permanent reduction of transmural myocardial perfusion at rest.

Adult↗
PubMed2005

Regional desensitization of beta-adrenergic receptor signaling in swine with chronic hibernating myocardium.

Contractile reserve during submaximal beta-adrenergic stimulation is attenuated in patients and swine with hibernating myocardium. We tested the hypothesis that this arises as a regional adaptive response in beta-adrenergic adenylyl cyclase coupling. Pigs (n=8) were studied 3 months after instrumentation with a left anterior descending artery (LAD) stenosis when flow (LAD, 0.7+/-0.2 versus 1.2+/-0.1 mL/min per gram in normal remote; P<0.05) and wall thickening (LAD, 15.5 [corrected]+/-3.2% versus 40.0+/-5.5% in remote; P<0.05) were reduced in the absence of infarction. Whereas basal cAMP production was normal (LAD, 87+/-18 versus 91+/-19 pmol/mg per minute; P=NS), responses to isoproterenol were blunted (LAD, 83+/-6 versus 146+/-25 pmol/mg per minute in remote; P<0.05). beta-receptor density and subtype were unchanged, but there was a reduction in the number of high-affinity binding sites (LAD, 40+/-4% versus 53+/-7% in normal remote; P<0.05). The Gialpha2/Gsalpha ratio increased (LAD, 1.8+/-0.3 versus 0.99+/-0.3 in remote myocardium; P<0.05), although GppNHp-stimulated cAMP production was equivocally reduced. Forskolin responses were unchanged and similar to shams. These data indicate regional attenuation of beta-receptor adenylyl cyclase signaling in hibernating myocardium. This blunts the local contractile response to beta-adrenergic stimulation and may serve to protect against a myocardial supply/demand imbalance when external determinants of myocardial workload increase during sympathetic activation.

Adenylyl Cyclases↗
PubMed1995

Mechanism of impaired myocardial function during progressive coronary stenosis in conscious pigs. Hibernation versus stunning?

The major goal of this study was to determine whether impaired myocardial contractile function during the development of progressive coronary artery stenosis induced by ameroid constriction in conscious pigs reflected myocardial "hibernation" or "stunning." Minipigs were instrumented with a coronary ameroid constrictor and hydraulic occluder, regional wall thickness crystals, a left ventricular (LV) pressure gauge, and aortic and left atrial catheters. In the seven pigs in which it was measured, systolic wall thickening (WT) distal to the ameroid fell by a maximum of 56 +/- 6% at 20 +/- 3 days after ameroid implantation and then began to recover. At 1 day after ameroid implantation, brief complete coronary artery occlusion (CAO) resulted in wall thinning distal to the ameroid (-113 +/- 4%) and transmural decreases in myocardial blood flow in endocardial (from 0.82 +/- 0.08 to 0.02 +/- 0.01 mL/min per gram) and epicardial (from 0.73 +/- 0.13 to 0.03 +/- 0.02 mL/min per gram) layers. At 20 +/- 3 days, baseline myocardial blood flow was not altered either in endocardial (0.92 +/- 0.10 mL/min per gram) or epicardial (0.85 +/- 0.12 mL/min per gram) layers, whereas brief complete coronary artery occlusion still reduced WT (-83 +/- 12%) and myocardial blood flow in endocardial (to 0.21 +/- 0.03 mL/min per gram) and epicardial (to 0.43 +/- 0.12 mL/min per gram) layers, indicating that the coronary artery was not totally occluded. Pathology in four pigs demonstrated no gross necrotic myocardium shortly after this time point. Transient reductions in WT distal to the ameroid were observed during progressive coronary artery stenosis in response to spontaneous increases in activity. Beat-by-beat analysis of these episodes revealed that acute reductions in WT followed increases in LV dP/dt and heart rate and exhibited delayed recovery. These data suggest that the reduced function during ameroid-induced coronary stenosis reflected cumulative myocardial stunning rather than a primary deficit in coronary blood flow or "hibernating myocardium."

Animals↗
PubMed2000

Detecting viable hibernating myocardium in chronic coronary artery disease--a comparison of resting 201Tl single photon emission computed tomography (SPECT), 99mTc-methoxy-isobutyl isonitrile SPECT after nitrate administration, and 201Tl SPECT after 201Tl-glucose-insulin infusion.

To identify and quantify the amount of viable hibernating myocardium in patients with chronic coronary artery disease, resting 201Tl single photon emission computed tomography (SPECT) was compared with 99mTc-methoxy-isobutyl isonitrile (MIBI) SPECT after nitrate infusion (nitrate-99mTc-MIBI) and 201Tl SPECT after 201Tl with glucose-insulin-potassium infusion (201Tl-GIK) in 25 patients. Twenty-one patients also underwent completely left ventriculography beforehand and 5+/-4 months afterwards. SPECT images were divided into 9 segments and scored visually from 0 (normal uptake) to 3 (absent). The defect score was calculated as the summation of the total scores (TDS) in each patient. The TDS of nitrate-99mTc-MIBI images (6.3+/-4.3) and 201Tl-GIK images (5.8+/-4.2) were significantly lower than the 7.4+/-4.3 of resting 201Tl images (p<0.01). Based on the improvement of wall motion after coronary revascularization, the sensitivity of 201Tl-GIK imaging (85%) was significantly higher (p<0.05), and that of nitrate-99mTc-MIBI imaging (79%) also tended to be higher (p=0.08), than that of 201Tl imaging (62%) in detecting viable myocardium. The specificity of the 3 methods was almost the same. The nitrate-99mTc-MIBI and 201Tl-GIK methods were more useful than the resting 201Tl method for evaluating viable hibernating myocardium. Furthermore, the 201Tl-GIK method may provide a more accurate estimate of the amount of viable myocardium than the nitrate-99mTc-MIBI method.

Aged↗
PubMed2005

Hibernating myocardium in heart failure.

Ischemic left ventricular systolic dysfunction may result from myocardial necrosis or from hypocontractile areas of viable myocardium. In some cases, recovery of contractility may occur on revascularization--this reversibly dysfunctional tissue is commonly referred to as hibernating myocardium. Observational data suggest that revascularization of patients with ischemic left ventricular systolic dysfunction and known viable myocardium provides a survival benefit over medical therapy. Identification of viable, dysfunctional myocardium may be especially worthwhile in deciding which patients with ischemic left ventricular systolic dysfunction will benefit from revascularization procedures. Randomized, prospective trials evaluating this are currently ongoing. This review will provide an overview of the complex pathophysiology of viable, dysfunctional myocardium, and will discuss outcomes after revascularization. Of the techniques used to determine the presence of hibernating myocardium, functional methods such as stress echocardiography and cardiac magnetic resonance appear more specific, but less sensitive, than the nuclear modalities, which assess perfusion and metabolic activity. Currently, the availability of all methods is variable.

Heart Failure↗
PubMed2000

[Evaluation of hibernating myocardium in patients with heart insufficiency].

Myocardial dysfunction due to chronic hypoperfusion (so-called hibernating myocardium) is potentially reversible if the normal coronary flow is restored. Stress echocardiography (dobutamine, post-extrasystolic potentiation) may elicit contractile reserve of the hibernating myocardium and predict accurately its functional recovery after coronary revascularization. Thus, the identification of dysfunctioning but viable myocardium may be crucial to select patients with ischemic congestive heart failure who might benefit from coronary revascularization.

Cardiotonic Agents↗
PubMed2002

Myocardial hibernation: a noninvasive physician's point of view.

In a large subset of patients with coronary artery disease and left ventricular (LV) dysfunction. LV performance is reduced on the basis of regionally ischemic or hibernating myocardium rather than irreversibly infarcted myocardium. The detection of reversibly dysfunctional myocardium is clinically relevant, as regional and global LV function in such patients may improve substantially after revascularization. Noninvasive imaging methods to assess myocardial metabolic activity, membrane integrity, and inotropic reserve are ideally suited for this assessment. Among these are the unique potential of nuclear cardiology techniques to distinguish viable regions on the basis of perfusion, cell membrane integrity, and metabolic activity and the ability of dobutamine echocardiography to assess regional inotropic reserve. Contrast-enhanced magnetic resonance imaging has also emerged as important method for viability. assessment. Patients with LV dysfunction and extensive regions of hibernating myocarduim appear to have the potential not only for improved left ventricular function after revascularization, but also for improved symptoms and improved survial. This, assessing myocardial viability may provide important information regarding the selection of patients with LV dysfunction for myocardial revascularization procedures.

Coronary Artery Disease↗
PubMed2002

[Acute focal dystrophy of the myocardium with hibernating or stunned myocardium].

Opportunities of clinical, laboratory and device diagnosis of acute focal dystrophy (AFD) with hibernating or stunned myocardium are postulated. Myocardial AFD belongs to intermediate coronary syndrome and is a clinico-morpho-functional manifestation of one of the acute coronary syndromes in ischemic heart disease. Differentiation of hibernating with stunned myocardium is made after myocardial revascularization. 230 coronaroventriculographies have been made, of them 72 were urgent with balloon angioplasty and stenting.

Acute Disease↗
PubMed2002

[Hibernating and stunned myocardium. Pathogenetic mechanisms during and after myocardial ischemia].

In this paper the Authors consider the concept of stunning/hibernating myocardium, analizing the most recent articles and reviews in literature, until April 2002 (database PubMed). Dysfunctional segments with normal perfusion and normal glucose utilization are considered to be "stunned", and dysfunctional segments with reduced perfusion and preserved glucose utilization are considered to be "hibernated". Together with the two major hypothesis (generation of oxygen-derived free radicals and transient calcium overload) in developing of dysfunctional myocardium after ischaemia, recent studies have demonstrated an important role in down-regulation of beta-adrenergic receptors both in the stunned and in the hibernated segments. Moreover, the increase of negatively inotropic cytokines TNF-alpha and NOS2 has been observed in dysfunctional segments. The number of copies of mRNA has been quantified by reverse transcription-polymerase chain reaction (reverse-PCR).

Humans↗
PubMed2003

Increased glycolysis as protective adaptation of energy depleted, degenerating human hibernating myocardium.

In the current study on human hibernating myocardium (HHM), we tested the hypothesis that increased glycolysis might exert a positive effect during a supply-demand balance situation by augmentation of myocardial energy formation. In 14 patients HHM was preoperatively detected by clinical methods and validated by the recovery of contractile function three months following revascularization. During open-heart surgery, transmural biopsies were removed from the hibernating areas and analyzed using biochemical and morphologic methods. Metabolite contents were normalized for the degree of fibrosis (control: 9.8 +/- 0.5%, HHM 28.1 +/- 3.0%; p < 0.05), providing values for cardiomyocytes only. In energy depleted HHM, severe intracellular degeneration, glycogen accumulation and myocyte loss were found. Elevated lactate levels (2.22 +/- 0.26 vs. 25.38 +/- 3.53 micromol/wet wt, p < 0.001) were indicative of an increased anaerobic glycolytic flux. In conclusion the presence of abundant intracellular glycogen and an increased anaerobic glycolysis in HHM is indicative of a protective adaptation of this myocardium, which might balance energy deficit and may limit structural damage.

Adaptation, Physiological↗
PubMed1975

[Experience with artificial hibernation of patients with severe craniocerebral injuries].

The artificial hibernation (hypothermia) of patients with severe cranio-cerebral lesion is discussed. The authors' experiences have shown that re-establishment of the normothermia reduces considerably the symptoms of the neurovegetative syndrome, thus it contributes to the improvement of the prognosis and in many cases it assures the patient's survival. Artificial hibernation is an important task during the intensive therapy of patients with cranio-cerebral lesions.

Brain Injuries↗
PubMedDate not supplied

Myocardial hibernation.

Myocardial hibernation is a potentially reversible cause of resting left ventricular dysfunction in some patients with coronary artery disease. Successful revascularisation in these patients can lead to improved ventricular function and hence improved prognosis. This review discusses the pathophysiology of myocardial hibernation and the methods that are currently available to detect it.

Coronary Circulation↗
PubMed1995

[Identification of hibernating myocardium using 99m sestamibi tomoscintigraphy at rest].

The aim of this study was to assess the value of resting 99m Tc-Sestamibi scintigraphy for the detection of hibernating myocardium in zones of contractile dysfunction. Based on a series of 25 patients, 27 segments of supposedly hibernating myocardium were identified. All these segments corresponded to left ventricular wall motion abnormalities confirmed by contrast angiography and were perfused by a stenosed coronary artery: none of these zones were infarcted. Before revascularisation, comparison of the results of ventriculography and scintigraphy showed a correlation (p < 0.001) between the severity of regional contractile dysfunction appreciated by the center line method and the degree of myocardial hypofixation of 99m Tc MIBI. Three months after revascularisation, improvement of regional wall motion, assessed by control contrast angiography, was observed in 21 of the 27 segments studied (78%). Of these 21 segments, the viability of which was confirmed, 13 had a non-transmural uptake defect and 8 were normal on pre-revascularisation scintigraphy. The 6 segments without improvement at the 3 month control, had a transmural uptake defect on scintigraphy in 67% of cases. The authors concluded that when a residual uptake defect of 99m Tc sestamibi is present, viable myocardium may also be present.

Aged↗
PubMed1995

[Postischemic ("stunned") and chronic ischemic ("hibernating") cardiac muscle].

Stunning of the heart muscle is a postischaemic dysfunction observed after reperfusion. The stunned heart muscle is functional, the restoration of contractility is slow. The stunning of the heart muscle is probably due to a partial disorder of the electromechanical mechanisms caused by impaired calcium homeostasis. Substances which protect against the development of stunning are substances which eliminate oxygen radicals and calcium channel blockers which adjust the calcium homeostasis in cells. The "hibernating myocardium" is a state of contractile dysfunction during chronic hypoperfusion of the heart muscle. When the blood flow is restored, the contractility improves gradually. The second generation of calcium antagonists is effective in hibernated heart muscles due to their selective coronary artery dilating effect.

Animals↗
PubMed1994

[Thallium scintigraphy for determining myocardial vitality. Evaluation of the "stunned and hibernating myocardium"].

Myocardial uptake of 201thallium is not only a function of regional myocardial blood flow, but also reflects cellular uptake by intact cell membranes and thus can not be merely regarded a signal of perfusion but also of structural cell integrity. Especially in the setting of severely depressed left ventricular function evidence of viable but dysfunctional myocardium has impact on recovery potential and prognosis after myocardial revascularization. Hibernating myocardium, a reversible chronically ischemic state of reduced aerobic metabolism and depressed contractile function, may be identified after injection of 201thallium at rest and rest-redistribution SPECT imaging. Since 201thallium uptake in initial defect areas may occur as a function of time allowed for redistribution, even partial late uptake may be considered a reliable signal for viable, but hibernating tissue, 75% of which demonstrating contractile recovery after revascularization. Uptake of 201thallium at rest or with redistribution, thus, is indicative of myocardial viability irrespective of function. Conversely, lack of 201thallium uptake after stress and redistribution does not always indicate necrosis, since 45 to 83% of myocardium with no uptake may improve function after revascularization. These defects, however, often resolve with reinjection of 201thallium and subsequent imaging at rest. This observation led to a triphasic imaging protocol including conventional rest-redistribution imaging and a third set of images after reinjection of 1 mCi 201thallium at rest. This concept ensures uptake of 201thallium in 31 to 49% of presumably persistent defects and increases sensitivity for detection of viable tissue. In 80 to 87% of areas with reinjection 201thallium uptake function improved after revascularization compared to 0 to 8% of segments with no uptake at all. Redistribution imaging should not be omitted for logistical reasons, since important information not only on ischemia but also on viability may be lost. Useful imaging protocols for detection of both ischemia and viability comprise either a sequence of stress, redistribution and reinjection imaging or a series of stress, reinjection and 24 hour redistribution images; both protocols have similar sensitivity for detection of tissue viability. In the setting of stunned myocardium mainly after thrombolytic therapy the assessment of residual viability may be important for both additional therapeutic and prognostic reasons. 201Thallium uptake preferentially using a re-redistribution protocol may help to differentiate viable from non-viable myocardium; however 201 thallium imaging should be performed after the hyperemic phase following successful thrombolysis (> or = 24 to 48 hours after thrombolysis).(ABSTRACT TRUNCATED AT 400 WORDS)

Coronary Disease↗
PubMed1993

[Synchronized coronary vein retroperfusion for identification of myocardium with chronic ischemic disorders of wall movement ("hibernating myocardium")].

UNLABELLED: ECG-synchronized retroperfusion (SRP) via the coronary sinus has been recently demonstrated to efficiently deliver arterial blood to ischemic myocardium in an experimental setting and during PTCA. To assess the potential of SRP for identifying hibernating myocardium by improved contractile function resulting from retrograde delivery of oxygen, 10 patients (M/F = 9/1; age 56 +/- 9 years) with ischemic wall motion abnormalities, but, according to ECG-criteria, no transmural infarction in the territory of a totally occluded LAD, underwent 30 min of SRP at a flow rate of 145-250 ml/min prior to mechanical recanalization. Serial digital ventriculograms were obtained before, after 30 min of SRP and, finally, after successful PTCA at follow-up of 28 +/- 4 days. RESULTS: Wall motion analysis revealed improved global and regional contractile function in seven of 10 patients, which was maintained after successful PTCA. Continuous SRP over 30 min resulted in an improvement of global and segmental systolic function. Left ventricular ejection fraction (LVEF) increased from 53 +/- 8% to 58 +/- 5% with 30 min of SRP (p < 0.03) and significant improvement in regional function was detected in the anterobasal, apical and inferior segment of the left ventricular circumference (p < 0.05). CONCLUSION: An improved contractile response to retrograde delivery of oxygen by SRP appears to document the reversibility of myocardial hibernation. Thus, ECG-synchronized SRP via the coronary sinus has the potential to unmask viable myocardium likely to completely recover from contractile dysfunction after successful antegrade recanalization. Moreover, continuous SRP procedure over 30 min was safe and had no hazardous side-effects.

Adult↗
PubMed1997

[The hibernating myocardium--its use in clinical practice].

Hibernated myocardium is a term used to describe a state of myocardial hypocontractility which is due to chronic hypoperfusion of the heart muscle. The myocardium remains, however, viable and therefore revascularization can significantly improve the reduced mechanical function of the left ventricle. Differentiation between hibernated myocardium and a myocardium which was irreversibly damaged and replaced by scar tissue is particularly important in patients with ischemic dysfunction of the left ventricle. Information on the viability of dysfunctional areas of the myocardium helps in reflections on the indication and strategy of the revascularization operation.

Coronary Circulation↗