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Evaluation of hibernating myocardium

Evaluation of hibernating myocardium
Literature review current through: Jan 2024.
This topic last updated: Jan 27, 2023.

INTRODUCTION — It has become apparent that impaired left ventricular (LV) function in patients with coronary heart disease (CHD) is not always an irreversible process, but may be the result of stunned or hibernating myocardium:

Transient postischemic dysfunction is called "stunned" myocardium

Chronic but potentially reversible ischemic dysfunction due to a stenosed coronary artery is called "hibernating" myocardium

From 20 to more than 50 percent of patients with chronic ischemic LV dysfunction have a significant amount of viable hibernating myocardium and, therefore, the potential for clinically important improvement in LV function after revascularization (figure 1) [1-4]. (See "Treatment of ischemic cardiomyopathy".)

The approach to the detection of hibernating myocardium will be reviewed here (table 1). The pathophysiology of and clinical syndromes associated with hibernation are discussed separately. (See "Pathophysiology of stunned or hibernating myocardium" and "Clinical syndromes of stunned or hibernating myocardium" and "Treatment of ischemic cardiomyopathy".)

DEFINITION — Ischemic cardiomyopathy is defined as myocardial dysfunction (with reduced LV systolic function) with resultant heart failure (HF) symptoms that are a direct result of coronary artery disease (CAD) [5]. Patients with ischemic cardiomyopathy may have scarring from one or more prior myocardial infarctions (MI), viable but hibernating myocardium resulting from chronic myocardial ischemia, or a combination of the two.

Hibernating myocardium is defined as a region of depressed myocardial contractility at rest due to persistently impaired coronary blood flow [6-9]. It may be present in chronic stable or unstable angina, acute MI, HF with or without severe LV systolic dysfunction, and an anomalous coronary artery. (See "Clinical syndromes of stunned or hibernating myocardium".)

Since the ischemic myocardium remains viable, the LV dysfunction can be partially or completely restored to normal by improving blood flow or by reducing oxygen demand. Both the reduction in resting coronary blood flow in hibernating segments and the improvement following percutaneous coronary intervention have been directly demonstrated by cardiovascular magnetic resonance (CMR) imaging [10].

Positron emission tomography (PET) has shown that regions with abnormal wall motion may still be metabolically active; these are the regions that can improve after revascularization [11]. In an autopsy series, 52 percent of myocardial segments that were hypokinetic had normal myocardium when examined histologically, compared with only 7 percent of akinetic or dyskinetic segments [12].

Hibernating myocardium has been thought to be different from stunned myocardium in which myocardial dysfunction persists for a variable period after transient myocardial ischemia. However, several observations suggest that the difference between hibernation and stunning may be one of degree: in hibernation, resting blood flow is low, whereas in stunning, resting flow is normal but maximal blood flow is reduced, leading to the hypothesis that hibernation may result in some cases from repetitive stunning, secondary to repeated episodes of ischemia, or from chronic stunning (figure 2) [13]. Hibernation has more damage than stunned myocardium; recovery may thus also take longer after revascularization [14]. (See "Pathophysiology of stunned or hibernating myocardium", section on 'Relation between hibernation and stunning'.)

DIAGNOSIS — The presence of ischemic cardiomyopathy is an independent predictor of mortality; in addition, the extent of CAD as determined by angiography contributes more prognostic information than the clinical diagnosis of an ischemic cardiomyopathy alone [15]. The diagnostic approach to ischemic cardiomyopathy consists of two steps: the detection of clinically significant CAD and the detection of potentially reversible hibernating (ie, viable) myocardium [16].

Detection of coronary disease — Because of the frequency of ischemic heart disease as a cause of HF and the observation that it also accounts for some cases of initially unexplained HF [17], evaluation for CAD is usually part of the evaluation of patients with newly diagnosed HF. This issue is discussed in detail separately. (See "Determining the etiology and severity of heart failure or cardiomyopathy", section on 'Detection of coronary artery disease'.)

Summarized briefly, chest pain alone is not sufficient to make the diagnosis, since up to one-third of patients with nonischemic cardiomyopathy have chest pain that may resemble angina or be atypical. The evaluation for CAD typically consists of exercise stress testing, often with some form of myocardial imaging, which can detect ischemia and provides prognostic information by assessment of exercise capacity, and/or coronary arteriography.

The 2013 American College of Cardiology Foundation/American Heart Association guidelines on HF recommended that cardiac catheterization with coronary angiography is reasonable in patients with new onset HF of uncertain cause who would be eligible for revascularization [18]. In addition, noninvasive imaging to detect myocardial ischemia and viability was considered reasonable in patients with new onset HF who are known to have CAD but no angina, again assuming that the patient is eligible for revascularization.

It is essential that the angiographic findings be considered in the context of the patient's history and other data. As mentioned above, the presence of asymptomatic angiographic CAD in patients with dilated cardiomyopathy does not prove causality unless there is evidence of prior infarction or hibernating myocardium [19,20]. (See 'Definition' above.)

Although scintigraphic and echocardiographic techniques have traditionally been the noninvasive ischemia tests of choice, noninvasive coronary arteriography, including the use of multidetector row or electron beam computed tomography (CT) and CMR are also being evaluated. The options include CT or CMR angiography and detection of coronary artery calcification by CT or late gadolinium enhancement by CMR. (See "Cardiac imaging with computed tomography and magnetic resonance in the adult" and "Coronary artery calcium scoring (CAC): Overview and clinical utilization" and "Clinical utility of cardiovascular magnetic resonance imaging", section on 'Cardiomyopathy'.)

Detection of viable (hibernating) myocardium — Unless the patient is not a candidate for revascularization of any kind, noninvasive imaging to detect myocardial ischemia and viability is reasonable in patients with known CAD and no angina [18]. The guidelines also noted that, although the efficacy is less well established, noninvasive imaging may be considered to define the likelihood of CAD in other patients with HF and LV dysfunction. The efficacy of the methods used to detect regions of viable myocardium in which function might improve after revascularization is discussed in detail below. (See 'Efficacy of imaging tests' below.)

EFFICACY OF IMAGING TESTS — Several tests can assist in the evaluation of myocardial viability and contractile reserve and identification of patients in whom there is the potential for recovery of LV function with revascularization. These tests include radionuclide myocardial perfusion imaging (rMPI), dobutamine echocardiography, positron emission tomography (PET) scanning, and an increase in segmental contraction with pharmacologic or nonpharmacologic stimulation (postextrasystolic potentiation) during left ventriculography.

Computed tomography (CT) and CMR also can detect hibernating myocardium, but their roles have not been systematically evaluated and comparisons with rMPI are limited. (See "Clinical utility of cardiovascular magnetic resonance imaging".)

Radionuclide myocardial perfusion imaging — Noninvasive testing with thallium or technetium sestamibi rMPI or PET is often performed to identify the presence of dysfunctional segments that are viable. The major rMPI techniques are thallium stress-redistribution-reinjection single photon emission computed tomography (SPECT), thallium rest-redistribution SPECT, and technetium-sestamibi SPECT. PET with the use of tracers to detect myocardial metabolism is an alternative method. The role of myocardial imaging in the detection of myocardial viability is discussed in detail elsewhere and the relative efficacy of the different tests is reviewed below. (See 'Pooled analysis of rMPI and DE studies' below and "Assessment of myocardial viability by nuclear imaging in coronary heart disease".)

Echocardiography

End-diastolic wall thickness — Since myocardial necrosis is associated with thinning of the myocardial wall, preserved end-diastolic wall thickness may provide a simple method for determining myocardial viability. This was investigated in a study that compared the end-diastolic wall thickness, obtained on a resting two-dimensional echocardiography, with the results of dobutamine stress echocardiography (DSE) and rest-distribution thallium-201 scan [21]. An end-diastolic wall thickness ≤0.6 cm excluded the potential for functional recovery with a sensitivity and specificity of 94 and 48 percent, respectively, which was similar to the results with thallium scanning. Combination of the end-diastolic wall thickness with the results of DSE had a sensitivity and specificity of 88 and 77 percent.

However, the presence of a thinned wall does not exclude the possibility of myocardial viability. (See 'Magnetic resonance imaging' below.)

Dobutamine echocardiography — DSE is an important noninvasive clinical tool for the detection of hibernating myocardium (figure 3 and figure 4) [22,23]. (See "Dobutamine stress echocardiography in the evaluation of hibernating myocardium".)

Dobutamine echocardiography examines the "inotropic reserve" of dysfunctional but viable myocardium.

Viable myocardium shows improved regional contractile function (inotropic reserve), as assessed by simultaneous transthoracic echocardiography, in response to these agents. The prevalence of contractile reserve in patients with CHD and LV dysfunction is independent of the angiographic extent and severity of coronary disease [24] and the improvement in contractility in hypoperfused viable myocardium does not require an increase in regional myocardial perfusion [25] although dobutamine may also increase myocardial blood flow [26].

A contractile response to dobutamine appears to require at least 50 percent viable myocytes in a given segment and correlates inversely with the extent of interstitial fibrosis on myocardial biopsy [27]. In comparison, rMPI can identify segments with fewer viable myocytes. In one series, for example, dobutamine echocardiography and thallium imaging showed equivalent sensitivity among segments with more than 75 percent viable myocytes (78 versus 87 percent) but dobutamine was much less sensitive among segments with 25 to 50 percent viable myocytes (15 versus 82 percent) [28].

Atropine may be given with dobutamine to enhance the diagnostic value of the technique by increasing myocardial blood flow; in one series, atropine was necessary in 36 percent of patients to evaluate myocardial viability [29]. In addition to atropine therapy, other methods to improve the predictive value are to combine dobutamine echocardiography with myocardial contrast echocardiography (MCE) [30], Doppler assessment of mitral inflow pattern [31], and strain rate imaging (SRI) with tissue Doppler [32,33].

Another possible approach is nitroglycerin given with dobutamine. Potential efficacy was illustrated in a report of 32 patients in whom 309 of 512 myocardial segments were akinetic or dyskinetic. In terms of improved contractility after revascularization, nitroglycerin-dobutamine echocardiography had a lower sensitivity than rest-redistribution thallium and MCE (63 versus 95 and 87 percent, respectively), but was the most specific (83 versus 37 and 48 percent) [34]. Nitroglycerin alone increased regional thickening in 20 percent of viable akinetic segments, suggesting that it may be a useful addition to dobutamine stimulation.

TDE/strain rate imaging — A refinement in the assessment of regional LV function has been SRI from tissue Doppler echocardiography (TDE). SRI involves mathematical subtraction of the whole heart or translational motion from regional thickening velocity using a transmural data set from color-coded TDE. The results are less subjective than with wall motion scoring with traditional dobutamine echocardiography. (See "Tissue Doppler echocardiography", section on 'Strain and strain rate imaging'.)

When used with low dose dobutamine, TDE is a useful method for assessing the degree of myocardial viability [32,33]. The possible incremental value SRI to wall motion scoring was illustrated in review of 55 stable patients with a prior myocardial infarction (MI) and mean LVEF of 36 percent [33]. The following findings were noted:

Global functional recovery was seen after CABG in 21 patients (mean LVEF 35 percent at baseline to 47 percent at follow-up). There remaining patients had no increase in LVEF after CABG (38 to 39 percent).

The combination of SRI and wall motion scoring significantly increased the sensitivity for predicting recovery of function after CABG compared with wall motion scoring alone (82 versus 73 percent).

Mitral inflow pattern — Limited data indicate that the early diastolic deceleration time may correlate with the extent of myocardial viability. The value of measuring the early diastolic deceleration time (DT) on Doppler was assessed in 40 patients with ischemic cardiomyopathy who also underwent dobutamine echocardiography and rMPI [31]. (See "Echocardiographic evaluation of left ventricular diastolic function in adults".)

The following findings were noted:

There was a linear relationship between DT and both the number of viable segments on dobutamine echocardiography and the increase in LVEF after CABG surgery.

A DT >150 msec predicted an increase in LVEF after CABG of ≥5 percent (mean 29 percent at baseline to 40 percent after surgery) with a sensitivity and specificity of about 80 percent. In comparison, a DT ≤150 msec predicted an increase in LVEF <5 percent (mean 27 percent before and after CABG).

At one year, the rate of death or heart transplantation was much lower in the patients with a DT >150 msec (5 versus 37 percent).

Pooled analysis of rMPI and DE studies — The relative predictive value of the different forms of rMPI and of dobutamine echocardiography for detecting hibernating myocardium was evaluated in an analysis from 52 published studies that utilized thallium stress-redistribution-reinjection SPECT, thallium rest-redistribution SPECT, fludeoxyglucose (FDG)-PET scanning, technetium-sestamibi SPECT, or low dose dobutamine echocardiography [35,36]. The following findings were noted (figure 5):

For each technique, the negative predictive value was higher than the positive predictive value. The highest negative predictive values were seen with FDG-PET, reinjection thallium SPECT, and dobutamine echocardiography, while lower values were noted for rest-redistribution thallium SPECT and technetium-sestamibi SPECT.

The highest positive predictive value was seen with dobutamine echocardiography, with intermediate values for FDG-PET, rest-redistribution thallium SPECT, and technetium-sestamibi SPECT, and the lowest value for reinjection thallium SPECT.

Most of these studies did not compare imaging techniques in the same patients. In a subset of studies in which two techniques were compared to detect viability, the pooled results showed that dobutamine echocardiography had significantly higher positive predictive value than nuclear imaging (84 versus 75 percent) and a significantly lower negative predictive value (69 versus 80 percent).

Data were also available on the relationship between the change in LVEF after revascularization and the presence or absence of hibernating myocardium on imaging [35,36]. There was a mean increase in LVEF of about 8 percent after revascularization when hibernating myocardium was present (37 versus 45 percent) compared with no change in the absence of hibernation (36 versus 37 percent). The pooled results suggested that dobutamine echocardiography had a slightly higher positive and negative predictive values than nuclear imaging (77 versus 70 percent and 85 versus 78 percent, respectively) [35]. (See "Treatment of ischemic cardiomyopathy", section on 'Additional imaging'.)

Magnetic resonance imaging

Wall thickness — As with echocardiography, CMR evidence of reduced end-diastolic wall thickness (thinned wall) has been proposed as an indicator of lack of viability. In a study of 35 patients with prior MI and regional akinesia or dyskinesia, resting end-diastolic wall thickness and low dose dobutamine-induced systolic wall thickening were assessed by CMR [37]. Dobutamine-induced wall thickening was a better predictor of residual metabolic activity on PET (sensitivity 81 percent specificity 95 percent) than end-diastolic wall thickness (sensitivity 72 percent and specificity 89 percent). If at least one CMR parameter was used to identify viability, the sensitivity was 88 percent and specificity was 87 percent.

However, a region of thinned myocardium may be viable with potential for structural and functional recovery following revascularization [38]. Also, normal ventricles have significant regional variation in viable myocardial thickness. Therefore, identification of the extent of scar (eg, through contrast enhancement) along with the extent of viable tissue may provide a more accurate means of evaluating viability.

Contrast-enhanced imaging — Contrast-enhanced CMR imaging can be used to identify the extent of myocardial viability. Regions of myocardium exhibiting late (or delayed) gadolinium enhancement (LGE) coincide with regions of myocardial necrosis and irreversible injury; regions that fail to hyperenhance are viable. In addition, quantitative perfusion assessment can document the reduction in resting coronary blood flow in hibernating segments [10]. (See "Clinical utility of cardiovascular magnetic resonance imaging", section on 'Myocardial viability'.)

In one series of 24 patients with stable CAD and LV dysfunction, delayed (3 to 15 minute) enhancement of contrast-enhanced CMR images were associated with nonviability as established with rest-distribution thallium imaging and dobutamine echocardiography [39]. The absence of enhancement correlated with radionuclide and echocardiographic viability, regardless of the status of resting contractile function.

The degree of enhancement with contrast-enhanced CMR can predict recovery of LV function after revascularization [40,41]. This was illustrated in a study of 50 patients with CAD who had LV dysfunction prior to surgical or percutaneous revascularization; 33 percent of myocardial segments in 80 percent of patients had late myocardial enhancement; 38 percent of segments had abnormal contractility [40]. After revascularization, more dysfunctional segments without enhancement improved (78 versus 17 percent with enhancement of >75 percent of the tissue).

The likelihood of improvement in regional contractility after revascularization decreased progressively as the transmural extent of hyperenhancement increased. The percentage of the LV that was dysfunctional and not enhanced was significantly related to the degree of improvement in LVEF.

A similar relationship was noted in another series [41]. An additional finding was that, among the nonenhancing or minimal enhancing segments that did not improve after revascularization, 36 percent showed new late enhancement on the early postoperative CMR scan.

Magnetic resonance myocardial tagging is another CMR method that quantifies local myocardial segment shortening throughout the LV myocardium at sites across the LV wall thickness. When combined with low dose dobutamine, this method can quantify the amount of myocardial viability, based upon myocardial shortening and thickening, after an acute MI and may provide prognostic information. (See "Clinical utility of cardiovascular magnetic resonance imaging", section on 'Myocardial viability'.)

Kidney disease — Gadolinium administration during CMR imaging to patients with moderate to severe kidney disease (particularly dialysis patients) has been associated with the often severe syndrome of nephrogenic systemic fibrosis. It is recommended that gadolinium-based imaging be avoided in such patients. This issue, including the definition of patients at risk, is discussed separately. (See "Nephrogenic systemic fibrosis/nephrogenic fibrosing dermopathy in advanced kidney disease".)

Newer methods — Several newer methods may be useful in the evaluation of hibernating myocardium.

Electroanatomic mapping — Electroanatomic mapping, which uses low-intensity magnetic field energy to determine the location of sensor-tipped catheter electrodes in the LV, has been widely applied for mapping of arrhythmias. (See "Invasive diagnostic cardiac electrophysiology studies", section on 'Mapping and ablation'.)

By simultaneously measuring the electrical data (amplitude of endocardial electrical signals) and mechanical data (regional wall motion reflecting average local shortening) from the myocardium, which correlate inversely with the extent of myocardial ischemia, this technique may also have a role in distinguishing between infarcted and ischemic, but still viable, myocardium (image 1A-C) [42-46].

The sensitivity and specificity for viable myocardium compared with other imaging studies has ranged from 70 to 80 percent [42,44,45]. In one report of 20 patients in whom testing for viability was directly compared with the results of revascularization, the diagnostic performance of electroanatomic mapping was not as good as that of rMPI with PET or SPECT [46].

Myocardial contrast echocardiography — MCE utilizes intravenous infusion of microbubbles, which have a distinct ultrasonic density from blood or tissue and which can traverse the microvasculature, permitting visualization of myocardial perfusion. This technique compares favorably with other modalities in the detection of hibernating myocardium, although contrast agents have not yet been US Food and Drug Administration (FDA) approved for this purpose.

The potential value of MCE was illustrated in a study in which 20 patients with coronary disease and ventricular dysfunction underwent MCE, dobutamine echocardiography, and rest-redistribution thallium scintigraphy prior to coronary artery bypass grafting (CABG) [47]. Echocardiography was repeated three to four months after surgery. The sensitivity of MCE in detecting segments with recovery of function after surgery was comparable to that of dobutamine echocardiography or thallium scintigraphy (90, 80, and 92 percent, respectively), and the specificity was significantly greater (63, 54, and 45 percent, respectively).

A second report compared these three approaches in 32 patients in whom 309 of 512 myocardial segments were akinetic or dyskinetic [34]. In terms of predicting functional recovery after revascularization, MCE had the intermediate sensitivity (87 versus 95 and 63 percent with rest-redistribution thallium and nitroglycerin-dobutamine echocardiography) and specificity (48 versus 37 and 83 percent with rest-redistribution thallium and nitroglycerin-dobutamine echocardiography).

Ventriculography — Ventriculography is the oldest imaging technique and is rarely used clinically today.

Assessment of regional wall motion by ventriculography, and its improvement with nitroglycerin or positive inotropic stimulation has at least two limitations:

Due to the subjective nature of this evaluation, it may not be accurate [48]

The technique used to superimpose the end-systolic silhouette on the end-diastolic silhouette may influence the assessment of regional wall motion function [49]

Thus, some assessments that regional wall motion function has improved or deteriorated could be erroneous. The finding of improved wall motion function would be accepted more confidently if it were reflected in improved global LV systolic function or LV ejection fraction (LVEF). However, for LVEF to improve, it appears that wall motion function must improve in at least two to three myocardial regions.

Use of nitroglycerin — Since the hibernating myocardium is a result of reduced myocardial blood flow, one way to demonstrate its presence would be to show an improvement in function after reducing the myocardial oxygen requirement with nitrates [50,51]. Nitroglycerin and/ or isosorbide dinitrate with contrast medium, two dimensional echocardiography, or radionuclide ventriculography can be utilized for this purpose. The sensitivity, specificity, and predictive accuracy of nitroglycerin contrast ventriculography for the detection of hibernating myocardium is only 76 percent, 65 percent, and 70 percent, respectively. However, if LV wall segments improve with nitroglycerin preoperatively, there is an 85 percent chance of their improving with coronary artery bypass grafting (CABG) [52].

Inotropic stimulation/postextrasystolic potentiation — With inotropic stimulation caused by low-dose dobutamine or postextrasystolic potentiation, the ventriculogram may appear to show an improvement in akinetic wall motion segments by increasing the force of contraction of the normal myocardium leading to a tethering effect on the akinetic segment.

Despite this limitation, inotropic stimuli may demonstrate reversible abnormal wall motion, a response that appears to be similar to that seen with nitroglycerin [51]. As an example, one study found that low-dose dobutamine left ventriculography is a useful technique for identifying myocardial viability, especially in patients with a suboptimal dobutamine echocardiographic study [53]. A positive response to inotropic stimuli predicts a better short-and long-term survival with CABG [54-56].

In patients with global LV dysfunction due to an ischemic cardiomyopathy, improvement in global LV function or LVEF with dobutamine may be of greater importance than reversibility of a regional wall motion abnormality. In one study of 56 patients with an ischemic cardiomyopathy and multivessel coronary disease, a dobutamine radionuclide ventriculogram, which provides an objective quantification of LV function, was performed to assess viability; a 10 percent increase in global LVEF with low dose dobutamine had a sensitivity, specificity, and positive and negative predictive values of 67, 93, 91, and 72 percent, respectively, for improvement in LV function after CABG [57].

Concern about the augmentation of myocardial oxygen demand with dobutamine infusion has led to the evaluation of inamrinone (formerly known as amrinone), an inotropic agent which does not significantly increase oxygen demand because it also induces coronary vasodilation. One study evaluated 44 patients with coronary disease and an LVEF below 40 percent; inamrinone was infused at a dose of 1 mg/kg body weight and LVEF measured with radionuclide ventriculography [58]. An increase in LVEF of ≥10 percent with inamrinone predicted the same increase in LVEF after CABG, while those with a lesser change with inamrinone had little, if any, improvement after CABG [58].

Increased inotropy can also be observed on ventriculography or echocardiography by measuring the change in LVEF following an induced or spontaneous premature beat (ie, the degree of postextrasystolic potentiation) [59].

RECOMMENDED APPROACH — The major imaging tests used to detect hibernating myocardium include thallium stress-redistribution-reinjection, thallium rest-redistribution, positron emission tomography (PET) scanning, technetium sestamibi imaging, and low dose dobutamine echocardiography. All of these tests are highly sensitive and can predict the benefit from revascularization, although there are some differences (figure 5) [1,35,36,60]. (See 'Pooled analysis of rMPI and DE studies' above.)

We agree with the following conclusions from a Study Group of the European Society of Cardiology [36]:

Assessment for hibernation is most relevant in patients with dyspnea rather than angina.

Radionuclide myocardial perfusion imaging (rMPI) and dobutamine echocardiography have similar test performance for the detection of viable myocardium. Thus, the choice may depend upon availability, local expertise, and whether a more sensitive (rMPI) or a more specific technique (dobutamine echocardiography) is required for predicting recovery of LV function.

PET scanning or CMR imaging is usually performed if clarification is required after echocardiography and/or rMPI. However, if readily available, PET scanning is an alternative initial test and CMR is an acceptable alternative to echocardiography when assessment of LV function at rest and during stress is also desired.

The American College of Cardiography/American Heart Association guidelines on chronic HF reached the following conclusions on noninvasive imaging, unless the patient is not eligible for revascularization of any kind [18]:

Noninvasive imaging to detect myocardial ischemia and viability is reasonable in patients with known CAD and no angina.

Noninvasive imaging may be considered (evidence less well established) to define the likelihood of CAD in patients with HF and LV dysfunction.

TREATMENT — The detection of viable myocardium is of importance because the restoration of blood flow with revascularization can reverse depressed LV contractility, improve LV function, and reduce long-term mortality, although the latter has not been proven. These issues are discussed in detail separately. (See "Treatment of ischemic cardiomyopathy".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Heart failure in adults" and "Society guideline links: Chronic coronary syndrome" and "Society guideline links: Multimodality cardiovascular imaging appropriate use criteria".)

SUMMARY AND RECOMMENDATIONS

Hibernating myocardium, defined as a region of depressed myocardial contractility at rest due to persistently impaired coronary blood flow, can occur in a variety of clinical scenarios (eg, chronic stable or unstable angina, acute myocardial infarction [MI], heart failure). Since the ischemic myocardium remains viable, the left ventricular (LV) dysfunction can be partially or completely restored to normal by improving blood flow or by reducing oxygen demand. (See 'Definition' above.)

Several tests, including radionuclide myocardial perfusion imaging (rMPI), dobutamine echocardiography, positron emission tomography (PET) scanning, and cardiovascular magnetic resonance (CMR) imaging, can assist in the evaluation of myocardial viability and contractile reserve and identification of patients in whom there is the potential for recovery of LV function with revascularization. (See 'Efficacy of imaging tests' above.)

Our recommended approach to the evaluation of hibernating myocardium is to begin with either rMPI or dobutamine echocardiography depending upon availability and local expertise. PET scanning or CMR imaging are acceptable alternatives which may have greater sensitivity but are more challenging to perform and not as widely available. (See 'Recommended approach' above.)

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Topic 1474 Version 15.0

References

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