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 Table of Contents  
CONTEMPORARY TOPIC
Year : 2017  |  Volume : 1  |  Issue : 1  |  Page : 32-38

Assessment of myocardial viability by echocardiography


Department of Cardiology, Jupiter Hospital, Thane, Maharashtra, India

Date of Web Publication7-Apr-2017

Correspondence Address:
Nitin J Burkule
Jupiter Hospital, Thane, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jiae.JIAE_21_17

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  Abstract 

Clinical application of myocardial viability testing to improve patient outcome is still a concept in evaluation. The various echocardiographic, nuclear, and magnetic resonance imaging techniques of assessment of myocardial viability evaluate different aspects of ischemic pathophysiology and have certain distinct advantages and limitations. A clinical algorithm combining “anatomic” and “flow/function” imaging gives more specific result of myocardial viability. Different modalities of echocardiography form the basic and cost-effective tools to assess the anatomic and functional aspect of viability.

Keywords: Dobutamine stress echocardiography, myocardial contrast echocardiography, myocardial viability, strain and strain rate


How to cite this article:
Burkule NJ. Assessment of myocardial viability by echocardiography. J Indian Acad Echocardiogr Cardiovasc Imaging 2017;1:32-8

How to cite this URL:
Burkule NJ. Assessment of myocardial viability by echocardiography. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2017 [cited 2017 Jun 24];1:32-8. Available from: http://www.jiaecho.org/text.asp?2017/1/1/32/204066


  Introduction Top


Patients with coronary artery disease and depressed left ventricular (LV) function often present with heart failure symptoms without exertional angina. In this group of patients, assessment of myocardial viability is still a popular but controversial concept to decide “for” or “against” surgical revascularization. Nonrandomized, retrospective, single-center studies show that revascularization of viable myocardium results in recovery of regional wall motion, global LV ejection fraction (LVEF), LV reverse remodeling,[1] reduce cardiac events,[2],[3] and improved survival.[4] This concept was challenged later by more systematic, prospective studies such as surgical treatment for ischemic heart (STICH)[5] and STICH extension study.

The low-dose dobutamine stress echocardiography (LD-DSE) is the most practical and low-cost test for detecting myocardial viability in large number of patients.


  Pathophysiology of Myocardial Ischemia and Myocardial Dysfunction Top


A myocardial segment may become akinetic due to transient coronary occlusion followed by reperfusion (myocardial stunning) or due to chronically reduced resting coronary blood flow with many structural changes in myocardium and interstitium (myocardial hibernation).[6] The akinetic myocardial segment is defined as “viable” if it regains contractility after restoration of adequate coronary blood flow.

The subendocardial layer is the major contributor of regional myocardial systolic thickening and is also most susceptible to ischemic injury. In ST-elevation myocardial infarction (STEMI), the wave front of myocardial necrosis extends from endocardium to epicardium, to a variably extent, depending upon the rapidity of reperfusion. Therefore, in the late recovery of STEMI, more the transmural (TM) extent of myocardial necrosis less is the myocardial segmental thickness and less is the recovery of wall motion and global LV systolic function.[6]

In stable epicardial coronary artery stenosis, TM myocardial blood flow (TM-MBF) may be near normal or mildly reduced at rest, but the coronary flow reserve (CFR) is significantly reduced or absent. In the perfusion territory of severe coronary artery stenosis, the subendocardial layer MBF (SE-MBF) is significantly reduced even at rest.[7] A physical activity or tachycardia provokes a significant subendocardial ischemia. The postischemic hyperemia is maldistributed to mid- and epi-cardial layer, and the SE-MBF remains severely reduced for a long period of time.[6] Approximately 25% reduction in TM-MBF results in a 50% reduction in SE-MBF. Since subendocardial layer contributes to segmental thickening, up to 50%–75% reduction of SE-MBF results in segmental akinesia. In a setting of critical coronary stenosis, this demand-supply mismatch, with every physical activity or tachycardia, causes repetitive stunning and persistent akinesia.

In ischemic dilated cardiomyopathy, multiple factors lead to myocardial remodeling in both “ischemic” and “nonischemic” LV territories. These factors include increased wall stress due to dilated LV, increased exposure to systemic neurohumoral activation and the ultrastructural adaptation of myocytes, and interstitial tissue to chronically reduced capillary blood flow. In chronically ischemic territory, the microvasculature shows sparse capillary network and reduced resting and hyperemic capillary blood volume.[8] The myocytes shut down energy-intensive cellular processes such as actin-myosin coupling and decoupling, mitochondrial adenosine triphosphate (ATP) generation, and activity of sarcoplasmic reticulum ionic channels. The sarcomeres, myofilaments, and sarcoplasmic reticulum degenerate, and the space is filled by glycogen. The cytoskeletal proteins and mitochondria undergo ultrastructural changes. The interstitial matrix increase in volume due to laying down of large amounts of Type I and III collagen and fibronectin. In both ischemic and nonischemic remote territories, these adaptive pathological changes are seen to a variable extent, leading to global LV dysfunction.[9],[10]

In chronic ischemic LV dysfunction, regional akinesia or hypokinesia is a result of a spectrum of pathologies such as variable extent of TM scarring, remodeled myocardium, reduced myocardial capillary volume, and interstitial fibrosis. Segments with less fibrosis and less myocardial remodeling are more likely to improve contractility on LD-DSE or after revascularization. Similarly, the time to recovery of hibernating myocardium, after revascularization, depends on the baseline severity of myocardial ultrastructural changes.[6]


  Multimodality Imaging for Myocardial Viability Top


Different anatomical or functional characteristics of the ischemic and dysfunctional myocardium are studied by different imaging modalities to predict the functional recovery after revascularization. A combination of “anatomic imaging” and “flow–function imaging” is required to improve specificity of detecting myocardial viability. The “anatomic imaging” consists of wall thickness on echo, gadolinium scar on magnetic resonance imaging (MRI), and rest-redistribution or metabolic imaging by nuclear tracer. The “flow–function imaging” involves contractile reserve on LD-DSE or dobutamine stress MRI, stress sestamibi perfusion, and MBF reserve on nuclear imaging.


  Low -Dose Dobutamine Stress Echocardiography Top


Administering LD dobutamine 2.5–10 mcg/kg/min leads to mild systemic and coronary vasodilatation causing reduced afterload and increase in myocardial perfusion and myocardial blood volume. It has mild inotropic effect mediated through beta-receptors without any significant chronotropic effect. Therefore, in an akinetic, ischemic segment wall motion and systolic thickening may improve without steep rise in oxygen demand. The positive LD-DSE response depends on the TM myocytes mass, presence of intact contractile apparatus, and baseline residual coronary vasodilatory reserve. The dobutamine-induced contractile response is highly specific predictor of viability.[6] However, despite having sufficient viable myocytes, negative LD-DSE response may occur due to virtually absent baseline coronary vasodilatory reserve, ischemia provoked by dobutamine-induced tachycardia, and presence of complete loss of subendocardial layer due to subendocardial infarction. The positive dobutamine stress echo result is useful to confidently “rule in” viability, but the negative dobutamine stress echo result is not certain to “rule out” viability.


  Myocardial Contrast Echocardiography Top


The ultrasound contrast is made of inert gas bubbles with lipid shell. Currently, it is the only true intravascular tracer available in imaging field. It does not cross capillary endothelial barrier to enter the interstitial space. The viable myocardium has sufficient myocardial capillary blood volume to sustain the metabolism of the surviving myocytes.[8] The myocardial contrast perfusion is visualized by electrocardiogram (ECG) triggered, intermittent imaging sequences, using low ultrasound power to prevent destruction of contrast bubbles. The akinetic segment showing good TM perfusion on gray scale imaging indicates intact capillary network, good capillary blood volume, and hence indirect evidence of good viability. When the wall thickness is well preserved, the myocardial contrast echocardiography (MCE) can be evaluated with certainty. In STEMI patients, who have undergone primary percutaneous intervention (PPCI), the wall thickness is preserved due to reperfusion edema. Hence, MCE is most useful bedside test in this patient population to predict recovery of infarct territory post-PPCI. MCE does not test functional status of the myocytes similar to nuclear perfusion imaging studies. It has good sensitivity but modest specificity for detecting viability as discussed later. It can be a convenient and cost-effective tool when combined with LD-DSE.


  Nuclear Perfusion And Metabolic Imaging Top


The thallium-201 or technetium-99m tracers are transported across the cell membrane via sodium-potassium ATP system just like potassiumions, through the sodium-potassium ATP system. The tracers enter the myocytes only if the cell membrane and mitochondria are intact and have active ion exchange channels. The backscatter from these tracers, in ischemic myocardium, on single-photon emission computed tomography (SPECT) is compared with that from normal myocardium, and an estimate of viable myocardium is achieved. Although the cell membrane may be intact, the contractile apparatus may be nonfunctional or degraded in chronically ischemic myocytes. Less than 50% of thallium uptake on SPECT imaging indicates a small probability of viability.

The 18 F-2-fluoro-2-deoxyglucose (FDG) tracer uptake is restricted to the myocytes which have metabolically active mitochondria. Myocytes with enhanced glucose metabolism through Krebs cycle are deemed viable. The backscatter signals are picked up by positron emission tomography (PET) (FDG-PET). The glucose analog FDG shows increased uptake in hypoperfused but viable myocardium. This is termed as metabolism-perfusion mismatch. Among all the modalities, FDG-PET is the most sensitive test for viability, however, with modest specificity.


  Late Gadolinium Enhancement On Magnetic Resonance Imaging Top


The infarcted myocardium has increased volume of extravascular space due to degraded myocytes and capillary network. After intravenous (IV) injection, the gadolinium tracer enters the expanded extravascular space and gets retained there due to delayed washout. The infarcted territory appears white, on inversion recovery images, acquired 10–20 min after gadolinium administration. The cardiac MRI (CMRI), with its superb spatial resolution, can exactly delineate the TM extent of the infarct (late gadolinium enhancement [LGE]) from endocardium to epicardium. More the extent of TM fibrosis less are the chances of functional recovery. More than 50% LGE on CMR indicates a small probability of contractile recovery after revascularization. The LGE-MRI can be combined with LDD-MRI to add functional information to the anatomical scar imaging.[11] The LGE-MRI and LDD-MRI combine anatomical and functional imaging and achieve optimal sensitivity (lower than FDG-PET) and optimal specificity (lower to LD-DSE).


  Step-By-Step Approach to Myocardial Viability Assessment by Low-Dose Dobutamine Stress Echocardiography Top


Patient should be fasting for 2–3 h. Chest shaving is required for flawless ECG signals. It is advisable to secure left arm IV access if patient is imaged in the left lateral decubitus position. The antianginal drugs and beta-blockers can be stopped for 24 h if deemed safe. The layout of pharmacological stress echo laboratory is shown in [Figure 1]. The patient is monitored by the 12-lead ECG cable of the stress test monitor and by 3-lead ECG cable of the echo machine. The resting images of 4 chamber (4 CH), 2 CH, apical long axis, parasternal short axis at base, and apex are recorded with or without LV contrast opacification (LVO). One may record tissue Doppler velocity-encoded images (tissue velocity imaging [TVI]) for off-line analysis postprocedure.
Figure 1: Layout of dobutamine stress echo laboratory

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Dobutamine is an inexpensive drug with good safety profile. IV dobutamine is administered as a continuous infusion, by syringe pump, staring at a dose of 2.5 mcg/kg/min. The dose is increased every 3–5 min to 5, 7.5, and 10 mcg/kg/min for viability testing. The same set of images is recorded at the end of each step. Most of the viability response occurs between 5 and 10 mcg/kg/min dose range. It is better to avoid tachycardia and provocation of ischemia. The higher dosages of dobutamine 20, 30, and 40 mcg/kg/min are used to provoke biphasic response or reversible ischemia only if clinically indicated. Atropine boluses of 0.3–0.6 mg are rarely required in this patient population to achieve target heart rate. Since these patients have critical coronary disease and LV dysfunction, one should not routinely use higher dosages of dobutamine. One should carefully monitor the patient during and ½ h postprocedure if higher dosages of dobutamine are used. IV metoprolol (2–10 mg) is administered at the end of the test to rapidly reverse dobutamine-induced tachycardia or arrhythmia.

As recommended by the American Society of the Echocardiography,[12] the 16-segment model (not including apical cap) for LV myocardial segmentation is used for wall motion analysis. Wall motion of myocardial segments at rest and at every stage of dobutamine is analyzed “one segment” at a time by qualitatively noting the extent of “endocardial excursion” and “wall thickening.”

Dobutamine increases cardiac contractility at LD (2.5–10 μg/kg/min) without significant increase in myocardial oxygen demand. At higher dose, there is a progressive increase in heart rate and myocardial oxygen demand. The hibernating myocardial segment will improve at low dose but worsens again at peak dose (biphasic response). The nonischemic, stunned myocardial segments as well as the tethered or remodeled segments will demonstrate a sustained improvement in contractility at low and peak dose. When there is no change in contractility at low or high dose, it suggests the absence of myocardial viability. Rarely, a dysfunctional segment may deteriorate at low dose due to critically low resting MBF without any CFR. Viable segments which do not show improved contractility on LD-DSE usually have completely exhausted CFR. The completely exhausted CFR, advanced myocardial ultrastructural changes, and downregulation of beta-adrenergic receptors may all contribute to the lack of dobutamine-induced contractile response in akinetic but viable segments.

Four different types of responses are described in LD-DSE:[13]

  • Biphasic: improvement in contractility at LD and akinesia at higher dose suggesting viable and ischemic segment [Figure 2]. It is the most specific sign of viability with modest sensitivity
  • Sustained: Continued improvement in contractility with increasing dobutamine dose [Figure 3]. It suggests nonischemic, stunned, remodeled, tethered segments or segment with subendocardial infarct. It has lower specificity to predict improvement postrevascularization. In routine practice, both biphasic and sustained responses are reported as viability to improve sensitivity
  • Deterioration: hypokinetic segments becoming akinetic to dyskinetic with dobutamine. These are the segments with critical resting low MBF
  • No response: Segments continue to be akinetic. These are either nonviable, scarred segments or myocytes with critical low MBF and exhausted CFR or advanced ultrastructural changes. These segments may have low myocyte mass, more TM extent of fibrosis, and are unlikely to improve with revascularization [Figure 4].
Figure 2: Biphasic response on low-dose dobutamine stress echocardiography. End-systolic left ventricular apical long-axis images (endocardium and epicardium marked by red outline and segment marked by yellow arrow). The baseline akinetic apical septal segment (left upper quadrant) shows improved systolic thickening at 5 mcg/kg (right upper quadrant) and 20 mcg/kg (left lower quadrant) dosages suggesting viability. At higher dose of 40 mcg/kg (right lower quadrant), the apical segment shows thinning and akinesia due to ischemia provoked by high dose and tachycardia

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Figure 3: Sustained response on low-dose dobutamine stress echocardiography. End-systolic left ventricular apical long-axis images (endocardium and epicardium marked by red outline and segment marked by yellow arrow). The baseline akinetic left ventricular mid and apical segment shows progressively sustained improvement in thickening and excursion on increasing dosages of dobutamine with reduction in left ventricular end-systolic cavity size

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Figure 4: No response on low-dose dobutamine stress echocardiography. End-systolic left ventricular apical 4 chamber images (endocardium and epicardium marked by red dotted outline and segment marked by yellow arrow). The entire lateral wall shows no improvement in akinesia or systolic thickening with increasing dosages of dobutamine suggesting nonviability. Note the improved systolic thickening of septum with higher dosages of dobutamine

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In ischemic dilated cardiomyopathy, the LV volumes and dimensions can give insight into advanced LV remodeling which is unlikely to show global LVEF recovery postrevascularization.[6] The LV end-diastolic volume index >170 ml/m 2, LV end-systolic volume index >90 ml/m 2, and LV end-diastolic diameter index >55 mm/m 2 (end-diastolic volume greater than twice the upper limit of normal) may suggest a threshold beyond which LV functional recovery with revascularization seems improbable.


  Sensitivity and Specificity of Dobutamine Stress Echocardiography for Detecting Myocardial Viability Top


A preserved end-diastolic wall thickness (EDWT) indicates the presence of sufficient mass of myocytes for functional recovery which can effectively contribute to systolic thickening and global LV function [Figure 5]. EDWT >6 mm and thallium uptake >60% predict postrevascularization functional recovery with high sensitivity (>90%) but low specificity (40%–50%).[14] EDWT <5 mm is highly accurate in identifying no improve after revascularization.[6]
Figure 5: Measurement of end-diastolic wall thickness by left ventricular contrast opacification. The yellow arrows show normal anterior wall thickness while the red arrows show partially thinned posterolateral wall

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LD-DSE studies give average sensitivity of 75%–80% and a specificity of 80%–85% for the prediction of functional recovery postrevascularization either after myocardial infarction or in the setting of ischemic dilated cardiomyopathy.[6] “Biphasic response” is most specific for detection of myocardial viability. The specificity of biphasic response is 89% but the sensitivity is modest at 74%.[15] The “sustained” response shows higher sensitive but has a much lower specificity. The combination of “biphasic” and “sustained” responses is reported as evidence of viability, to improve sensitivity (86%) but with drop in specificity (68%). Combining any response on dobutamine (biphasic, sustained, or worsening) improves sensitivity (88%) further at the cost of significant drop in specificity (61%).[16]

Diagnostic sensitivity and accuracy improves significantly when dobutamine response is reported only in segments with diastolic wall thickness of at least 6 mm or more. Combining EDWT >6 mm and DSE “any improvement” gives clinically optimum sensitivity (88%) and specificity (77%).[14] The combination of “diastolic wall thickness >5 mm plus LD-DSE” or “diastolic wall thickness >5 mm plus thallium-201 scintigraphy” results in similar higher positive predictive values as combined “LD-DSE plus thallium-201 scintigraphy.”[6]

The degree of global LV functional recovery postrevascularization is directly proportional to the number of myocardial viable segments on baseline LD-DSE. The improvement in LVEF is approximately 5%–6% for baseline 2–5 viable segments and more than 10% for baseline six or more viable segments.[17] A significant LVEF improvement with low-dose dobutamine echocardiography at baseline is associated with more global LV functional recovery and LV reverse remodeling after bypass surgery.[18]


  Strain and Strain Rate Analysis for Detection of Viability Top


In TVI encoded images of LD-DSE, the improvement in systolic and early diastolic strain rates (SRs) in akinetic segments can be quantified. Increase in systolic SR (>0.23) or increase in early diastolic SR (>0.8) has sensitivity of 83% and specificity of 84% to predict viability.[19],[20],[21] In another study, a systolic SR increment of >0.25/s predicted functional recovery, postrevascularization, with sensitivity of 80% and specificity of 75%.[22] In a head-to-head comparison study between Doppler TVI and speckle-tracking echocardiography (STE), only the TVI longitudinal strain and SR on LD-DSE showed incremental value over visual wall motion analysis in detecting viability. STE could identify viability only in left anterior descending (LAD) territory, but TVI strain and SR could identify viability in both LAD and left circumflex/right coronary artery territories.[23]

In a study by Park et al., SR measurement was better than myocardial tissue velocity for identification of viable myocardium in patients with STEMI who underwent PPCI. Patients with functional recovery from anterior wall STEMI showed better diastolic function, better early diastolic SR, and more isovolumic contraction in LAD territory.[24] Zhang et al. studied correlation of systolic SR and transmurality of infarction. Systolic SR − 0.59/s or lower detected a TM infarction with high sensitivity of 90.9% and high specificity of 96.4% while systolic SR between − 0.98/s and −1.26/s identified subendocardial infarction from normal myocardium with sensitivity of 81.3% and specificity of 83.3%.[25]


  Comparison of Echocardiography With Other Imaging Modalities Top


The use of ultrasound microbubble contrast for LV opacification gives accurate measurement of diastolic wall thickness. The intensity of myocardial contrast perfusion is directly proportional to the surviving myocardial capillary network. Myocardial contrast perfusion echocardiography may be used to evaluate of myocardial viability in dobutamine nonresponsive segments with preserved thickness. However, the ten MCE studies evaluating viability in literature have shown sensitivity ranging from 62% to 92% and specificity ranging from 67% to 87% in identifying myocardial viability. This suggests nonstandardization of protocols and nonuniformity of imaging skills.[6]

Compared with nuclear or MRI methods, LD-DSE is more specific but less sensitive. In case of negative DSE results, in myocardial segments more than 5 mm thickness, it is imperative to get additional data from MRI or nuclear study.[26] Meta-analysis of LD-DSE trials involving 1090 patients showed sensitivity of 81% and specificity of 80% for predicting myocardial viability. Similar meta-analysis of SPECT thallium trials involving 858 patients showed sensitivity of 86%–88% and specificity of 50%–60% while meta-analysis of FDG-PET trials involving 598 patients showed sensitivity of 93% and specificity of 58% for predicting myocardial viability. Thirteen MRI studies involving 420 patients showed sensitivity of 80%–82% and specificity of 68%–70% for predicting myocardial viability.[26]


  Clinical Algorithm for Multimodality Myocardial Viability Assessment Top


Using multiple costly imaging modalities to assess viability in given patient is not cost-effective and leads to more uncertainties due to discordant results. The clinicians and imaging experts should follow a systematic algorithm for myocardial viability assessment in ischemic dilated cardiomyopathy. The algorithm proposed by Rahimtoola et al.[6] consists of stepwise utilization of different imaging modalities alone or in combination in a most cost-effective way. The first step is to accurately measure EDWT of the akinetic segment on echocardiography with or without contrast LVO. CMRI may be used in patients with poor echo window. A preserved segment, with EDWT more than 5 mm, has more than 50% probability of functional recovery while a thinned-out segment, with EDWT <5 mm, has <5% probability of recovery.[6] In the presence of preserved wall thickness more than 5–6 mm, either LD-DSE or SPECT imaging is sufficient to establish viability in large number of patients. However, in the presence of EDWT of 5 mm or less, the role of LD-DSE is limited. In segments with wall thickness of 5 mm or less, if LD-DSE results are negative or equivocal, “LGE-MRI” or “FDG-PET” is planned.


  Current Relevance of Myocardial Viability in Cardiology Practice Top


STICH trial utilized LD-DSE or SPECT thallium scan for assessing viability in a subset of patients with LV dysfunction randomized to undergo coronary bypass graft surgery or optimal medical treatment.[5],[27] There was a significant association between myocardial viability and outcome in both medically treated and revascularized patients in univariate analysis. This association was not significant in multivariate analysis which included clinical and other echo parameters. When assessed by either intention to treat or by treatment actually received, myocardial viability failed to show discriminatory power on the outcome of medical versus surgical treatment. The fall out of STICH trial is that the clinicians can no longer use presence or absence of myocardial viability, to choose between medical versus surgical treatment for patients with ischemic heart disease and LV dysfunction. In short, the assessment of myocardial viability does not identify patients who will have greater survival benefit by adding coronary artery bypass grafting to aggressive medical therapy.

In cardiology literature, myocardial viability is defined as myocardial systolic function recovery after revascularization. This dichotomy of “yes” or “no” contractile recovery postrevascularization does not consider the beneficial effects of revascularization on the complex pathophysiology of chronic ischemic myocardium. Myocardial segments with viable myocytes but no contractile recovery may still benefit by revascularization. The revascularization theoretically may prevent reinfarctions and arrhythmias. The revascularization may preserve epicardial layer which may influence global LV remodeling and diastolic function. Finally, the value of viability testing by various modalities should be evaluated by its impact on postrevascularization reduction in the hard end points such as cardiac mortality and nonfatal myocardial infarction.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Ferrari R. Myocardial hibernation. An adaptive phenomenon? In: Yellon DM, Rahimtoola SH, Opic LH, editors. New Ischemic Syndromes. New York: Authors Publishing House; 1997. p. 204-14.  Back to cited text no. 1
    
2.
Carluccio E, Biagioli P, Alunni G, Murrone A, Giombolini C, Ragni T, et al. Patients with hibernating myocardium show altered left ventricular volumes and shape, which revert after revascularization: Evidence that dyssynergy might directly induce cardiac remodeling. J Am Coll Cardiol 2006;47:969-77.  Back to cited text no. 2
    
3.
Rahimtoola SH, La Canna G, Ferrari R. Hibernating myocardium: Another piece of the puzzle falls into place. J Am Coll Cardiol 2006;47:978-80.  Back to cited text no. 3
    
4.
Allman KC, Shaw LJ, Hachamovitch R, Udelson JE. Prognostic valve of myocardial viability testing: A meta-analysis. Circulation 2000;102 Suppl II:576.  Back to cited text no. 4
    
5.
Velazquez EJ, Lee KL, Deja MA, Jain A, Sopko G, Marchenko A, et al. Coronary-artery bypass surgery in patients with left ventricular dysfunction. N Engl J Med 2011;364:1607-16.  Back to cited text no. 5
    
6.
Rahimtoola SH, Dilsizian V, Kramer CM, Marwick TH, Vanoverschelde JL. Chronic ischemic left ventricular dysfunction: From pathophysiology to imaging and its integration into clinical practice. JACC Cardiovasc Imaging 2008;1:536-55.  Back to cited text no. 6
    
7.
Selvanayagam JB, Jerosch-Herold M, Porto I, Sheridan D, Cheng AS, Petersen SE, et al. Resting myocardial blood flow is impaired in hibernating myocardium: A magnetic resonance study of quantitative perfusion assessment. Circulation 2005;112:3289-96.  Back to cited text no. 7
    
8.
Shimoni S, Frangogiannis NG, Aggeli CJ, Shan K, Quinones MA, Espada R, et al. Microvascular structural correlates of myocardial contrast echocardiography in patients with coronary artery disease and left ventricular dysfunction: Implications for the assessment of myocardial hibernation. Circulation 2002;106:950-6.  Back to cited text no. 8
    
9.
Heusch G. Hibernating myocardium. Physiol Rev 1998;78:1055-85.  Back to cited text no. 9
    
10.
Borgers M, Thoné F, Wouters L, Ausma J, Shivalkar B, Flameng W. Structural correlates of regional myocardial dysfunction in patients with critical coronary artery stenosis: Chronic hibernation? Cardiovasc Pathol 1993;2:237-45.  Back to cited text no. 10
    
11.
Schuster A, Morton G, Chiribiri A, Perera D, Vanoverschelde JL, Nagel E. Imaging in the management of ischemic cardiomyopathy: Special focus on magnetic resonance. J Am Coll Cardiol 2012;59:359-70.  Back to cited text no. 11
    
12.
Lang RM, Badano LP, Mor-Avi V, Afilalo J, Armstrong A, Ernande L, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: An update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr 2015;28:1-39.e14.  Back to cited text no. 12
    
13.
Elhendy A, Cornel JH, Roelandt JR, van Domburg RT, Nierop PR, Geleÿnse ML, et al. Relation between contractile response of akinetic segments during dobutamine stress echocardiography and myocardial ischemia assessed by simultaneous thallium-201 single-photon emission computed tomography. Am J Cardiol 1996;77:955-9.  Back to cited text no. 13
    
14.
Cwajg JM, Cwajg E, Nagueh SF, He ZX, Qureshi U, Olmos LI, et al. End-diastolic wall thickness as a predictor of recovery of function in myocardial hibernation: Relation to rest-redistribution T1-201 tomography and dobutamine stress echocardiography. J Am Coll Cardiol 2000;35:1152-61.  Back to cited text no. 14
    
15.
Afridi I, Kleiman NS, Raizner AE, Zoghbi WA. Dobutamine echocardiography in myocardial hibernation. Optimal dose and accuracy in predicting recovery of ventricular function after coronary angioplasty. Circulation 1995;91:663-70.  Back to cited text no. 15
    
16.
Qureshi U, Nagueh SF, Afridi I, Vaduganathan P, Blaustein A, Verani MS, et al. Dobutamine echocardiography and quantitative rest-redistribution 201Tl tomography in myocardial hibernation. Relation of contractile reserve to 201Tl uptake and comparative prediction of recovery of function. Circulation 1997;95:626-35.  Back to cited text no. 16
    
17.
Meluzín J, Cerný J, Frélich M, Stetka F, Spinarová L, Popelová J, et al. Prognostic value of the amount of dysfunctional but viable myocardium in revascularized patients with coronary artery disease and left ventricular dysfunction. Investigators of this Multicenter Study. J Am Coll Cardiol 1998;32:912-20.  Back to cited text no. 17
    
18.
Pasquet A, Lauer MS, Williams MJ, Secknus MA, Lytle B, Marwick TH. Prediction of global left ventricular function after bypass surgery in patients with severe left ventricular dysfunction. Impact of pre-operative myocardial function, perfusion, and metabolism. Eur Heart J 2000;21:125-36.  Back to cited text no. 18
    
19.
Voigt JU, Arnold MF, Karlsson M, Hübbert L, Kukulski T, Hatle L, et al. Assessment of regional longitudinal myocardial strain rate derived from Doppler myocardial imaging indexes in normal and infarcted myocardium. J Am Soc Echocardiogr 2000;13:588-98.  Back to cited text no. 19
    
20.
Hoffmann R, Altiok E, Nowak B, Heussen N, Kühl H, Kaiser HJ, et al. Strain rate measurement by Doppler echocardiography allows improved assessment of myocardial viability inpatients with depressed left ventricular function. J Am Coll Cardiol 2002;39:443-9.  Back to cited text no. 20
    
21.
Hoffmann R, Altiok E, Nowak B, Kühl H, Kaiser HJ, Buell U, et al. Strain rate analysis allows detection of differences in diastolic function between viable and nonviable myocardial segments. J Am Soc Echocardiogr 2005;18:330-5.  Back to cited text no. 21
    
22.
Hanekom L, Jenkins C, Jeffries L, Case C, Mundy J, Hawley C, et al. Incremental value of strain rate analysis as an adjunct to wall-motion scoring for assessment of myocardial viability by Dobutamine echocardiography: A follow-up study after revascularization. Circulation 2005;112:3892-900.  Back to cited text no. 22
    
23.
Bansal M, Jeffriess L, Leano R, Mundy J, Marwick TH. Assessment of myocardial viability at dobutamine echocardiography by deformation analysis using tissue velocity and speckle-tracking. JACC Cardiovasc Imaging 2010;3:121-31.  Back to cited text no. 23
    
24.
Park SM, Miyazaki C, Prasad A, Bruce CJ, Chandrasekaran K, Rihal C, et al. Feasibility of prediction of myocardial viability with Doppler tissue imaging following percutaneous coronary intervention for ST elevation anterior myocardial infarction. J Am Soc Echocardiogr 2009;22:183-9.  Back to cited text no. 24
    
25.
Zhang Y, Chan AK, Yu CM, Yip GW, Fung JW, Lam WW, et al. Strain rate imaging differentiates transmural from non-transmural myocardial infarction: A validation study using delayed-enhancement magnetic resonance imaging. J Am Coll Cardiol 2005;46:864-71.  Back to cited text no. 25
    
26.
Schinkel AF, Bax JJ, Poldermans D, Elhendy A, Ferrari R, Rahimtoola SH. Hibernating myocardium: Diagnosis and patient outcomes. Curr Probl Cardiol 2007;32:375-410.  Back to cited text no. 26
    
27.
Velazquez EJ, Lee KL, Jones RH, Al-Khalidi HR, Hill JA, Panza JA, et al. Coronary-artery bypass surgery in patients with ischemic cardiomyopathy. N Engl J Med 2016;374:1511-20.  Back to cited text no. 27
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]



 

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  In this article
   Abstract
  Introduction
   Pathophysiology ...
   Multimodality Im...
   Low -Dose Dobuta...
   Myocardial Contr...
   Nuclear Perfusio...
   Late Gadolinium ...
   Step-By-Step App...
   Sensitivity and ...
   Strain and Strai...
   Comparison of Ec...
   Clinical Algorit...
   Current Relevanc...
   References
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