The accuracy of viability imaging can be improved by combining approaches. In particular, the likelihood of functional recovery is uncertain in patients showing dysfunctional myocardium with preserved EDWT and in those presenting with intermediate grades of scar transmurality (ie, 25% to 75%). Additional low-dose dobutamine stress imaging may provide valuable information with regard to viability in these dysfunctional segments.54–56 Kühl et al57 assessed the thickness of the nonenhanced rim of myocardial segments showing LGE. A cutoff value of 3 mm was superior to a cutoff value of 5.4 mm for EDWT to assess viability. As PET and CMR assess dysfunctional myocardium from a different perspective—that is, metabolic versus scar imaging±contractile reserve, respectively—they can be considered complementary. As such, the emergence of hybrid PET-MR scanners raises new expectations with regard to improved viability detection—for example, to study myocardial metabolism in the nonenhanced rim on LGE-CMR.58 Although initial results are promising, several hurdles need to be overcome to integrate this novel hybrid technique into clinical routine59,60 (Table 1).
If deemed necessary, viability imaging can be combined with stress imaging to exclude concomitant myocardial ischemia. For these combined purposes, stress-rest SPECT/PET imaging, high-dose DSE (±atropine), high-dose dobutamine CMR (±atropine), and/or stress perfusion CMR can be performed.61,62
Finally, with the advent of multidetector CT technology more than a decade ago, reliable cardiac imaging became a reality. Although the focus has mainly been on coronary imaging, this technique has the intrinsic potential to offer a comprehensive approach in evaluating a heart failure patient merging coronary artery imaging, myocardial perfusion, and myocardial viability imaging into a single examination.63–65 However, it should be emphasized that many patients with IHF have advanced CAD with high coronary calcium values hampering an accurate evaluation of coronary artery lumen. Radiation doses for a CT-based myocardial perfusion/viability study remain high (≈15 mSv),65 and in patients with comorbidities such as renal failure, administration of iodinated contrast agents may be contraindicated. Nevertheless, a greater role for CCT in viability imaging might be expected in the coming years.
From a clinical perspective, recovery of global ventricular function and ultimately improved patient survival are more important than regional improvement (Fig. 8).7 Revascularization of the myocardium deemed viable is only indicated if LV ejection fraction is assumed to increase significantly (ie, ≥5%) after revascularization, thereby improving patient survival, stressing the importance to define an optimal cutoff of viability extent. This can be achieved by expressing viable myocardium as a percentage of LV mass or by the number of viable segments, as determined using the standardized myocardial segmentation approach as proposed by the American Heart Association.66 There is substantial evidence that patients with significant myocardial viability treated medically had a significantly worse prognosis compared with patients treated with revascularization.67,68 Importantly, those without proof of viability had intermediate rates of mortality regardless of treatment option.68 The minimal extent of myocardial viability to predict improvement of survival varies among techniques. PET requires the least amount of viable myocardium (25.8%) in comparison with DSE (35.9%) and SPECT (38.7%).69 On CMR, a patient is typically considered to have a viable myocardium when ≥4 dysfunctional segments are considered viable, showing an LGE transmurality ≤50% or improved contractility during low-dose dobutamine stress.68
Since the initial observations of improved contractility in severely dysfunctional myocardium after CABG 4 decades ago, it has become clear that predicting outcome in patients with IHF is difficult, multifactorially determined, and definitely not driven by the presence and extent of myocardial viability alone (Table 3). It is a misunderstanding to consider viability as binomially distributed (ie, viable vs. nonviable); rather than this dichotomy, many shades of gray are present that influence outcome. As preservation of myocyte fraction is an important determinant of functional recovery after revascularization, it is obvious that a higher myocyte fraction is required to maintain contractile reserve than to achieve significant tracer uptake. This may explain, for example, the higher sensitivity of SPECT imaging compared with DSE in the identification of myocardial hibernation.70 Moreover, both myocardial viability and adverse ventricular remodeling (ie, increase in end-systolic volume) provide independent, incremental prognostic value, and thus viability should not be assessed in isolation.71 Although, as discussed above, increasing extent of viability generally implies increased potential for recovery, this coincides with an increased risk for major adverse events.14 Moreover, progression of LV remodeling adversely affects outcome, and once the LV has become too dilated, the ability for functional improvement is lost, and revascularization will not improve patient outcome despite the presence of viable myocardium. In addition, ancillary morbidities related to severe LV dilatation such as mitral regurgitation and thrombus formation also negatively influence patient outcome. Several other issues come into play when considering functional recovery after revascularization. Time between viability assessment and intervention is important with improved survival if an early intervention is performed.72 Moreover, the time frame of recovery is highly variable within patients; in some of them it may take longer than 1 year depending on the severity of myocardial hibernation.16,17 In these patients, it may be difficult to differentiate between an unsuccessful revascularization procedure, evolving CAD, or a false-positive myocardial viability test. Moreover, an increasing number of patients are elderly patients with comorbidities such as renal failure or diabetes mellitus that may substantially contribute to mortality in the follow-up period. Conversely, lack of functional recovery not necessarily implies lack of improved patient outcome, suggesting that revascularization may have a beneficial impact on other factors such as protection against future infarction and death possibly by improving myocardial electrical stability.73 Another potentially confounding issue, not yet highlighted, is the periprocedural necrosis after percutaneous coronary intervention or CABG evidenced by elevation of cardiac enzymes, altered myocardial perfusion, and new myocardial enhancement on LGE-CMR, which is associated with increased long-term mortality.74,75 These and other confounding factors explain to a large extent the controversies on predicting patient outcome in literature, and hopefully may help better design future viability studies (Table 3).12,76
Although current standard care of treatment in IHF patients is largely focused on improving heart failure symptoms and minimizing the risk for premature death using optimal medical treatment with/without coronary revascularization, an increasing number of patients receives cardiac resynchronization therapy and/or an implantable cardioverter-defibrillator (Fig. 9).77 Although beyond the scope of this paper, noninvasive imaging may provide valuable information with regard to the presence and severity of ventricular dyssynchrony, to visualize coronary venous anatomy, and to determine the presence, location, and extent of myocardial scarring (using LGE-CMR or PET). This information is helpful to select the optimal access (eg, intravascular vs. pericardial), to locate the cardiac resynchronization therapy leads, and to estimate the risk for future adverse cardiac events. Information with regard to LV geometry may be of interest in patients scheduled for surgical ventricular reconstruction. Although the STICH trial did not show an added benefit of this procedure to bypass surgery, the trial’s inclusion criteria did not contain shape or viability parameters.78 CMR may contribute to a better patient selection, providing information on 2-dimensional or 3-dimensional LV geometry (eg, sphericity index, apical conicity index), scar tissue assessment and the consequences on regional and global function, and evaluate the reshaping and functional recovery after surgery.79 In patients with chronic total occlusions, CCT provides important preprocedural data regarding the occlusion length, degree of calcification, vessel tortuosity, and bridging collaterals, whereas LGE-CMR may show evidence of chronic MI in territories subtended by the occluded coronary artery.80,81
In the appropriate clinical setting, viability imaging has been recommended for patients with CAD and severe LV dysfunction by both the American College of Cardiology/American Heart Association (ie, class IIa recommendation) and by the European Society of Cardiology and European Association for Cardio-Thoracic Surgery.14 Although these recommendations date from before publication of the STICH trial results, a recent conjoint appropriate use document (2013 ACCF/ACR/ASE/ASNC/SCCT/SCMR) has recommended CMR and PET for investigating viability in patients with severe LV dysfunction, while at the same time indicating the possibility for the use of stress imaging with SPECT and echocardiography.4,14
1. Gheorghiade M, Sopko G, De Luca L, et al..Navigating the crossroads of coronary artery disease and heart failure
2. Yeh RW, Sidney S, Chandra M, et al..Population trends in the incidence and outcomes of acute myocardial infarction.N Engl J Med.2010;362:2155–2165.
3. Lloyd-Jones D, Adams RJ, Brown TM, et al..Heart disease and stroke statistics – 2010 update: a report from the American Heart Association.Circulation.2010;121:e46–e215.
4. Platel MR, White RD, Abbara S, et al..ACCF/ACR/ASE/ASNC/SCCT/SCMR appropriate utilization of cardiovascular imaging in heart failure
. A joint report of the American College of Radiology Appropriateness Criteria Committee and the American College of Cardiology Foundation Appropriate Use Criteria Task Force.J Am Coll Cardiol.2013;61:2207–2231.
5. Wijns W, Vatner SF, Camici PG.Hibernating myocardium
.N Engl J Med.1998;339:173–181.
6. Allman KC, Shaw LJ, Hachamovitch R, et al..Myocardial viability testing and impact of revascularization on prognosis in patients with coronary artery disease and left ventricular dysfunction: a meta-analysis.J Am Coll Cardiol.2002;39:1151–1158.
7. Camici PG, Prasad SK, Rimoldi OE.Stunning, hibernation, and assessment of myocardial viability.Circulation.2008;117:103–114.
8. Schinkel AF, Bax JJ, Poldermans D, et al..Hibernating myocardium
: diagnosis and patient outcomes.Curr Probl Cardiol.2007;32:375–410.
9. Bonow RO, Maurer G, Lee KL, et al..Myocardial viability and survival in ischemic left ventricular dysfunction.N Engl J Med.2011;364:1617–1625.
10. Beanlands RS, Nichol G, Huszti E, et al..F-18-Fluorodeoxyglucose positron emission tomography imaging-assisted management of patients with severe left ventricular dysfunction and suspected coronary disease. A randomized, controlled trial (PARR-2).J Am Coll Cardiol.2007;50:2002–2012.
11. Velazquez EJ, Lee KL, Deja MA, et al..Coronary-artery bypass surgery in patients with left ventricular dysfunction.N Engl J Med.2011;364:1607–1616.
12. Shah BN, Khattar RS, Senior R.The hibernating myocardium
: current concepts, diagnostic dilemmas, and clinical challenges in the post-STICH era.Eur Heart J.2013;34:1323–1334.
13. Chareonthaitawee P, Gersh BJ, Panza JA.Is viability imaging still relevant in 2012?JACC Cardiovasc Imaging.2012;5:550–558.
14. Allman KC.Noninvasive assessment myocardial viability: current status and future directions.J Nucl Cardiol.2013;20:618–637.
15. Maes A, Flameng W, Nuyts J, et al..Histological alterations in chronically hypoperfused myocardium: correlation with PET findings.Circulation.1994;90:735–745.
16. Bax JJ, Visser FC, Poldermans D, et al..Time course of functional recovery of stunned and hibernating segments after surgical revascularization.Circulation.2001;104:I314–I318.
17. Bondarenko O, Beek AM, Twisk JW, et al..Time course of functional recovery after revascularization of hibernating myocardium
: a contrast-enhanced cardiovascular magnetic resonance study.Eur Heart J.2008;29:2000–2005.
18. Rahimtoola SH.The hibernating myocardium
.Am Heart J.1989;117:211–220.
19. Selvanayagam JB, Jerosch-Herold M, Porto I, et al..Resting myocardial blood flow is impaired in hibernating myocardium
. A magnetic resonance study of quantitative perfusion assessment.Circulation.2005;112:3289–3296.
20. Wu M, D’Hooge J, Ganame J, et al..Non-invasive characterization of the area-at-risk using magnetic resonance imaging
in chronic ischemia.Cardiovasc Res.2011;89:166–174.
21. Kim RJ, Wu E, Rafael A, et al..The use of contrast-enhanced magnetic resonance imaging
to identify reversible myocardial dysfunction.N Engl J Med.2000;343:1445–1453.
22. Cwajg JM, Cwajg E, Nagueh SF, et al..End-diastolic wall thickness as a predictor of recovery of function in myocardial hibernation. Relation to rest-redistribution Tl-201 tomography and dobutamine stress echocardiography
.J Am Coll Cardiol.2000;35:1152–1161.
23. Romero J, Xue X, Gonzalez W, et al..CMR imaging assessing viability in patients with chronic ventricular dysfunction due to coronary artery disease. A meta-analysis of prospective trials.JACC Cardiovasc Imaging.2012;5:494–508.
24. Shah DJ, Kim HW, James O, et al..Prevalence of regional myocardial thinning and relationship with myocardial scarring in patients with coronary artery disease.JAMA.2013;309:909–918.
25. Bogaert J, Rademakers FE.Regional nonuniformity of the normal adult human left ventricle.Am J Physiol Heart Circ Physiol.2001;280:H610–H620.
26. Dawson DK, Maceira AM, Raj J, et al..Regional thicknesses and thickening of compacted and trabeculated myocardial layers of the normal left ventricle studied by cardiovascular magnetic resonance.Circ Cardiovasc Imaging.2011;4:139–146.
27. Moon JC, Lorenz CH, Francis JM, et al..Breath-hold FLASH and FISP cardiovascular MR imaging: left ventricular volume differences and reproducibility.Radiology.2002;223:789–797.
28. Symons R, Doulaptsis R, Masci PG, et al..Post-infarction left ventricular remodeling is significantly influenced by myocardial infarction severity. Assessment by cardiovascular magnetic resonance. Poster no. 2040. Proceedings of the European Society of Cardiology (ESC) 31 August-4 September 2013
. Amsterdam, The Netherlands; 2013.
29. Ganame J, Messalli G, Masci PG, et al..Time course of infarct healing and left ventricular remodelling in patients with reperfused ST segment elevation myocardial infarction using comprehensive magnetic resonance imaging
30. Mesotten L, Maes A, Hambye AS, et al..Nuclear cardiology, part IV: viability.J Nucl Med Technol.1999;27:93–102.
31. Wagner A, Mahrholdt H, Holly TA, et al..Contrast-enhanced MRI and routine single photon emission computed tomography
(SPECT) perfusion imaging for detection of subendocardial myocardial infarcts: an imaging study.Lancet.2003;361:374–379.
32. Simonetti OP, Kim RJ, Fieno DS, et al..An improved MR imaging technique for the visualization of myocardial infarction.Radiology.2001;218:215–223.
33. Mahrholdt H, Wagner A, Judd RM, et al..Delayed enhancement cardiovascular magnetic resonance assessment of non-ischaemic cardiomyopathies.Eur Heart J.2005;26:1461–1474.
34. Abdel-Aty H, Zagrosek A, Schulz-Menger J, et al..Delayed enhancement and T2-weighted cardiovascular magnetic resonance imaging
differentiate acute from chronic myocardial infarction.Circulation.2004;109:2411–2416.
35. Dymarkowski S, Ni Y, Miao Y, et al..Value of T2-weighted magnetic resonance imaging
early after myocardial infarction in dogs: comparison with bis-gadolinium-mesoporphyrin enhanced T1-weighted magnetic resonance imaging
and functional data from cine magnetic resonance imaging
36. Schroeder MA, Swietach P, Atherton HJ, et al..Measuring intracellular pH in the heart using hyperpolarized carbon dioxide and bicarbonate: a 13
C and 31
P magnetic resonance spectroscopy study.Cardiovasc Res.2010;86:82–91.
37. Sun KT, Yeatman LA, Buxton DB, et al..Simultaneous measurement of myocardial oxygen consumption and blood flow using [1-carbon-11] acetate.J Nucl Med.1998;39:272–280.
38. Horn HR, Teichholz LE, Cohn PF, et al..Augmentation of left ventricular contraction pattern in coronary artery disease by an inotropic catecholamine: the epinephrine ventriculogram.Circulation.1974;49:1063–1071.
39. Mahrholdt H, Wagner A, Parker M, et al..Relationship of contractile function to transmural extent of infarction in patients with chronic coronary artery disease.J Am Coll Cardiol.2003;42:505–512.
40. Wahl A, Paetsch I, Gollesch A, et al..Safety and feasibility of high-dose dobutamine-atropine stress cardiovascular magnetic resonance for diagnosis of myocardial ischaemia: experience in 1000 consecutive cases.Eur Heart J.2004;25:1230–1236.
41. Senior R, Lahiri A.Enhanced detection of myocardial ischemia by stress dobutamine echocardiography
utilizing the “biphasic” response of wall thickening during low and high dose dobutamine infusion.J Am Coll Cardiol.1995;26:26–32.
42. Cigarroa CG, deFilippi CR, Brickner ME, et al..Dobutamine stress echocardiography
identifies hibernating myocardium
and predicts recovery of left ventricular function after coronary revascularization.Circulation.1993;88:430–436.
43. Baer FM, Theissen P, Crnac J, et al..Head to head comparison of dobutamine-transesophageal echocardiography
and dobutamine-magnetic resonance imaging
for the prediction of left ventricular functional recovery in patients with chronic coronary artery disease.Eur Heart J.2000;21:981–991.
44. Vitarelli A, Montesano T, Gaudio C, et al..Strain rate dobutamine echocardiography
for prediction of recovery after revascularization in patients with ischemic left ventricular dysfunction.J Card Fail.2006;12:268–275.
45. Bree D, Wollmuth JR, Cupps BP, et al..Low-dose dobutamine tissue-tagged magnetic resonance imaging
with 3-dimensional strain analysis allows assessment of myocardial viability in patients with ischemic cardiomyopathy.Circulation.2006;114supplI33–I36.
46. Korosoglou G, Lossnitzer D, Schellberg D, et al..Strain-encoded cardiac MRI as an adjunct for dobutamine stress testing: incremental value to conventional wall motion analysis.Circ Cardiovasc Imaging.2009;2:116–122.
47. Mahrholdt H, Wagner A, Holly TA, et al..Reproducibility of chronic infarct size measurement by contrast-enhanced magnetic resonance imaging
48. McCrohon JA, Moon JCC, Prasad SK, et al..Differentiation of heart failure
related to dilated cardiomyopathy and coronary artery disease using gadolinium-enhanced cardiovascular magnetic resonance.Circulation.2003;108:54–59.
49. Cheong BYC, Muthupillai R, Wilson JM, et al..Prognostic significance of delayed-enhancement magnetic resonance imaging
. Survival of 857 patients with and without left ventricular dysfunction.Circulation.2009;120:2069–2076.
50. Ramani K, Judd RM, Holly TA, et al..Contrast magnetic resonance imaging
in the assessment of myocardial viability in patients with stable coronary artery disease and left ventricular dysfunction.Circulation.1998;98:2687–2694.
51. Klein C, Nekolla SG, Bengel FM, et al..Assessment of myocardial viability with contrast-enhanced magnetic resonance imaging
. Comparison with positron emission tomography.Circulation.2002;105:162–167.
52. Kühl HP, Lipke CSA, Krombach GA, et al..Assessment of reversible myocardial dysfunction in chronic ischaemic heart disease: comparison of contrast-enhanced cardiovascular magnetic resonance and a combined positron emission tomography – single photon emission computed tomography
imaging protocol.Eur Heart J.2006;27:846–853.
53. Bello D, Shah DJ, Farah GM, et al..Gadolinium cardiovascular magnetic resonance predicts reversible myocardial dysfunction and remodeling in patients with heart failure
undergoing β-blocker therapy.Circulation.2003;108:1945–1953.
54. Baer FM, Theissen P, Schneider CA, et al..Dobutamine magnetic resonance imaging
predicts contractile recovery of chronically dysfunctional myocardium after successful revascularization.J Am Coll Cardiol.1998;31:1040–1048.
55. Kaandorp TAM, Bax JJ, Schuijf JD, et al..Head-to-head comparison between contrast-enhanced magnetic resonance imaging
and dobutamine magnetic resonance imaging
in men with ischemic cardiomyopathy.Am J Cardiol.2004;93:1461–1464.
56. Wellnhofer E, Olariu A, Klein C, et al..Magnetic resonance low-dose dobutamine test is superior to scar quantification for the prediction of functional recovery.Circulation.2004;109:2172–2174.
57. Kühl HP, van der Weerdt A, Beek A, et al..Relation of end-diastolic wall thickness and the residual rim of viable myocardium by magnetic resonance imaging
to myocardial viability assessed by fluorine-18 deoxyglucose positron emission tomography.Am J Cardiol.2006;97:452–457.
58. Knuesel PR, Nanz D, Wyss C, et al..Characterization of dysfunctional myocardium by positron emission tomography and magnetic resonance. Relation to functional outcome after revascularization.Circulation.2003;108:1095–1100.
59. Rischpler C, Nekolla SG, Dregely I, et al..Hybrid PET/MR imaging of the heart: potential, initial experiences, and future prospects.J Nucl Med.2013;54:402–415.
60. Nensa F, Poeppel T, Beiderwellen K, et al..Hybrid PET/MR imaging of the heart: feasibility and initial results.Radiology.2013;268:366–373.
61. Morton G, Schuster A, Perera D, et al..Cardiac magnetic resonance imaging
to guide complex revascularization in stable coronary artery disease.Eur Heart J.2010;31:2209–2216.
62. Kelle S, Nagel E, Voss A, et al..A bi-center cardiovascular magnetic resonance prognosis study focusing on dobutamine wall motion and late gadolinium enhancement in 3,138 consecutive patients.J Am Coll Cardiol.2013;61:2310–2317.
63. Lardo AC, Cordeiro MAS, Silva C, et al..Contrast-enhanced multidetector computed tomography
viability imaging after myocardial infarction. Characterization of myocyte death, microvascular obstruction, and chronic scar.Circulation.2006;113:394–404.
64. Bettencourt N, Chiribiri A, Schuster A, et al..Direct comparison of cardiac magnetic resonance and multidetector computed tomography
stress-rest perfusion imaging for detection of coronary artery disease.J Am Coll Cardiol.2013;61:1099–1107.
65. Vliegenthart R, Henzler T, Moscariello A, et al..CT of coronary heart disease: part I, CT of myocardial infarction, ischemia, and viability.Am J Roentgenol.2012;198:531–547.
66. Cerqueira MD, Weissman NJ, Dilsizian V, et al..Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart. A statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association.Circulation.2002;105:539–542.
67. Desideri A, Cortigiani L, Christen AI, et al..The extent of perfusion-F18-fluorodeoxyglucose positron emission tomography mismatch determines mortality in medically treated patients with chronic ischemic left ventricular dysfunction.J Am Coll Cardiol.2005;46:1264–1269.
68. Gerber BL, Rousseau MF, Ahn SA, et al..Prognostic value of myocardial viability by delayed-enhanced magnetic resonance in patients with coronary artery disease and low ejection fraction: impact of revascularization therapy.J Am Coll Cardiol.2012;59:825–835.
69. Inaba Y, Chen JA, Bergmann SR.Quantity of viable myocardium required to improve survival with revascularization in patients with ischemic cardiomyopathy: a meta-analysis.J Nucl Cardiol.2010;17:646–654.
70. Gunning MG, Kaprielian RR, Pepper J, et al..The histology of viable and hibernating myocardium
in relation to imaging characteristics.J Am Coll Cardiol.2002;39:428–435.
71. Kwon DH, Hachamovitch R, Popovic ZB, et al..Survival in patients with severe ischemic cardiomyopathy undergoing revascularization versus medical therapy. Association with end-systolic volume and viability.Circulation.2012;126suppl 1S3–S8.
72. Tarakji KG, Brunken R, McCarthy PM, et al..Myocardial viability testing and the effect of early intervention in patients with advanced left ventricular systolic dysfunction.Circulation.2006;113:230–237.
73. Samady H, Elefteriades JA, Abbott BG, et al..Failure to improve left ventricular function after coronary revascularization for ischemic cardiomyopathy is not associated with worse outcome.Circulation.1999;100:1298–1304.
74. Ricciardi MJ, Wu E, Davidson CJ, et al..Visualization of discrete microinfarction after percutaneous coronary intervention associated with mild creatine kinase-MB elevation.Circulation.2001;103:2780–2783.
75. Prasad A, Singh M, Lerman A, et al..Isolated elevation in troponin T after percutaneous coronary intervention is associated with higher long-term mortality.J Am Coll Cardiol.2006;48:1765–1770.
76. O’Meara E, Mielniczuk LS, Wells GA.Alternative imaging modalities in ischemic heart failure
(AIMI-HF) IMAGE HF project I-A: study protocol for a randomized controlled trial.Trials.2013;14:218.
77. Al Jaroudi W, Chen J, Jaber WA, et al..Nonechocardiographic imaging in evaluation for cardiac resynchronization therapy.Circ Cardiovasc Imaging.2011;4:334–343.
78. Jones RH, Velazquez EJ, Michler RE, et al..Coronary bypass surgery with or without surgical reconstruction.N Engl J Med.2009;360:1705–1717.
79. Hüther J, Doenst T, Nitzsche S, et al..Cardiac magnetic resonance imaging
for the assessment of ventricular function, geometry, and viability before and after surgical reconstruction.J Thorac Cardiovasc Surg.2011;142:1515–1522.
80. Courtney BK, Munce NR, Anderson KJ, et al..Innovations in imaging for chronic total occlusions: a glimpse into the future of angiography’s blind-spot.Eur Heart J.2008;29:583–593.
81. Choi J-H, Chang S-A, Choi J-O, et al..Frequency of myocardial infarction and its relationship to angiographic collateral flow in territories supplied by chronically occluded coronary arteries.Circulation.2013;127:703–709.