Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Myocardial viability

6,236 views

Published on

Published in: Health & Medicine
  • Be the first to comment

Myocardial viability

  1. 1. ASSESSMENT OF MYOCARDIAL VIABILITY Dr. RAGHURAM SCTIMST
  2. 2. VIABILITY
  3. 3. CORONARY ARTERY DISEASEACUTE CORONARY SYNDROMEUndergo revascularisation procedures Increased number of patients with residual LV dysfunctionImproved survival undergoing progressive LV remodeling and congestive heart failure
  4. 4. ADD TO THIS 1. rising age of our population 2. Higher prevalence of comorbidities, eg., DM-2Typically, these patients have multivessel disease, increased LV volumes, and variable degrees of regional or global systolicdysfunctionAmong these patients, coronary revascularization maylead to symptomatic and prognostic improvement, andthese clinical benefits are accompanied by evidence ofreverse LV remodeling.
  5. 5. In the early 1980s, Rahimtoola et al reviewed the results of coronarybypass surgery trials and identified patients with CAD and chronic LVDthat improved upon revascularization.CORNERSTONE FOR ALL FUTURE STUDIES CASS (coronary artery surgery study ) REGISTRY
  6. 6. Data from the coronary artery surgery study(CASS) registry for patients with LVEF < 35%involved 651 patients.The five year survival was significantly better insurgical patients (68%) than in the medical group(54%).The contrast was even more in patients with LVEF< 26% whose five year survival was 63% withsurgery, but 43% with medical treatment
  7. 7. Thus came the concept of myocardialviability and with it came the new termssuch as hibernation and stunning
  8. 8. THE MYOCARDIAL RESPONSE TO ISCHEMIC INJURY
  9. 9. Onset of severe ischemia Within seconds aerobic changes to anaerobic metabolism Decrease in the production of high-energy phosphates, namely adenosine triphosphate (ATP) and phosphocreatine (PCr)Ultrastructural changes occur  mitochondrial swelling, loosening of intercellular attachments, the presence of small, lipid-rich amorphous mitochondrial densities, dilation of the sarcoplasmic reticulum, disaggregation of SR polysomes, and myofibrillar relaxation
  10. 10. within 1 min of acute onset The myocardium is functionally sensitive to ischemia and will exhibit marked contractile dysfunction HOWEVER, these ultrastructural defects areentirely reversible if reperfusion occurs within 20– 40 min.
  11. 11. Irreversible InjuryBegins in the subendocardial tissue and progresses towardsthesubepicardium.In humans, it may take as long as 6–12 hr forcomplete infarction of the myocardium at riskthe necrotic changes are usually evident, about4–12 hr after onsetThis may include the denaturation ofcytoplasmic proteins, swelling, and enzymaticdigestion of organelles and the sarcolemma.
  12. 12. MYOCARDIAL VIABILITY
  13. 13. If tissue is viable,  restoration ofnormal blood flow.  will improve theventricular functionThus, the patient‘s prognosis will alsoimprove, as a result of an increase in ejectionfraction, systolic and diastolic performance,exercise capacity, and most importantly,survival.
  14. 14. Viable myocardium must have the followingcharacteristics1. The ability to generate HEP (PCr and ATP)2. have an intact sarcolemma, in order to maintain ionic/electrochemical gradients, and3. have sufficient perfusion, both for the delivery of substrates and O2 and for the adequate washout of potentially noxious metabolites ? contractility.
  15. 15. There are two tissue states that exhibitsustained contractile dysfunction despitemeeting the three criteriaStunned myocardium &Hibernating myocardium.
  16. 16. Myocardial stunningFirst documented by Heyndrickx et al. in the mid-1970s Heyndrickx GR, Millard RW, McRitchie RJ, Maroko PR, Vatner SF. Regional myocardial functional and electrophysiological alterations after brief coronary artery occlusion in conscious dogs. J Clin Invest 1975;56:978–985.
  17. 17. They had concluded that brief periods of coronary occlusion resulted in prolongeddepression of myocardial function in the ischemic zone.While regional electrograms return to normal within seconds and the coronary flowdebt is repaid rapidly, functional derangement lasts for several hours. Published October, 1975
  18. 18. The stunned myocardium: prolonged, postischemic ventriculardysfunction and RA E Braunwald Circulation 1982;66;1146-1149 KlonerCoined the term ‗‗myocardial stunning‘‘, for thisphenomenon of ‗‗delayed recovery of regionalmyocardial contractile function after reperfusiondespite the absence of irreversible damage anddespite restoration of normal flow
  19. 19. Pathogenesis of stunningEarlier,loss of and reduced ability to synthesize high-energy phosphates,Impairment of microvascular perfusion,impairment of sympathetic neuralresponsiveness,reduction in the activity of creatine kinase, Were believed to be the causes
  20. 20. PresentlyThere are 2 major hypotheses for myocardial stunning:(1)a oxygen-free radical hypothesis and(2)a calcium overload hypothesis time-course of myocardial stunning dysfunction may persist for hours or for as long as 6 weeks post-insult both the duration and severity of ischemia determine the duration of post-ischemia/reperfusion dysfunction
  21. 21. Mechanism of contractile dysfunction in stunningNormal cardiac contraction depends on the maintenance ofcalcium cycling and homeostasis across themitochondrial membrane and sarcoplasmic reticulum duringeach cardiac cycle.Brief ischemia followed by reperfusion- accumulation ofcalcium and a partial failure of normal beat to beat calciumcycling - damages Ca2+ pump and ion channels of thesarcoplasmic reticulum.This results in the electromechanical uncoupling of energygeneration from contraction that characterizes myocardialstunning.
  22. 22. Hibernating MyocardiumHibernating myocardium is a state of persistentlyimpaired myocardial and left ventricular function atrest due to reduced coronary blood flows.It can be defined as an exquisitely regulated tissuesuccessfully adapting its activity to prevailingcircumstances.
  23. 23. Hibernating myocardium:Episodic and/or chronically reduced blood flow, which isdirectly responsible for the decrease in the myocardialcontractile function.Tissue ischemia and resultant remodeling withoutnecrosisResidual contractile reserve in response to inotropicstimulation (in at least half of clinical cases).Recovery of contractile function after successfulrevascularization.
  24. 24. Myocardial Hibernation is primarily a clinicalobservation3 mechanisms whereby this may occur Decreased flow at rest  decreased metabolism decreased function Chronically depressed contractile function. Demand ischemia Recovery  Repeated stunning Chronically depressed contractile function. Genomic trigger for cell survival Survival proteinsproduced by antiapoptotic, cytoprotective, and growth-promotinggenes Protection against apoptosis, activation of autophagyAll these mechanisms lead to cell survival in the face of and inspiteof reduced perfusion.
  25. 25. STUNNING AND HIBERNATION
  26. 26. IDENTIFYING VIABLEMYOCARDIUM
  27. 27. The gold standard for the assessment of viability, in theclinical setting is limited…….Noninvasive techniques can only identify tissue thatmight benefit from revascularization.Further we should know that the determination ofviability is indirect and depends on a given region‘sfunctional response to revascularization.
  28. 28. Key non invasive methods to identifyviability1.Echocardiography2.Single Photon Emission Computed Tomography3.Positron Emission Tomography4.Magnetic Resonance
  29. 29. Echocardiography-Extremely useful tool-document the early and late functionalchanges at rest,Stress echocardiography withdobutamine has also been used toidentify viable, yet chronicallydysfunctional myocardium.
  30. 30. Multiple, step-wise doses of dobutamine isadministeredBasally the hibernating tissue may be hypokinetic ,akinetic or dyskinetic.With dobutamine infusion, it may demonstrate abiphasic response- at lower doses(5–10mg/kg/min),  an improvement in contractileperformance at higher doses (>15mg/kg/min)  Contractility regresses as themetabolic demand stimulated overwhelms thetissue‘s capacity to respond
  31. 31. Nagueh et al studied the transmural myocardialbiopsies obtained from patients with hibernatingmyocardiumShowed that tissue with >17% fibrosis failed toexhibit contractile reserve when challenged withlow-dose dobutamine Circulation 1999, 100, 490–496.
  32. 32. In a study by Pagano et al , they reported that thediagnostic accuracy of dobutamine-echocardiography wasreduced with increasing severity of regional and global LVdysfunction.That is, the technique appeared to underestimate the extentof viability: 39% of all recovering LV segments failed toexhibit inotropic contractile reserve. Heart 1998;79:281-288Wiggers et al studied the functional recovery pre- and 6months post-revascularization, and showed that low-dosedobutamine failed to identify 45% of the segments thatultimately regained function Am. Heart. J. 2000, 140, 928–936.
  33. 33. Value of Dobutamine stress echoReductions in blood flow that lead to hibernation likely do soacross a significant range of flows, with a correspondingspectrum of metabolic reserve.Those regions with greater metabolic reserve will likely retain theability to respond to an inotropic stimulus while those regions withprofoundly reduced flow—just on the threshold ofviability—will have no ability to respond.Such regions will therefore appear to be nonviable on adobutamine-echocardiography challenge.Hence dobutamine-echocardiography may be consideredan easily accessible tool however with sub-optimalsensitivity for the detection of residual tissue viability
  34. 34. Myocardial contrast echocardiographyMyocardial contrast echocardiography (MCE) usingintracoronary contrast administration has emerged as amodality for assessing myocardial perfusion, and it has thepotential to predict myocardial viability.Basis :- Myocardial contrast enhancement depends onan intact microcirculation.The combination of intravenous MCE and destruction andreplenishment contrast intensity curves have allowed forthe noninvasive quantification of myocardial blood volumeand velocity and, thus, myocardial blood flow.
  35. 35. Left ventricular opacification (LVO) obtained withmicrobubbles improves the definition of the LV border.This provides better quantitation of LV volume by theSimpson method.The correlation between LV volume measured withcardiac magnetic resonance (CMR) and that measuredwith echocardiography is better with the use of LVO.Regional wall motion analysis can also be better withLVO.
  36. 36. Identification of Hibernating Myocardium With Quantitative IntravenousMyocardial Contrast Echocardiography: Comparison With DobutamineEchocardiography and Thallium-201 Scintigraphy Twenty patients with coronary artery disease and ventricular dysfunction underwent MCE 1 to 5 days before bypass surgery and repeat echocardiography at 3 to 4 months. Patients also underwent DE (n=18) and rest-redistribution Tl201 tomography (n=16) before revascularization. MCE images were analyzed both qualitatively and quantitatively. Qualitatively, 0, no opacification; 1, patchy or epicardial opacification only; or 2, homogeneous opacification. Quantitative analysis was performed using a prototype software – They constructed Myocardial contrast intensity (MCI) replenishment curves to derive quantitative MCE indices of blood velocity and flow. Circulation Volume 107(4), 4 February 2003, pp 5
  37. 37. Identification of Hibernating Myocardium With Quantitative Intravenous Myocardial ContrastEchocardiography: Comparison With Dobutamine Echocardiography and Thallium-201 Scintigraph(Contd….)Results :Recovery of function occurred in 38% of dysfunctionalsegments.The best MCE parameter for predicting functional recoverywas Peak MCI×[beta], an index of myocardial blood flowMCE parameters of perfusion in hibernating myocardiumwere similar to segments with normal function and washigher than that in dysfunctional myocardium withoutrecovery of functionMCE parameters were higher in segments with contractilereserve and Tl201 uptake >60% and identified viable segmentswithout contractile reserve by DE.
  38. 38. Single Photon EmissionComputedTomography
  39. 39. SA VLA STANDARDSPECT IMAGING DISPLAY HLA
  40. 40. SPECTSPECT requires injection of a gamma-emitting radioisotopeThallium-201 and Technetium Tc 99m–Labeled Tracersare the commonly used radionuclides01Tl is a monovalent cation with biologic propertiessimilar to those of potassium (major intracellular cation inmuscle and is virtually absent in scar tissue ) 201Tl is awell-suited radionuclide for differentiation of normal andischemic myocardium from scarred myocardium.The initial myocardial uptake early after intravenousinjection of thallium is proportional to regional blood flow.
  41. 41. VARIOUS SPECT MODALITIES TOIDENTIFY VIABLE MYOCARDIUM
  42. 42. 201Tl stress redistributionThe uptake of 201Tl is an energy-dependentprocess requiring intact cell membrane integrity,and the presence of 201Tl implies preservedmyocyte cellular viability.Imaging is done- 1) immediately following stress, with eitherexercise or pharmacologically induced coronaryhyperemia with dipyridamole or adenosine, and 2) after 3–4 hr redistribution of Tl-201
  43. 43. INTERPRETATIONDefects on post-stress images, may ―fill in‖ by the time therest-redistribution images are acquired, indicating viability.A defect that persists and appears again on the 3–4 hr images(i.e., a fixed-defect) may be due to: (1) markedly reduced regional perfusion, (2) impaired cellular membrane integrity, inadequate forthe active sequestration of the tracer into the cell, (3) cell death (acute infarction), or (4) scar tissue.Thus, fixed-defects on 3– 4 hr redistribution images mayrepresent only severely hypoperfused—and not necessarilyinfarcted tissue
  44. 44. INTERPRETATIONLate redistribution imagesAcquire a third set of images at 24 hoursThis would allow for redistribution of the tracer to very-ischemic (yet viable) tissueIt has been shown that 22% of fixed defects (at earlyredistribution imaging) demonstrate normal Tl-201 uptakeat later redistribution.This may indicate a poorly perfused, yet viable region
  45. 45. 201Tl reinjectionThis may be necessary because redistribution depends onthe continued delivery of the tracer over the 3–4 hr period.If the blood concentration of Tl- 201 decreases a great deal,there may be insufficient delivery of the tracer and the defectmay not fill-in during redistribution imagingThe second injection of thallium with delayed imaging afterthis repeat injection will give the myocytes with reducedperfusion the greatest opportunity to sequester thallium
  46. 46. 201Tl rest redistribution Here we compare images between 3- to 4-hourversus 15- to 20-minute images. The identification of a "reversible resting defect“reflects preserved viability.  Is Insensitive  BUT is a specific sign ofpotential improvement in regional function.
  47. 47. 99mTc-sestamibi and tetrofosminThey do not share the redistribution properties of201TlBUT their characteristics for predicting improvementin regional function after revascularization appear tobe similar
  48. 48. Relation between tracer uptake in a dysfunctional territory and thesubsequent probability of functional recovery after revascularization. Modified from Bonow RO: Assessment of myocardial viability with thallium-201
  49. 49. AN EXERCISE…..1. Severe apical defect  Fixed defect2. Basal and mid inferior and lateral wall defect Reversibl e
  50. 50. The impact of viability assessment using myocardialperfusion imaging on patient management and outcome.Hage FG et al J Nucl Cardiol. 2010 Jun;17(3):378-89. Epub 2010 Feb 26.They studied 246 consecutive ICM patients with rest-redistribution gated SPECT thallium-201 MPI.Size and severity of perfusion defects were assessed byautomated method.Regions with <50% activity vs normal were considerednonviable
  51. 51. The impact of viability assessment using myocardial perfusion imaging onpatient management and outcome. (Contd…)RESULTS:•Of the 246 patients, 37% underwent CR within 3 months of MPI.•Independent predictors of CR included chest pains (OR 2.74) and rest-delayed transient ischemic dilatation (OR 4.49), while a prior history ofCR or ventricular arrhythmias favored Medical therapy.•The cohort was followed-up for 41 +/- 30 m•Survival was better with CR than MT (P < .0001).•For CR, survival was better for those with a smaller area of nonviablemyocardium (risk of death increased by 5%/1% increase in size ofnonviable myocardium, P = .009) but this was not seen in MT.•CR had a mortality advantage over MT when the area of nonviablemyocardium was <or=20%LV but not larger.
  52. 52. Late reversibility of tomographic myocardial thallium-201 defects:an accurate marker of myocardial viability. J Am Coll Cardiol. 1988 Dec;12(6):1456-63.Twenty-one patients were studied who underwent thallium-201 stress-redistributionsingle photon emission computed tomography (SPECT) both before and aftercoronary artery bypass grafting (n = 15) or transluminal coronary angioplasty (n =6). All patients underwent thallium imaging 15 min, 4 h and late (18 to 72 h) afterstress as part of the preintervention thallium-201 scintigram. There were a total of 201 tomographic myocardial segments with definite post- stress thallium-201 perfusion defects The 4 h redistribution images did not predict the postinterventionscintigraphic improvement: 67 (85%) of the 79, 4 h reversible as well as 88 (72%) of the 122, 4 h nonreversible segments improved(p = NS).The 18 to 72 h late redistribution images effectively subcategorized the 4h nonreversible segments with respect to postintervention scintigraphicimprovement: 70 (95%) of the 74 late reversible segments improved afterintervention, whereas 18 (37%) of the 48 late nonreversible segments improved (p
  53. 53. Positron emission tomography
  54. 54. MECHANISMFDG is transported into the cell by the same sarcolemmalcarrier as glucose, where it is phosphorylated to FDG-6-phosphate by the enzyme, hexokinase.This unidirectional reaction results in the intracellularaccumulation of FDG-6-phosphate.Since FDG does not undergo further metabolism, its uptakeis proportional to the overall rate of trans-sarcolemmaltransport and hexokinase phosphorylation of circulatingglucose by the myocardium
  55. 55. MECHANISM (Contd…)Although fatty acid oxidation stops shortly after the onsetof severe ischemia, the ischemic myocytes will deriveenergy from stored glycogen through anaerobic glycolysis.After glycogen stores have been depleted, the ischemicmyocyte makes extremely efficient use of its meager supplyof circulating glucose.Even under conditions of extremely diminished glucosedelivery, there is evidence that certain sarcolemmal glucosetransporters are up-regulated to allow for increased uptakeof this substrate
  56. 56. INTERPRETATIONAs there should be no uptake of glucose by infarctedmyocardium—which is metabolically inert—nonviablemyocardium will appear as a region of low-FDGconcentration in such images.In areas of reversibly injured myocardium, glucoseutilization is normal and even above normalThus, stunned or hibernating myocardium may beindistinguishable from normal tissue in an FDG PET image.
  57. 57. PET perfusion imagingEstimations of myocardial perfusion have been performedwith 13NH3 and H215OAlthough its initial uptake is in proportion to myocardial bloodflow, the retention of 13NH3 is thought to depend on themetabolic integrity of the myocytesThus, late-distribution 13NH3 PET images may prove usefulin the assessment of myocardial viability PET imaging with 82Rb does not need a cyclotron facility henceis attractive alternative to 13NH3 orH215Oimaging Late-distribution 82Rb images reflect myocardial viability asthe successful uptake of 82Rb depends on an intact myocyte membrane(a functional Na/K ATPase pump)
  58. 58. The Combined Value of Perfusion/Metabolism PETThe combination of perfusion PET and FDG PET has longbeen considered the gold-standard for the identification ofhibernating myocardium;The identification of a region with low perfusion reserve by13NH3 despite normal FDG uptake is highly predictive ofboth functional recovery and survivalpostrevascularization.
  59. 59. PET•CT cardiac perfusion and viability mismatchstudy
  60. 60. Prevalence of Myocardial Viability as Detected by Positron EmissionTomography in Patients With Ischemic Cardiomyopathy Circulation Volume 99(22), 8 June 1999, pp 2921-2926Methods:- PET studies of 283 patients (age, 63 +/- 10 years) with IHD(mean EF- 26 +/- 8%) were analysedThe extent of viable myocardium was considered "functionally" significant if > 5 segments ([approximate]25% ofthe left ventricular myocardium) exhibited a blood flow/metabolismmismatch "prognostically" significant if 1 to 4 left ventricularsegments did so.Of all patients, 41% had no evidence of viable myocardium, 55% had viable myocardium, and 4% had normal blood flow and metabolism within anenlarged left ventricle.Functionally significant viability was found in 27% and prognosticallysignificant viability in 28% of the patients. Multivariate analysisrevealed the presence of angina to be the only clinical parameter
  61. 61. FDG PET in Myocardial Viability- various studiescombined sensitivity and specificity of 88 and 73%,
  62. 62. SPECT VS FDG PETBrunken et al published data from a comparison oftomographic thallium images with PET images; 47% of theirreversible thallium defects were identified as viable onPET images Circulation. Nov 1992;86(5):1357-69.Tamaki et al subsequently confirmed these findings in 2comparative studies of SPECT and PET in which 38-42%of the irreversible thallium defects had enhanced FDGuptake suggestive of viable myocardium. Am J Cardiol. Oct 15 1989;64(14):860-5
  63. 63. Magnetic resonance Imaging
  64. 64. WHY THE NEED FOR MRI?Dobutamine echocardiography (DbE) and thallium single-photon emission computed tomography are widely available.Dbe - contractile reserve and SPECT  membrane integrity.SO in a patient with a scar may exhibit small residua ofviable myocardium which is picked up by SPECT , however it isinsensitive to DbEHence a smaller scar may respond to DbEThus the size of the scar becomes the keyResting systolic thickening is abolished by the transmuralextent of scar (TES) >20%Increasing TES may be associated with poorer contractilereserveHence the need to evaluate the scar usingdelayed hyperenhancement after gadolinium injection
  65. 65. Gd-DTPA is the most widely available and tested MRcontrast agent.It is a freely diffusible, extracellular tracer with a molecularsize of 550 Da. This tracer results in contrast enhancementby reducing the T1 of tissue in a concentration dependentfashionFree Gd3þ is toxic, BUT when chelated to DTPA, the tracerhas an excellent safety profile and clearance ispredominantly via glomerular filtration.The chelator, DTPA, is the moiety responsible for thedistribution and kinetics of the whole Tracer: healthy cells(with intact, selectively permeable cell membranes) willexclude Gd-DTPA and thereforethis agent is restricted to the extravascular andinterstitial spaces
  66. 66. ORIGINAL ARTICLEThe Use of Contrast-Enhanced Magnetic Resonance Imaging to Identify ReversibleMyocardial DysfunctionRaymond J. Kim, M.D., Edwin Wu, M.D., Allen Rafael, M.D., Enn-Ling Chen, Ph.D.,Michele A. Parker, M.S., Orlando Simonetti, Ph.D., Francis J. Klocke, M.D., RobertO. Bonow, M.D., and Robert M. Judd, Ph.D.N Engl J Med 2000; 343:1445-1453Gadolinium-enhanced MRI was performed in 50 patients with ventriculardysfunction before they underwent surgical or percutaneousrevascularization.The transmural extent of hyperenhanced regions was postulated torepresent the transmural extent of nonviable myocardium.The extent of regional contractility at the same locations was determinedby cineMRI before and after revascularization in 41 patients.
  67. 67. AKINETIC SEGMENT NO SCAR ON MRI VIABLE SEGMENTBECAME FUNCTIONALPOSTREVASCULARISATION REVERSIBLEDYSFUNCTION
  68. 68. AKINETIC SEGMENT SCAR ON MRI NON VIABLE SCAR ANDAKINESIS WASPERSISTENT POSTREVASCULARISATION IRREVERSIBLE DYSFUNCTION
  69. 69. RESULTSAn absence of delayed enhancement in segments that exhibitabnormal contractility has a positive predictive value of 78% forrecovery after revascularization.A <25% delayed enhancement has a positive predictive value of71%.The percentage of the left ventricle that was both dysfunctionaland not hyperenhanced before revascularization was stronglyrelated to the degree of improvement in the global mean wall-motionscore (P<0.001) andthe ejection fraction (P<0.001) after revascularization.
  70. 70. DIFFERENTIAL DIAGNOSIS OF HYPERENHANCEMENT ON MRI
  71. 71. Meta-analysis demonstrating outcome of patients with ischemic left ventricular dysfunction after viability testing J Am Coll Cardiol 39:1151, 2002
  72. 72. Accuracy of currently available techniques for prediction of functional recovery afterrevascularization in patients with left ventricular dysfunction due to chronic coronary arterydisease: comparison of pooled data METHODSA systematic review of all reports on prediction of functional recovery after revascularization in patients withchronic coronary artery diseaseMODALITIES : Thallium-201 (Tl-201) stress-redistribution-reinjection, Tl-201 rest-redistribution, fluorine-18fluorodeoxyglucose with positron emission tomography, technetium-99m sestamibi imaging and low dosedobutamine echocardiographyRESULTS:Sensitivity for predicting regional functional recovery after revascularization was high for all techniques. Thespecificity of both Tl-201 protocols was significantly lower (p < 0.05) and LDDE significantly higher (p <0.01) than that of the other techniquesCONCLUSIONSAlthough all techniques accurately identify segments with improved contractile function after revascularization,the Tl-201 protocols may overestimate functional recovery. The evidence available thus far indicates thatLDDE appears to have the highest predictive accuracy. J Am Coll Cardiol, 1997; 30:1451-1460
  73. 73. Impact of scar thickness on the assessment of viability using dobutamineechocardiography and thallium single-photon emission computed tomographyA comparison with contrast-enhanced magnetic resonance imagingBACKGROUND: Discrepancies between DbE and Tl-SPECT are oftenattributed to differences between contractile reserve and membraneintegrity, but may also reflect a disproportionate influence ofnontransmuralscar on thickening at DbE.METHODS: Sixty patients (age 62 ± 12 years; 10 women and 50men) with postinfarction left ventricular dysfunction underwentstandard rest-late redistribution Tl-SPECT and DbE.Viable myocardium was identified when dysfunctional segmentsshowed Tl activity >60% on the late-redistribution image or by low-dose augmentation at DbE.Contrast-enhanced magnetic resonance imaging (ceMRI) was used todivide TES into five groups: 0%, <25%, 26% to 50%, 51% to 75%, and>75% of the wall thickness replaced by scar. C. et al. J Am Coll Cardiol 2004;43:1248-1256 Nelson,
  74. 74. Correlation between dobutamine echocardiography and thalliumsingle-photon emission computed tomography (Tl-SPECT)
  75. 75. Relationship between transmual extent of scar (TES) and thallium (Tl) activity at lateredistribution (left) and increase in wall motion score (WMS) with low-dose dobutamine (right)
  76. 76. CONTD.RESULTS: As TES increased, both the mean Tl uptake and change in wall motion scoredecreased significantly (both p < 0.001).However, the presence of subendocardial scar was insufficient to prevent thickening;>50% of segments still showed contractile function with TES of 25% to 75%, althoughresidual function was uncommon with TES >75%.The relationship of both tests to increasing TES was similar, but Tl-SPECT identified VMmore frequently than DbE in all groups. Among segments without scar or with smallamounts of scar (<25% TES), >50% were viable by SPECT.CONCLUSIONS: Both contractile reserve and perfusion are sensitive to the extent ofscar. However, contractile reserve may be impaired in the face of no or minor scar, andthickening may still occur with extensive scar.
  77. 77. Commonly Used Noninvasive Testing Modalities to Predict Regional Functional Improvement SENSITIVITY (%) SPECIFICITY (%) MODALITY MEAN (95% CI) MEAN (95% CI) Dobutamine 76 (72-80) 81 (77-84) echocardiography Delayed enhancement by 97 (91-100) 68 (51-85) MRI FDG PET 89 (85-93) 57 (51-63) SPECT 89 (84-93) 68 (61-75) Circulation 117:103, 2008.
  78. 78. ACC/AHA/ASNC GuidelinesRecommendations for the Use of Radionuclide Techniques to Assess Myocardial Viability J Am Coll Cardiol, 2003; 42:1318-1333Indication Test Class Level of Evidenc e1. Predicting improvement in Stress/redistribution/reinjection 201Tl I Bregional and global LV functionafter revascularization I B Perfusion plus PET FDG imaging I B Resting sestamibi imaging I B Gated SPECT sestamibi imaging IIa B Late 201Tl redistribution imaging (after IIb B stress) Dobutamine RNA IIb C Postexercise RNA IIb C Postnitroglycerin RNA IIb C2. Predicting improvement in Perfusion plus PET FDG imaging IIa Bheart failure symptoms afterrevascularization.3. Predicting improvement in 201Tl imaging (rest-redistribution and I Bnatural history after stress/redistribution/reinjection)revascularization
  79. 79. Myocardial Viability End Diastolic Thickness Contractile reserve (DS MRI) DE MRI (Delayed Enhancement MRI)
  80. 80. End Diastolic Thickness EDT <5.5 mm in previous MI : criterion for myocardial necrosis In PET these patients very low metabolically active myocardium The sensitivity and specificity of the end- diastolic thickness for the diagnosis of myocardial viability resulted to be respectively 72 and 89%. In akinetic segments (but with EDT preserved), 44% of segments found viable in PET
  81. 81. DS MRI (Dobutamine StressMRI)
  82. 82. Contractile reserve (DS MRI) Compared to SPECT with both thallium and Tc sestamibi DS MRI is less sensitive but more specific with respect to recovery of contractile function after revascularisation Sensitivity / Specificity :  50 / 81% for MRI, -- 76 and 44% for SPECT thallium -- 66 and 49% for SPECT Tc Compared PET (gold standard), sensitivity and specificity of dobutamine MRI for the diagnosis of myocardial viability have resulted to be 81 and 95%.
  83. 83. (Contrast Enhanced InversionRecovery MRI) CE IR MRI
  84. 84. DE MRI (Acute Myocardial Infarction) Three patterns of enhanced signal hyperintensity: 1) Early hypointensity  No late hyperintensity (hypo), 2) early Hyperintensity  late hyperintensity (hyper); 3)early hypointensity  late hyperintensity (comb).
  85. 85. Type I pattern (hypo) Indicated diffuse microvascular damage Severe myocardial damage / Myocardial necrosis Poor functional recovery after revascularisation
  86. 86. Recovery after Revasc. Dependson transmural extension Highly probable < 25%, intermediate 25 - 75%, Very low / null > 75% Hyperintensities restricted to Subendocardial area will recover contractility better
  87. 87. Myocardial ViabilityDE MRI Allows direct or indirect assessment of viability Infarct characterization In a study, presence of Microvascular obstruction, Increased LVEDV and Impaired LVEF in MRI are found to be independent predictors of adverse events
  88. 88. DE MRI compared to DSE Nelson et al: TEI by DE MRI is inversly related to contractile reserve by DSE Half of all segments which were fully viable by DE MRI had absence of contractile reserve. Due to thethering of viable regions to scar regions, myocyte cellular adaptations that impair dobutamine response, and absence of coronary flow reerve in chronically hypoperfused regions.
  89. 89. DE MRI with PET Various studies showed good correlation Kuhl et al: Inverse correlation between TEI by DEMRI and segmental glucose uptake by PET. 55% of subendocardial infarcts detected by DEMRI were detected as normal by PET. Reason may be the differential metabolism along the thickness of myocardium was not taken in PET.
  90. 90. DE MRI and SPECT DE MRI is more specific and sensitive 60 fold more spatial resolution. Wagner et al: Histopathology proved 75% thickness infarcts (all showed infarction in DE MRI and SPECT) But in <50% infarct thickness in HPE, DE MRI detected infarction in 92% and SPECT in 28% only. Conclusion: DE MRI systemically detects subendocardial infarcts missed by SPECT
  91. 91. DE MRI and SPECT Kitagawa et al: Post revascularisation functional recovery was better assessed by DE MRI than by SPECT. Sensitivity: 98% vs 90% Specificity: 75% vs 54%
  92. 92. MR Coronary angiography Limitations: small arterial size (<5mm) tortuosity complex anatomy cardiac and respiratory motion Mainly for assessing Proximal diameter stenosis and to rule out multivessel CAD At present assessment for surgical planning is difficult
  93. 93. 2D GE picture of MR coronary Angiography
  94. 94. 3D MR angio with True FISP
  95. 95. 3D MRA of LIMA
  96. 96.  Gerber et al: MR MDCT Sensitivity 62% 84% Specificity 79% 71%
  97. 97. Feasibility of MR coronary angio
  98. 98. Characterisation of Vessel Wall Tissues rich in Protons will have hyperintense signal. Calcifications have a low concentration of protons and appear hypointense. The lipid plaques have both a short T1 and a short T2 and will be hyperintense in T1-weighted images Fibrous plaques have a quite similar signal intensity in T1- and T2-weighted images
  99. 99.  Useful in imaging Proximal and medium segments of major epicardial coronary arteries Useful in identifying the origing and course of anomalous coronaries Useful in assessing Bypass graft patencies (both Venous and Arterial) Useful in Plaque characterisation of coronary vessel wall
  100. 100. THANK YOU

×