© 2007 Cardinal Health. All rights reserved. PET In Cardiology; Metabolic Imaging with 18-FDG.

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© 2007 Cardinal Health. All rights reserved. PET In Cardiology; PET In Cardiology; Metabolic Imaging Metabolic Imaging with 18-FDG with 18-FDG

Transcript of © 2007 Cardinal Health. All rights reserved. PET In Cardiology; Metabolic Imaging with 18-FDG.

Page 1: © 2007 Cardinal Health. All rights reserved. PET In Cardiology; Metabolic Imaging with 18-FDG.

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PET In Cardiology;PET In Cardiology;

Metabolic Imaging Metabolic Imaging with 18-FDGwith 18-FDG

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Introduction to Metabolic Cardiac Introduction to Metabolic Cardiac ImagingImaging

• Patients with severe left ventricular dysfunction and heart failure may have reduced cardiac performance due to irreversible (myocardial infarction or scarring), or reversible causes.

• Definitions: Infarction – artery blocked - heart attack Stenosis – narrowing of the blood vessel Ischemia – restriction in blood supply Perfusion – blood flow Akinesis – lack of wall motion in a myocardial segment Tachycardia – abnormal, rapid heart beat CABG – coronary artery bypass graft CHF – congestive heart failure

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Myocardial MetabolismMyocardial Metabolism

• Resting aerobic conditions: myocardium predominantly utilizes free fatty acids (FFA) as energy substrate.

• Glucose loading: insulin released by glucose loading downregulates FFA use, and increases glucose utilization.

• Chronic ischemia: FFA utilization suppressed; anaerobic glycolysis preferred. glucose utilization normal.

• Acute ischemia: FFA suppressed, enhanced glucose utilization to supranormal levels.

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Reversible Causes of Global and Reversible Causes of Global and Regional Myocardial DysfunctionRegional Myocardial Dysfunction

• Stunned myocardium: episode of severe ischemia causes acute cell injury, disruption of architecture, and transient myocardial dysfunction. Residual severe stenosis with patent artery.

• Hibernating myocardium: severe stenosis causes chronically ischemic myocardium. Contractility sacrificed for cell integrity.

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Myocardial Viability and PET Myocardial Viability and PET ImagingImaging

• Viable Myocardium> myocardium which exhibits regional dysfunction due to injury or ischemia and severely reduced blood flow (perfusion), but which is intact metabolically, and can achieve normal or near-normal contractility with revascularization.

• Goal of PET Imaging > Identify myocardial segments with poor contractility and severely reduced perfusion, which are intact metabolically (viable).

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Why 18-Fluorodeoxyglucose Why 18-Fluorodeoxyglucose Is A Good Cardiac TracerIs A Good Cardiac Tracer

• Glucose analogue with Fl-18 substituting for hydroxyl group. Trapped in glucose-pyruvate anaerobic glycolysis.

• On site synthesis not required. With a 110 min. half-life, off- site synthesis and delivery available.

• Studies performed in the non-fasting state, with oral glucose loading and insulin injection.

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FDG ProtocolsFDG Protocols

• Resting perfusion imaging performed as previously described.

• 18-FDG administered intravenously

• Oral glucose loading

• One hour given for equilibration

• Fingerstick glucose assessed

• Insulin administered if necessary

• 20 minute static acquisition

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Analysis of Perfusion/Metabolism Analysis of Perfusion/Metabolism PET ImagesPET Images

• Compare perfusion (Rb-82) with metabolic activity (18-FDG) in each myocardial segment.

• Evaluate for regions of mismatch between perfusion and metabolism, relate to wall motion.

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Perfusion/Metabolism Pattern IPerfusion/Metabolism Pattern I

• Perfusion metabolism match: severely reduced perfusion, with matching reduction in FDG uptake. This is consistent with low probability of viable myocardium

• The following slide shows a severe perfusion defect of the lateral and inferolateral walls (upper panels), with a matching severe metabolic defect in the lower panels. This is consistent with a low probability of viable myocardium in those regions.

• This patient would not benefit from an invasive revascularization procedure and would be treated medically.

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Perfusion Metabolism Perfusion Metabolism MatchMatch

Rb-82

FDG

Severe perfusion defect of the lateral and inferolateral walls (upper panels), with a matching severe metabolic defect in the lower panels

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Perfusion/Metabolism Pattern IIPerfusion/Metabolism Pattern II

• Perfusion metabolism mismatch: severely reduced perfusion. FDG uptake normal or near normal. Consistent with high probability of viable myocardium.

• The following slide shows a patient with a severe perfusion defect of the lateral wall (RB-82, upper panel). Metabolic study shows intact 18-FDG uptake in the lateral wall (lower panel), indicative of viable myocardium.

• Therefore, this patient would benefit from revascularization.

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Perfusion Metabolism Perfusion Metabolism MismatchMismatch

Rb-82

FDGSevere perfusion defect of the lateral wall (RB-82, upper panel).

Metabolic study shows intact 18-FDG uptake in the lateral wall (lower panel),

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Perfusion/Metabolism Pattern IIIPerfusion/Metabolism Pattern III

• Enhanced FDG uptake: severely reduced perfusion. FDG uptake increased, with downscaling of FDG uptake in other segments. Consistent with viable myocardium and resting silent ischemia.

• The following slide shows a patient with a severe perfusion defect of the lateral and inferolateral walls (upper two panels, NH3). Metabolic imaging (lower panel) shows hyper intense uptake of 18-FDG in the lateral and inferolateral walls, with relative downscaling of FDG uptake in other segments. This pattern is consistent with viable myocardium, and resting ischemia.

• Therefore, the patient would be treated??????

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Enhanced 18-FDG UptakeEnhanced 18-FDG Uptake

(ML Goris, Bretille J. Colour Atlas of Nuclear Cardiology. Chapman and Hall Medical. London. 1992. p. 216)

• Severe perfusion defect of the lateral and inferolateral walls

• Hyper intense uptake of 18-FDG in the lateral and inferolateral walls

• Viable Myocardium and Resting Ischemia

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Use of PET Metabolic Imaging to Use of PET Metabolic Imaging to Guide RevascularizationGuide Revascularization

• Revascularization of segments shown “viable” on PET has a high likelihood of improving cardiac function.

• Revascularization of nonviable segments is unlikely to improve function.

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Results of Revascularization in Results of Revascularization in Viable vs. Nonviable SegmentsViable vs. Nonviable Segments

Likelihood of improved wall motion:

• Mismatch 82%

• Match: 17%

Tillsch J. NEJM (1986) 314: 884-8.

Tamaki N. Am J Cardiol (1989) 64: 860-5

Von Dahl A. J Nuc Med (1993) 34:23

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Improvement in LV function with Improvement in LV function with Revascularization Based on PET Revascularization Based on PET Metabolic ImagingMetabolic Imaging

• The following table lists studies in which PET perfusion and metabolic imaging is used to identify viable myocardium and dictate coronary bypass surgery or angioplasty.

• In 109 total patients studied, mean LV ejection fraction rose from 34% to 47% post revascularization.

Schelbert H. Card Clin 1994; 12: 303-316

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PET Viability with 18-FDGPET Viability with 18-FDG

• Superior to SPECT: 30% of nonviable segments on Tl-201 are viable by PET FDG

• Extent of viability on PET FDG predicts extent of improvement in left ventricular function post-CABG

• Prognosis: Patients with viable myocardium and

revascularization < 10% event rate Patients with viable myocardium, no

revascularization > 27% event rate

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Pitfalls of PET Pitfalls of PET Perfusion/Metabolic ImagingPerfusion/Metabolic Imaging

• Early Post-Myocardial Infarction, there is a increased incidence of: False (+) Positive Studies: (Positive mismatch, but no viable

myocardium). Due to increased anaerobic glycolytic uptake by remodeling WBC’s (white blood cells) and macrophages.

False (--) Negative Studies: (Viable myocardium, but local metabolic factors, such as acidosis and lactate, impair glucose and FDG uptake by myocardium).

Gropler R. JACC (1992) 19:989 JACC (1993) 22: 1587. Range Effects: ß(+) energy F-18 (0.64 MeV) vs. Rb-82 (3.35 MeV)

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Case Study #1Case Study #1Anterior Wall Viability?Anterior Wall Viability?

Rb-82 FDG

History • 66 YOM• H/O anterior MI and CHF• Angiogram: 99% stenosis mid-

LAD; 50% stenosis LCX; akinesis anterior and apical walls.

PET Findings• Matched severe perfusion and

metabolic defects in the mid-distal anterior wall and apex

• Low prob. of viable myocardium

Outcome • No indications for

revascularization of LAD• Intensive medical treatment.

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Case Study #2;Case Study #2;Interior and/or Exterior Wall Viability?Interior and/or Exterior Wall Viability?

Rest Rb-82

FDG

History • 50 YOM with unstable angina,

cardiogenic shock, sustained ventricular tachycardia.

• Angiogram: 100% LAD; 80% RCA. Stenoses. LVEF 25% with severe diffuse hypokinesis. IABP placed

PET Findings• Perfusion/metabolism mismatch in the

anterior, apical and inferior wall regions.

• Indicates viable, hibernating myocardium in the LAD and RCA distributions

Outcome • PCI successfully performed to LAD

and RCA. IABP weaned. Patient discharged.

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Case Study #3Case Study #3Site of Resting Ischemia and Wall Viability?Site of Resting Ischemia and Wall Viability?

Rb-82

FDG

History • 68 YOF• DM: S/P CABG: recurrent angina• SPECT MPI: severe intensity,

slightly reversible lateral defect• Angiogram: Patent LIMA. Grafts

to LADD and LCX 100%; 100% RCA. Diffuse LV hypokinesis, LVEF 38%.

PET Findings• PET: mod-severe perfusion

defect of lateral and inferolateral walls with hyper-intense lateral wall FDG uptake.

• Resting lateral wall ischemia

Outcome • PCI of native LCX

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Case Study #4Case Study #4Evidence of viable myocardium in the anterior Evidence of viable myocardium in the anterior wall to justify catheterization and PCI?wall to justify catheterization and PCI?

History • 77 YOF• H/O of CHF. ECG reveals delayed

R-wave progression suggestive of anterior MI.

• Echocardiogram: severe hypokinesis to akinesis of the anterior, septal and apical walls.

PET Findings• Severe perfusion defect of the

anterior, apical, septal and inferoapical walls, with matched decrease in 18-FDG uptake in these regions.

• Low prob. of viable myocardium

Outcome • Continued medical therapy

Rest Rb-82

FDG

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Case Study #5Case Study #5Jeopardized or Viable Myocardium?Jeopardized or Viable Myocardium?

History • 68 YOM• H/O anterior MI, S/P CABG, now with

unstable angina.• Angiogram: patent LIMA, and patent

grafts to RCA and OM. Significant CAD proximal to grafts.

• LV gram: severe anterior wall hypokinesis

PET Findings• Anterior wall severe matched defect of

perfusion and metabolism• Low probability of viable myocardium.• Moderate defect in the anteroseptum

with slightly greater 18-FDG uptake vs. Rb-82 (mild mismatch).

Outcome • Continued medical therapy

Rb-82

FDG

NOTE: Rb-82 uptake in lateral wall is >> 18-FDG. This indicates viable myocardium

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Case Study #6Case Study #6Viable myocardium sufficient to justify Viable myocardium sufficient to justify revascularization and mitral valve replacement?revascularization and mitral valve replacement?

Rb-82 FDG

History • Pt. with history of MI. Admitted

with CHF and found to have mitral regurgitation. LVF severely reduced on echocardiogram.

PET Findings• Anteroapical

perfusion/metabolism mismatch - viable myocardium

• Inferior wall severe perfusion defect with matched FDG uptake - low prob. of viable myocardium

Outcome • CABG + MVR

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Case Study #7Case Study #7 Is LAD viable?Is LAD viable?

Rb-82

FDG

History • 66YOM• S/P anterior MI and stent to the LCX.

Now admitted with unstable angina.• Angiogram: 100% stenosis of

proximal LAD. 100% stenosis of LCX stent.

• LV gram: Severely reduced LVF with anteroapical akinesis. LVEF 25%.

PET Findings• Severe perfusion defect of the anterior,

anterolateral and apical walls, with matched 18-FDG uptake in those regions. FDG uptake and perfusion intact in the lateral wall.

• Low probability of anterior wall viable myocardium

Outcome • PCI LCX

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Case Study #8Case Study #8Viable myocardium in the LAD?Viable myocardium in the LAD?

Rb-82

FDG

History • 71YOM with abnormal ECG• Angiogram: 100% stenosis of

LAD• LV gram: akinesis of the distal

anteroapex

PET Findings• Severe perfusion defect in the

distal anterior and apical walls, with intact metabolic 18-FDG uptake.

• Perfusion/metabolism mismatch - viable myocardium

Outcome • PCI of LAD

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Case Study #9Case Study #9 Is Anterior Wall Viable?Is Anterior Wall Viable?

Rb-82 FDG

History • 81YOF with abnormal ECG• H/O stents to the RCA and LCX.

Recurrent angina• Angiogram: Patent stents of the

LCX. Occluded stent of the RCA. 100% occlusion of the mid LAD

• Ventriculogram: moderately reduced LV function with anteroapical akinesis

PET Findings• Perfusion/Metabolism mismatch

in the anteroapical, anterolateral and lateral walls, consistent with hibernating, viable myocardium

Outcome • CABG

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Case Study #10Case Study #10Is there viable myocardium in the anterior and Is there viable myocardium in the anterior and lateral walls to justify attempts at lateral walls to justify attempts at revascularization?revascularization?

Rb-82 FDG

History • 64 yo male with anterolateral MI, CHF• Angiography: 100% occlusion mid LAD.

100% occlusion mid LCX. RCA nonobstructive

• Echocardiogram: severely reduced LV function.. Akinesis of the distal septum and apex. Severe hypokinesis of the lateral wall.

PET Findings• Rb-82 perfusion: Severe perfusion defects

distal anterior, apical, lateral walls.• 18-FDG Metabolic study: severe defects

matching rubidium perfusion uptake. Consistent with low probability of viable myocardium

Outcome • Medical management

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Case Study #11Case Study #11 Is there viable myocardium in the anterior wall?Is there viable myocardium in the anterior wall?

Rb-82 FDG

History • 79 y.o. male with acute myocardial

infarction and cardiogenic shock• Coronary Angiography revealed 100%

occlusion of the proximal LAD, and 90% stenosis of the LCX. RCA was non-dominant

• Echo revealed severely reduced LV function with anterior, septal and apical akinesis.

PET Findings• PET study shows severe matching

perfusion defects in the LAD distribution. Viable myocardium present in the lateral and inferior walls (which was jeopardized on angiogram).

Outcome • PCI LCX

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ACC/ASNC Guidelines for ACC/ASNC Guidelines for PET ImagingPET Imaging

Class I

Adenosine or dipyridamole myocardial perfusion PET in patients in whom an appropriately indicated myocardial perfusion SPECT study has been found to be equivocal for diagnostic or risk stratification purposes. (Level of Evidence: B)

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ACC/ASNC Guidelines ACC/ASNC Guidelines for PET Imagingfor PET Imaging

Class IIa

1. Adenosine or dipyridamole myocardial perfusion PET to identify the extent, severity, and location of ischemia as the initial diagnostic test in patients who are unable to exercise. (Level of Evidence: B)

2. Adenosine or dipyridamole myocardial perfusion PET to identify the extent, severity, and location of ischemia as the initial diagnostic test in patients who are able to exercise but have LBBB or an electronically-paced rhythm. (Level of Evidence: B)

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ACC/ASNC Guidelines for ACC/ASNC Guidelines for Viability ImagingViability Imaging

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SummarySummary

• PET MPI: Due to higher energy isotopes, higher resolution and established attenuation correction, PET has superior sensitivity, specificity and accuracy for detecting, and evaluating the significance of CAD.

• PET has a unique and central role in diagnosing CAD in patients with prior equivocal or non-diagnostic non-invasive studies.

• PET metabolic imaging, with 18-FDG allows identification of high risk CAD patients who may benefit from revascularization.

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Andrew Van Tosh, M.DAndrew Van Tosh, M.D..

Associate Professor of Medicine

Albert Einstein College of Medicine

Lab Director, Nuclear Cardiology

Beth Israel Medical Center, New York