4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx

Post Graduate Intern
May. 27, 2023
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx
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4.15.21 NUCLEAR Cardiac Innervation, Sarcoidosis, Amyloidosis - Luna.pptx

Editor's Notes

  1. They may control the stimulatory and inhibitory physiologic effects of each system.
  2. These autonomic nervous systems regulate synthesis and storage of neurotransmitters and their release, reuptake, metabolism, and interaction with presynaptic and postsynaptic receptor sites
  3. Schema of myocardial adrenergic neuronal terminals and various radioligands used to probe adrenergic functions. illustrate representative positron emission tomography (PET) and single-photon emission computed tomography (SPECT) radiotracers to evaluate presynaptic and postsynaptic sympathetic and parasympathetic neuronal functions.
  4. any medications and substrates that may interfere with NE uptake, including opioids, antidepressants, and reserpine, should temporarily be discontinued An increase in sympathetic tone is associated with increased MIBG washout with decreased myocardial uptake
  5. ROIs are drawn in the heart (H) and upper mediastinum (M) in the anterior MIBG image to calculate the H/M ratio.
  6. Although MIBG yields high-quality images of myocardial neuronal function,
  7. I-123 MIBG images of a healthy subject. Planar image (top) and SPECT image (bottom). High MIBG uptake in the myocardium is noted in normal subjects in the anterior planar images. MIBG SPECT shows relatively homogenous distribution in the LV myocardium despite high liver uptake the normal H/M ratio ranged from 2.0 to 2.7 for the early image and from 2.1 to 2.9 for the delayed image.
  8. improvement in cardiac sympathetic nerve activity based on the H/M ratio on MIBG  associated with LV functional recovery and potential improvement in patient outcome improvement of MIBG uptake in relation to LVEF recovery after treatment with angiotensin-converting enzyme inhibitors in patients with HF.
  9. Assessment of adrenergic neuronal function in the myocardium has another important role in various other cardiovascular diseases. SCD due to fatal arrhythmia represents an important problem for health care. To prevent SCD due to fatal arrhythmias, implantable cardioverter- defibrillator (ICD) treatment has been used. it would be important to know whether patient selection for ICD treatment can be improved.
  10. Assessment of adrenergic neuronal function in the myocardium has another important role in various other cardiovascular diseases. SCD due to fatal arrhythmia represents an important problem for health care. To prevent SCD due to fatal arrhythmias, implantable cardioverter- defibrillator (ICD) treatment has been used. it would be important to know whether patient selection for ICD treatment can be improved.
  11. C-11 epinephrine - a radiolabeled true neurotransmitter, and the uptake and storage of this tracer resemble those of NE C-11 phenylephrine - PET tracer that is trapped in neuronal vesicles and metabolized by neuronal monoamine oxidase. Its kinetics may thus reflect MAO metabolism in addition to vesicular leakages HED - most widely used PET tracer for cardiac neuronal imaging. It has high affinity for presynaptic neuronal catecholamine transporter (uptake 1) without being metabolized by monoamine oxidase or catechol-O-methyl-transferase (COMT)
  12. Figure 23.9 HED PET image (top), time activity curve (bottom left), and retention index in each segment (bottom right).
  13. OVERVIEW Primary light-chain (AL) amyloid, amyloid fibrils are formed from immunoglobulin light chains that are produced by a clonal population of plasma cells in the bone marrow. Cardiac transthyretin amyloidosis (ATTR), misfolded monomers or dimers of the normally tetrameric transthyretin protein (TTR) from either mutant TTR (ATTRm) or wild-type TTR (ATTRwt) deposit as amyloid fibrils in the myocardium. ATTRwt is an aging disease predominately described in older adult males (senile systemic amyloidosis), associated with carpal tunnel syndrome, with prevalence of up to 30% in patients with HF with preserved ejection fraction (EF) in those aged 75 years and older (autopsy studies). ATTRm is inherited in an autosomal dominant fashion leading to familial amyloid cardiomyopathy or familial amyloid polyneuropathy and can affect individuals of all ages. Three percent to 4% of African Americans carry an amyloidogenic allele of the human serum protein transthyretin (TTR V122I), which appears to increase risk for cardiac amyloid deposition after 65 years of age.4
  14. The diagnosis of cardiac amyloidosis is challenging due to the variety of presenting symptoms. The signs and symptoms of cardiac amyloidosis often overlap with other causes of HF
  15. Cardiac transthyretin amyloidosis (ATTR),
  16. Transthyretin
  17. Figure 26.1 99mTc pyrophosphate (PYP) scan for the diagnosis of transthyretin cardiac amyloidosis in a 55-year-old female with known diagnosis of familial amyloidosis due to the Ala 60 TTR variant. A subcutaneous abdominal fat pad biopsy was positive for amyloid, indicating amyloid deposition in the tissues. Her history included mild sensory neuropathy, carpal tunnel syndrome, and episodes of dizziness. The LVEF was normal without significant increase in wall thickness on echocardiogram (12 mm). A 99Tc PYP SPECT scan showed diffuse intense uptake in the heart, confirming cardiac amyloidosis.
  18. Several noninvasive imaging tests can be used in cardiac amyloidosis
  19. Cardiac sarcoidosis is a form of focal myocardial inflammation that can be well imaged with cardiac MRI or radionuclide methods.
  20. . In the fasting state, free fatty acids account for up to 90% of oxygen consumption of normal myocytes as opposed to glucose utilization in the postprandial state.
  21. 13N-ammonia and 18F-FDG PET/CT imaging at baseline, after 6 months of therapy, and at 18 months. These images were obtained in a 52-year-old woman with episodes of rapidly progressing symptoms of dizziness and syncope with complete heart block necessitating pacemaker implantation. On her pacemaker interrogation she was found to have 22 episodes of nonsustained ventricular tachycardia. She underwent 18F-FDG CT for evaluation of possible sarcoidosis. These figures show baseline 13N- ammonia and 18F-FDG images with and without attenuation correction, in alternate rows displayed in SA, VLA, and HLA images along with partial whole-body 18F-FDG images in gray and color scale, in the coronal and sagittal views. On the baseline images (A), there is a small, severe perfusion defect involving the basal anterior septum, with evidence of mildly increased 18F-FDG uptake (perfusion–metabolic mismatch). There is a second small and severe perfusion defect involving the apical septal and inferior LV segments (perfusion–metabolic mismatch). The partial whole-body images show areas of 18F-FDG uptake in the myocardium (arrows) and multiple 18F-FDG–avid foci within the liver and spleen consistent with sarcoid. The patient underwent endomyocardial biopsy, which confirmed the diagnosis of cardiac sarcoidosis. Her pacemaker was upgraded to an implantable cardioverter-defibrillator for prevention of sudden cardiac death.
  22. 13N-ammonia and 18F-FDG images after 6 months of high-dose steroid therapy. There is a small and moderate- severity perfusion defect in the basal anterior septum and a small and severe perfusion defect involving the apical septum with no focal myocardial 18F-FDG uptake (only blood-pool activity). The absence of myocardial 18F-FDG uptake in the regions with previously increased 18F- FDG uptake (basal anterior septum and the apical septum) suggests an interval decrease in myocardial inflammation, and perfusion defect suggests fibrosis. Partial whole-body 18F-FDG images in gray and color demonstrate no focal 18F-FDG uptake within the myocardium, liver, or lungs. Steroid therapy was discontinued.
  23. Follow-up images after 18 months off of steroid therapy. On 13N-ammonia and 18F-FDG images there is a region of myocardial scar in the basal antero-septal and infero-septal walls that might represent burnt-out sarcoid. There is also a focal region of active inflammation in the apical septum and the apical inferior wall (perfusion defect with 18F-FDG uptake) suggestive of myocardial inflammation. Partial whole-body 18F-FDG images show multiple new foci of increased hepatic radiotracer uptake that may represent active hepatic sarcoidosis.
  24. 67Gallium SPECT and 18F-FDG PET/CT imaging in a patient with cardiac sarcoidosis. These images, obtained 2 years apart, show the improved spatial resolution of 18F-FDG PET/CT imaging when compared to 67Gallium SPECT(compare the left two columns).
  25. Three serial exams of PET with FDG over 25 months from a 46-year-old man with cardiac sarcoidosis treated with corticosteroids are shown. The color maps demonstrate the intensity of FDG uptake in a coronal view. The gray-scale images demonstrate serial perfusion images using 82- rubidium (top) and metabolism images using FDG (bottom) in three distinct axes at approximately the same location. For each scan, the measurements of LV ejection fraction, standard uptake value (SUV) maximum, and SUV volumes are displayed. Demonstrated is the serial decline in myocardial inflammation and rise in LVEF with therapy.