Cardiac innervation imaging as a risk stratification tool for potential device therapy candidates
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Division of Nuclear Medicine and Molecular Imaging, The Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD Department of Nuclear Medicine/Comprehensive Heart Failure Center, University Hospital ¨ rzburg, Wu ¨ rzburg, Germany Wu
Received Sep 19, 2018; accepted Sep 20, 2018 doi:10.1007/s12350-018-01475-0
As a scintigraphic approach evaluating cardiac nerve integrity, 123I-metaiodobenzylguanidine (123I-mIBG) has been recently Food and Drug Administration approved. A great deal of progress has been made by the prospective ADMIRE-HF trial, which primarily demonstrated the association of denervated myocardium assessed by 123I-mIBG and cardiac events. However, apart from risk stratification, myocardial nerve function evaluated by molecular imaging should also be expanded to other clinical contexts, in particular to guide the referring cardiologist in selecting appropriate candidates for specific therapeutic interventions. In the present issue of the Journal of Nuclear CardiologyÒ, the use of 123I-mIBG for identifying cardiomyopathy patients, which would most likely not benefit from ICD due to low risk of arrhythmias, is described. If we aim to deliver on the promise of cardiac innervation imaging as a powerful tool for risk stratification in a manner similar to nuclear oncology, studies such as the one reviewed here may imply an important step to lay the proper groundwork for a more widespread adoption in clinical practice. Key Words: Heart failure Æ cardiomyopathy Æ SPECT Æ cardiac innervation Æ molecular imaging Æ ICD
See related article, https://doi.org/10.10 07/s12350-018-01467-0. Alterations of the myocardial sympathetic nervous system (SNS) in Heart Failure (HF) patients are primarily driven by cardiac norepinephrine (NE) spillover, which in turn provokes severe damage of
Reprint requests: Rudolf A. Werner, MD, Division of Nuclear Medicine and Molecular Imaging, The Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, 601 N. Caroline St. JHOC 3230, Baltimore, MD 21287; [email protected]; [email protected] J Nucl Cardiol 1071-3581/$34.00 Copyright Ó 2018 American Society of Nuclear Cardiology.
cardiomyocytes, in particular by AMP-mediated calcium overload.1,2 Notably, such a continuous NE oversupply also triggers remodeling of the left ventricle or the development of hypertensive left ventricular hypertrophy.3 On a subcellular level, cardiac alterations of the SNS are reflected by impaired function of the NE transporter (uptake-1 mechanism) and by reduced plasma clearance of NE in the synaptic cleft.1,4 As a physiological rationale, NE is stored inside presynaptic vesicles and if a firing impulse has arrived at the nerve terminal, NE is released into the synaptic gap and provokes further downstream cascades at postsynaptic ßadrenoreceptors to achieve neurotransmission. After completing its primary task at the post-synapse, NE has to undergo a recycling mechanism via the uptake
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