Review ArticleDysinnervated but viable myocardium in ischemic heart disease
Introduction
A relationship between sympathetic nerve dysfunction and cardiovascular morbidity and mortality has been recognized for decades yet there has only recently been interest in applying sympathetic nerve imaging to the clinical management of patients with heart disease. With the increasing availability of nuclear tracers of norepinephrine it is likely that in the near future non-invasive imaging of sympathetic function will be translated from the realm of research to the clinical armamentarium. This brief review will focus on sympathetic nerve dysfunction in the setting of coronary artery disease with particular attention to pathophysiology, pre-synaptic molecular imaging, and potential clinical applications. A discussion of technologies for imaging the cardiac sympathetic nervous system can be found in the recent review by Link and Caldwell,1 and a detailed review of PET tracers and receptor ligands has been previously published by Bengel and Schwaiger.2
Section snippets
Pathophysiology of Dysinnervated but Viable Myocardium
There are various pathophysiological explanations for ischemically mediated sympathetic nerve dysfunction in the setting of viable myocardium that are analogous to the continuum of physiologies that occur with ischemia-induced myocardial dysfunction. These can range from complete anatomic denervation following transmural myocardial infarction3 to transient sympathetic nerve dysfunction in association with acute myocardial stunning.4 In this review, we will use “dysinnervation” or sympathetic
Prognostic Potential of Cardiac Sympathetic Imaging—Global or Regional?
There is now ample evidence to support the contention that the imaging of sympathetic nerve function (primarily with MIBG) provides independent prognostic information in patients with heart disease.35 For example, the recently completed ADMIRE-HF trial enrolled 961 subjects with NYHA Class II or III heart failure and left ventricular ejection fraction ≤35%.36 Their primary analysis confirmed that a low MIBG heart-to-mediastinum ratio predicted the time to first cardiac event. This was largely
Acknowledgments
We would like to thank Dr. Markus Schwaiger and Dr. James Caldwell for their contribution of figures, and Anne Coe for her help with the preparation of this manuscript. This study was supported by the National Heart, Lung and Blood Institute (HL-76252 and HL-81722); the Department of Veterans Affairs; and the Albert and Elizabeth Rekate Fund.
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