Imaging of cardiac sympathetic activity in heart failure: Not out of the woods yet

Excerpt

Currently, 5.7 million people are living with heart failure (HF) in the U.S., and given the aging of the population, the prevalence of HF continues to grow.1 In addition, HF is the leading cause of hospitalizations in people over the age of 65, thereby posing an increasing problem for global healthcare systems.2 In view of this burden, risk-based, personalized therapeutic strategies and a cost-effective management for patients with HF are needed. However, despite notable improvements in medical therapy, outcomes for HF patients are still unacceptable and precise risk stratification in HF remains challenging.2 In fact, various prognostic markers of mortality and morbidity of HF have been identified; however, their clinical applicability is limited. Similarly, tools contributing to the appropriate selection of therapeutic strategies or monitoring their efficacy are lacking. There is accumulating evidence that imaging of cardiac sympathetic activity by ¹²³I-metaiodobenzylguanidine (mIBG), a sympathetic neurotransmitter radionuclide analog (Figure 1), may help to direct therapy and clinical decision-making in HF patients. Indeed, given that dysfunction of the sympathetic nervous system is one of the key features of worsening systolic HF, pharmacological and non-pharmacological targeting of sympathetic dysfunction has emerged as a promising treatment strategy in HF.2 Accordingly, ¹²³I-mIBG imaging has been shown to have an incremental prognostic value in predicting disease progression, arrhythmic events, and cardiac death in HF patients beyond that provided by traditional functional and neurohormonal markers.3 However, despite its prognostic importance and its FDA approval for cardiac applications in 2013, the exact role of cardiac neuronal imaging in diagnosis and management of HF is still under debate, and therefore, ¹²³I-mIBG scintigraphy is currently mostly applied as a research tool.

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