Abstract
Heart failure, which is responsible for a high number of deaths worldwide, can develop due to chronic hypertension. Heart failure can involve and progress through several different pathways, including: fibrosis, inflammation, and angiogenesis. Early and specific detection of changes in the myocardium during the transition to heart failure can be made via the use of molecular imaging techniques, including positron emission tomography (PET). Traditional cardiovascular PET techniques, such as myocardial perfusion imaging and sympathetic innervation imaging, have been established at the clinical level but are often lacking in pathway and target specificity that is important for assessment of heart failure. Therefore, there is a need to identify new PET imaging markers of inflammation, fibrosis and angiogenesis that could aid diagnosis, staging and treatment of hypertensive heart failure. This review will provide an overview of key mechanisms underlying hypertensive heart failure and will present the latest developments in PET probes for detection of cardiovascular inflammation, fibrosis and angiogenesis. Currently, selective PET probes for detection of angiogenesis remain elusive but promising PET probes for specific targeting of inflammation and fibrosis are rapidly progressing into clinical use.
Highlights
Heart failure is one of the leading causes of death worldwide with ∼35% risk of death within the first year after diagnosis [1,2,3]
The variety of pathways and radiotracers included in this review indicates that positron emission tomography (PET) radiotracers explored for one type of pathology have the potential to become valuable tools in other conditions where the same pathways are involved
In addition to perfusion measurements, most cardiovascular PET imaging studies focus on assessing myocardial metabolism and viability using 18F-FDG, a marker of glucose metabolism that has over 90% accuracy for prediction of future recovery of myocardial function [60, 61]
Summary
Heart failure is one of the leading causes of death worldwide with ∼35% risk of death within the first year after diagnosis [1,2,3]. Changes in signals from the autonomic nervous system can affect progression of heart failure, with an associated increase in sympathetic drive shown to be worsening the condition, whereas parasympathetic activity has been suggested to be cardioprotective [70, 71] The integrity of both can be investigated with PET radiotracers. It has been used to visualize sympathetic nerves in the heart, focusing on the reuptake of norepinephrine at nerve terminals, and this could be a useful way to investigate the increased sympathetic drive in heart failure [72] Another radiotracer that targets sympathetic innervation is 18F-LMI1195 {N-[3-bromo-4-(3-18F-fluoro-propoxy)-benzyl]-guanidine}, which provides an option with a longer half-life compared to 11C- mHED, while investigating the same area of physiology. That this radiotracer when used in a mouse model of myocardial infarction was not successful at mapping presynaptic norepinephrine transporters, important
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