Phenotyping heart failure by nuclear imaging of myocardial perfusion, metabolism, and molecular targets

Nuclear imaging techniques can detect and quantify pathophysiological processes underlying heart failure, complementing evaluation of cardiac structure and function with other imaging modalities. Combined imaging of myocardial perfusion and metabolism can identify left ventricle dysfunction caused by myocardial ischaemia that may be reversible after revascularization in the presence of viable myocardium. High sensitivity of nuclear imaging to detect targeted tracers has enabled assessment of various cellular and subcellular mechanisms of heart failure. Nuclear imaging of active inflammation and amyloid deposition is incorporated into clinical management algorithms of cardiac sarcoidosis and amyloidosis. Innervation imaging has well-documented prognostic value with respect to heart failure progression and arrhythmias. Emerging tracers specific for inflammation and myocardial fibrotic activity are in earlier stages of development but have demonstrated potential value in early characterization of the response to myocardial injury and prediction of adverse left ventricular remodelling. Early detection of disease activity is a key for transition from broad medical treatment of clinically overt heart failure towards a personalized approach aimed at supporting repair and preventing progressive failure. This review outlines the current status of nuclear imaging in phenotyping heart failure and combines it with discussion on novel developments.

Automated summary

Nuclear imaging techniques play a significant role in detecting and quantifying pathophysiological processes in heart failure, providing complementary evaluation of cardiac structure and function. It enables the identification of left ventricle dysfunction caused by reversible myocardial ischemia in the presence of viable myocardium. Moreover, nuclear imaging allows assessment of various cellular and subcellular mechanisms of heart failure. It also has value in evaluating cardiac sarcoidosis and amyloidosis, predicting heart failure progression, arrhythmias, and characterizing the response to myocardial injury.