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

Abstract

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 ischemia 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 remodeling. 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.

Role of cardiac imaging in management of heart failure

“…When there are perfusion defects during stress but not at rest, it indicates reversible ischemia, while fixed defects indicate a myocardial infarction [ 62 ]. Moreover, a combination of perfusion and metabolic imaging can detect dysfunctional but potentially recoverable ischemic heart tissue, which may regain contractile function after revascularization [ 63 ]. The presence of preserved or increased uptake of 18F- Fluorodeoxyglucose (FDG) alongside reduced resting myocardial perfusion, referred to as flow-metabolism mismatch, strongly suggests the possibility of regional functional recovery after revascularization [ 64 ].…”

“…Nuclear techniques are also valuable for diagnosing cardiac amyloidosis. Scintigraphy with bone- avid radiotracers, 99m Tc-pyrophosphate (PYP), 99m Tc-3,3-diphosphono-1,2-propanodiacarboxylic acid (DPD), and 99m Tc-hydroxymethylene diphosphonate (HMDP), which bind to microcalcification associated with transthyretin fibrils, is used to identify transthyretin amyloid cardiomyopathy (ATTR-CM) [ 63 ]. Given the relatively common occurrence of transthyretin amyloid cardiomyopathy (ATTR-CM) and cardiac involvement in amyloid light-chain amyloidosis, patients with HFpEF should be screened for cardiac amyloidosis under certain circumstances.…”

“…These circumstances include increased LV wall thickness with no other explanation, a granular sparkling texture of the myocardium, bi-atrial enlargement and pericardial effusion, reduced LV GLS with apical sparing, and bilateral carpal tunnel syndrome [65][66][67]. Scans are analyzed semi-quantitatively or by visual grading, myocardial uptake of the tracer equal or higher than in the ribs (Grades 2 and 3) indicating the presence of ATTR [63].…”

Cardiovascular imaging in personalized medicine: focus issue on phenotyping heart failure

“…Separate state of the art articles addresses the utility of each of these modalities. 2 , 3 , 4 An additional article reviews methods to use when implementing clinical practice guidelines for management of HF. 5 Due to recent developments in therapy for HF with preserved EF, a separate state of the art article addresses use of imaging to guide treatment choices in these patients.…”