Left Ventricular Flow Analysis: Novel Imaging Biomarkers and Predictors of Exercise Capacity in Heart Failure.

Background: Cardiac remodeling, after a myocardial insult, often causes progression to heart failure. The relationship between alterations in left ventricular blood flow, including kinetic energy (KE), and remodeling is uncertain. We hypothesized that increasing derangements in left ventricular blood flow would relate to (1) conventional cardiac remodeling markers, (2) increased levels of biochemical remodeling markers, (3) altered cardiac energetics, and (4) worsening patient symptoms and functional capacity. Methods: Thirty-four dilated cardiomyopathy patients, 30 ischemic cardiomyopathy patients, and 36 controls underwent magnetic resonance including 4-dimensional flow, BNP (brain-type natriuretic peptide) measurement, functional capacity assessment (6-minute walk test), and symptom quantification. A subgroup of dilated cardiomyopathy and control subjects underwent cardiac energetic assessment. Left ventricular flow was separated into 4 components: direct flow, retained inflow, delayed ejection flow, and residual volume. Average KE throughout the cardiac cycle was calculated. Results: Patients had reduced direct flow proportion and direct-flow average KE compared with controls (P<0.0001). The residual volume proportion and residual volume average KE were increased in patients (P<0.0001). Importantly, in a multiple linear regression model to predict the patient’s 6-minute walk test, the independent predictors were age (β=−0.3015; P=0.019) and direct-flow average KE (β=0.280, P=0.035; R2 model, 0.466, P=0.002). In contrast, neither ejection fraction nor left ventricular volumes were independently predictive. Conclusions: This study demonstrates an independent predictive relationship between the direct-flow average KE and a prognostic measure of functional capacity. Intracardiac 4-dimensional flow parameters are novel biomarkers in heart failure and may provide additive value in monitoring new therapies and predicting prognosis.This study was supported by the British Heart Foundation [grant number FS/12/14/29354 to VMS]; Medical Research Council (ATH); Oxford British Heart Foundation Centre of Research Excellence (ATH and SN); Sir Henry Dale Fellowship from the Wellcome Trust and the Royal Society (098436/Z/12/B to CTR); National Institute for Health Research Oxford Biomedical Research Centre Programme (SN and SGM); Swedish Research Council (PD and TE); the Swedish Heart and Lung Foundation [grant number 20140398 to CJC]. The research leading to these results has received funding from the European Union's Seventh Framework Programme (FP7/2007-2013) under grant agreement 310612 to TE