Heart Failure With Normal Ejection Fraction: The Complementary Roles of Echocardiography and CMR Imaging

Abstract

Heart failure with normal ejection fraction (HFNEF), previously referred to as diastolic heart failure, has increased in prevalence as a cause of heart failure, now accounting for up to 50% of all cases. Contrary to initial evidence, the prognostic outlook in HFNEF may be similar to that of heart failure with reduced ejection fraction. According to current consensus statements, the diagnosis of HFNEF requires the demonstration of relatively preserved systolic left ventricular function and evidence of diastolic dysfunction. Noninvasive imaging techniques now permit evaluation of these parameters without need for cardiac catheterization in the large majority of patients. Echocardiography is the modality of choice in the evaluation of diastolic function but suffers from limitations in its assessment of systolic function. Cardiac magnetic resonance (CMR) imaging is the gold standard in the volumetric quantification of systolic function; however, it has limitations in its ability to characterize diastolic function. This report aims to review the strengths and weaknesses of both imaging modalities in the diagnosis of HFNEF. With regards to echocardiography, it will specifically describe limitations in measuring left ventricular ejection fraction, describe novel techniques to assess systolic function such as tissue velocity and strain analysis, and will review the measurements used in the evaluation of diastolic function. With respect to CMR, this review will highlight its value in the assessment of systolic left ventricular function, will review ancillary CMR findings that may support the diagnosis of HFNEF such as tissue characterization, and will provide a brief overview of CMR techniques to assess diastolic function. We propose that these 2 modalities may play a complementary role in the diagnosis of HFNEF. The importance of imaging in the diagnosis of HFNEF extends to both the individual patient and to clinical trials of therapies for this condition.

Clinical relevance of right ventricular diastolic stiffness in pulmonary hypertension

“…Moreover, future studies are needed to provide tools to noninvasively assess RV diastolic function. Currently, the available noninvasive techniques (echocardiography and MRI-measured relaxation velocities and filling patterns) have significant drawbacks (load dependency) which limit the clinical applicability of noninvasive load-independent RV diastolic evaluation [21][22][23]. However, studies on the assessment of diastolic wall strain in patients with left ventricular diastolic dysfunction have shown promising results, making diastolic wall strain a possible future evaluation tool for RV diastolic dysfunction in PAH [24,25].…”

Baseline diastolic dysfunction as a predictive factor of trastuzumab-mediated cardiotoxicity after adjuvant anthracycline therapy in breast cancer

“…Tissue characterization by delayed-enhancement CMR could play a major role in the future, as it may provide better understanding of the mechanisms involved in the occurrence and progression of TMC [7,27,52]. However, the evaluation of diastolic function by CMR still requires validation [53]. In contrast, RNA remains a robust technique for the evaluation of both systolic and diastolic function, with excellent intra-and inter-observer reproducibility.…”

Letter by Barison et al Regarding Article, “Cardiac Magnetic Resonance Postcontrast T1 Time Is Associated With Outcome in Patients With Heart Failure and Preserved Ejection Fraction”

“…In these patients, CMR has indeed become the gold standard method to assess not only biventricular, biatrial, and pericardial morphology, biventricular volumes, and systolic function, but also ultrastructural characterization. 3,4 Nevertheless, the authors did not provide a comprehensive analysis of myocardial tissue characterization: after excluding patients with ischemic heart disease, amyloidosis, and sarcoidosis, as well as myocardial areas with late gadolinium enhancement, they did not mention the presence and extent of late gadolinium enhancement in the study population as a conventional marker of macroscopic myocardial fibrosis compared with the microscopic fibrosis assessed with postcontrast T1 mapping. Moreover, no data about precontrast signal intensity (on T1 mapping, T2 mapping, or T2-short tau inversion recovery imaging) were presented as conventional markers of myocardial edema and ongoing cell damage.…”