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The extent of myocardial fibrosis is independently associated with lack of response to medical therapy in new-presentation DCM, and LGE-CMR may thus be an important risk-stratifying investigation in these patients. Accurate risk stratification may permit more targeted pharmacological and device therapies for patients with newly diagnosed DCM.

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Group 3 pulmonary hypertension (PH) is a common complication of chronic lung disease (CLD), including chronic obstructive pulmonary disease (COPD), interstitial lung disease, and sleep-disordered breathing. Development of PH is associated with poor prognosis and may progress to right heart failure, however, in the majority of the patients with CLD, PH is mild to moderate and only a small number of patients develop severe PH. The pathophysiology of PH in CLD is multifactorial and includes hypoxic pulmonary vasoconstriction, pulmonary vascular remodeling, small vessel destruction, and fibrosis. The effects of PH on the right ventricle (RV) range between early RV remodeling, hypertrophy, dilatation, and eventual failure with associated increased mortality. The golden standard for diagnosis of PH is right heart catheterization, however, evidence of PH can be appreciated on clinical examination, serology, radiological imaging, and Doppler echocardiography. Treatment of PH in CLD focuses on management of the underlying lung disorder and hypoxia. There is, however, limited evidence to suggest that PH-specific vasodilators such as phosphodiesterase-type 5 inhibitors, endothelin receptor antagonists, and prostanoids may have a role in the treatment of patients with CLD and moderate-to-severe PH.

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.

Background: Iron deficiency (ID) has a prevalence of ≈40% to 50% among patients in heart failure (HF) with reduced ejection fraction and is associated with worse prognosis. Several trials demonstrated that intravenous ferric carboxymaltose leads to early and sustained improvement in patient-reported outcomes and functional capacity in patients with HF with reduced ejection fraction with ID, yet morbidity and mortality data are limited. Methods: The objective of the HEART-FID trial (Ferric Carboxymaltose in Heart Failure With Iron Deficiency) is to assess efficacy and safety of ferric carboxymaltose compared with placebo as treatment for symptomatic HF with reduced ejection fraction with ID. HEART-FID is a multicenter, randomized, double-blind, placebo-controlled trial enrolling ≈3014 patients at ≈300 international centers. Eligible patients are aged ≥18 years in stable chronic HF with New York Heart Association functional class II to IV symptoms, ejection fraction ≤40%, ID (ferritin <100 ng/mL or ferritin 100–300 ng/mL with a transferrin saturation <20%), and documented HF hospitalization or elevated N-terminal pro-brain natriuretic peptide. Consented patients are assigned to ferric carboxymaltose or placebo at baseline, with repeated visits/assessments every 6 months for additional study drug based on hemoglobin and iron indices for the trial duration. The primary end point is a hierarchical composite of death and HF hospitalization at 12 months and change from baseline to 6 months in the 6-minute walk test distance. Conclusions: The HEART-FID trial will inform clinical practice by clarifying the role of long-term treatment with intravenous ferric carboxymaltose, added to usual care, in ambulatory patients with symptomatic HF with reduced ejection fraction with ID. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03037931.

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