Disclaimer:The ESC Guidelines represent the views of the ESC and were produced after careful consideration of the scientific and medical knowledge and the evidence available at the time of their publication. The ESC is not responsible in the event of any contradiction, discrepancy, and/or ambiguity between the ESC Guidelines and any other official recommendations or guidelines issued by the relevant public health authorities, in particular in relation to good use of healthcare or therapeutic strategies. Health professionals are encouraged to take the ESC Guidelines fully into account when exercising their clinical judgement, as well as in the determination and the implementation of preventive, diagnostic, or therapeutic medical strategies; however, the ESC Guidelines do not override, in any way whatsoever, the individual responsibility of health professionals to make appropriate and accurate decisions in consideration of each patient's health condition and in consultation with that patient and, where appropriate and/or necessary, the patient's caregiver. Nor do the ESC Guidelines exempt health professionals from taking into full and careful consideration the relevant official updated recommendations or guidelines issued by the competent public health authorities, in order to manage each patient's case in light of the scientifically accepted data pursuant to their respective ethical and professional obligations. It is also the health professional's responsibility to verify the applicable rules and regulations relating to drugs and medical devices at the time of prescription.

CHF is associated with marked insulin resistance, characterized by both fasting and stimulated hyperinsulinemia. Advanced heart failure (in terms of reduced peak VO2) is related to increased insulin resistance, but this is not directly mediated through ventricular dysfunction or increased catecholamine levels.

Peripheral loss of muscle tissue is a general finding in chronic heart failure. The wasting in cardiac cachexia affects all tissue compartments and is significantly related to neurohormonal and immunological abnormalities.

There is an inverse relationship between serum uric acid concentrations and measures of functional capacity in patients with cardiac failure. The strong correlation between serum uric acid and MVO2 suggests that in chronic heart failure, serum uric acid concentrations reflect an impairment of oxidative metabolism.

Di Marco, A. et al. (2017) Late gadolinium enhancement and the risk for ventricular arrhythmias or sudden death in dilated cardiomyopathy: systematic review and meta-analysis. JACC: Heart Failure, 5(1), pp. 28-38. (doi:10.1016/j.jchf.2016.09.017) This is the author's final accepted version.There may be differences between this version and the published version. You are advised to consult the publisher's version if you wish to cite from it.http://eprints.gla.ac.uk/133553/ Background: Risk stratification for SCD in DCM needs to be improved.

changes within the RV that are associated with adverse surgical outcomes and poorer prognosis following mitral valve surgery. Future studies are needed to confirm whether LGE is a new imaging biomarker that can be used to risk stratify severe asymptomatic MR patients for surgery. Abstract 110 Table 1 Features of patients with and without gadolinium enhancement Late gadolinium enhancement Number of patients MR fraction (%) Systolic RV volume (ml/ m 2) RV ejection fraction (%) Peak VO 2 (ml/ kg/min) VE/ VCO 2 None 43 32±12 28.5±7.7 61±8 24.6±6.9 31.1 ±5.0 RV insertion gadolinium 8 46±17* 31.4±7.6* 55±6* 23.1±8.7 33.2 ±3.2* LV myocardial gadolinium 10 42±19* 35.1±11.1* 55±8* 23.0±5.9 36.7 ±6.9* *denotes statistical significance of P0.05 compared to non-gadolinium cohort on Independent samples 2 tailed T-Test Abstract 110 Figure 1 Late gadolinium enhancement of the basal inferolateral LV

In patients with CHF, lower S(I) relates to higher mortality, independent of body composition and established prognosticators. Impaired S(I) may have implications in the pathophysiology of CHF disease progression. Therapeutically targeting impaired insulin sensitivity may potentially be beneficial in patients with CHF.

No abstract