CRT response is dictated by correction of multiple independent mechanisms of which LVDYS is only one. Long-axis DYS measurements alone failed to detect 40% of responders.

Cardiovascular Magnetic Resonance (CMR) is recognised as a valuable clinical tool which in a single scan setting can assess ventricular volumes and function, myocardial fibrosis, iron loading, flow quantification, tissue characterisation and myocardial perfusion imaging.The advent of CMR using extrinsic and intrinsic contrast-enhanced protocols for tissue characterisation have dramatically changed the non-invasive work-up of patients with suspected or known cardiomyopathy.Although the technique initially focused on the in vivo identification of myocardial necrosis through the late gadolinium enhancement (LGE) technique, recent work highlighted the ability of CMR to provide more detailed in vivo tissue characterisation to help establish a differential diagnosis of the underlying aetiology, to exclude an ischaemic substrate and to provide important prognostic markers.The potential application of CMR in the clinical approach of a patient with suspected non-ischaemic cardiomyopathy is discussed in this review.

Low-dose DSE increases and unmasks LBBB-induced dyssynchronous motion, easing its detection. The degree of clinical and echocardiographic response correlated with the extent of peak SF seen during low-dose DSE.

Changes in left atrial function due to hypertensive diastolic impairment are best reflected by LAVCONDUIT expansion. Hypertensive atrial dilatation is related to increase in PVREVERS. Left atrial S/SR offers a clinically valuable approach to detecting subclinical atrial dysfunction.

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In this large population, S' and RVFAC were sometimes discrepant, supporting the need for a multiparametric approach when evaluating RV function. Among seven less validated criteria, IVA and 2D strain had the best diagnostic value. Unlike 2D strain, IVA was not influenced by loading conditions.

Our study suggests that the biphasic SVP in the free walls is probably caused by interventricular interaction. Therefore the timing of maxima on SVP should be used with great caution when looking for intraventricular dyssynchrony as the peaks are influenced by RV function.

Decreased myocardial function results in a more symmetrical outflow, while very asymmetrical traces suggest increased contractility, potentially inducing intra-cavity gradients during DSE. Therefore, including outflow symmetry as a clinical measurement provides additional information on patients with CAD.