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Aims: MicroRNAs play a role in pathogenic mechanisms leading to heart failure. We measured a panel of 754 miRNAs in the myocardial tissue and in the serum of patients with heart failure with reduced ejection fraction due to dilatative idiopathic cardiomyopathy (DCM, N = 10) or ischaemic cardiomyopathy (N = 3), referred to left ventricular assist device implant. We aim to identify circulating miRNAs with high tissue co‐expression, significantly associated to echocardiographic and haemodynamic measures. Methods and results: We have measured a panel of 754 miRNAs in the myocardial tissue [left ventricular (LV) apex] and in the serum obtained at the same time in a well selected study population of end‐stage heart failure with reduced ejection fraction due to either DCM or ischaemic cardiomyopathy, referred to continuous flow left ventricular assist device implant. We observed moderate agreement for miR‐30d, miR‐126‐3p, and miR‐483‐3p. MiR‐30d was correlated to LV systolic as well as diastolic volumes (r = 0.78, P = 0.001 and r = 0.80, P = 0.005, respectively), while miR‐126‐3p was associated to mPAP and PCWP (r = −0.79, P = 0.007 and r = −0.80, P = 0.005, respectively). Finally, serum miR‐483‐3p had an association with right ventricular end diastolic diameter (r = −0.73, P = 0.02) and central venous pressure (CVP) (r − 0.68 p 0.03). Conclusions: In patients with DCM, few miRNAs are co‐expressed in serum and tissue: They are related to LV remodelling (miR‐30d), post‐capillary pulmonary artery pressure (miR‐126‐3p), and right ventricular remodelling/filling pressures (miR‐483‐3p). Further studies are needed to confirm their role in diagnosis, prognosis or as therapeutic targets in heart failure with reduced ejection fraction. [ABSTRACT FROM AUTHOR]

Left ventricular noncompaction (LVNC) can be defined as a cardiomyopathy characterised by a pattern of prominent trabecular structure and deep intertrabecular recesses, that is thought to be caused by an arrest of normal endomyocardial morphogenesis. Using patient-specific computational modelling, we assessed the cardiac mechanics of five patients with LVNC and compared myocardial stress and pump performance to those of healthy controls. Findings shown that patients with LVNC have impaired left ventricular (LV) function, making it possible that the lack of fibre shortening of noncompacted layer can determine poor heart function. Pronounced end-systolic wall stress on left ventricular wall of patients with LVNC was observed when compared to that of normal hearts, and this may lead to adverse cardiac remodelling and ultimately heart failure. We hereby suggest that computational modelling can be considered as a useful tool to assess the cardiac work and pump performance of LVNC, which are responsible for progressive left ventricular deterioration and poor clinical course. [ABSTRACT FROM AUTHOR]

Purpose: To assess endograft infolding for excessive bird-beak configurations in the aortic arch in relation to hemodynamic variables by quantifying device displacement and rotation of oversized stent-grafts deployed in a phantom model.Methods: A patient-specific, compliant, phantom pulsatile flow model was reconstructed from a patient who presented with collapse of a Gore TAG thoracic endoprosthesis. Device infolding was measured under different flow and pressure conditions for 3 protrusion extensions (13, 19, and 24 mm) of the bird-beak configuration resulting from 2 TAG endografts with oversizing of 11% and 45%, respectively.Results: The bird-beak configuration with the greatest protrusion extension exhibited the maximum TAG device displacement (1.66 mm), while the lowest protrusion extension configuration led to the minimum amount of both displacement and rotation parameters (0.25 mm and 0.6°, respectively). A positive relationship was found between the infolding parameters and the flow circulating in the aorta and left subclavian artery. Similarly, TAG device displacement was positively and significantly (p<0.05) correlated with the pulse pressure for all bird-beak configurations and device sizes. However, no collapse was observed under chronic perfusion testing maintained for 30 days and pulse pressure of 100 mm Hg.Conclusion: These findings suggest that endograft infolding depends primarily on the amount of aortic pulsatility and flow rate and that physiological flows do not necessarily engender hemodynamic loads on the proximal bird-beak segment sufficient to cause TAG collapse. Hemodynamic variables may allow for identification of patients at high risk of endograft infolding and help guide preventive intervention to avert its occurrence. [ABSTRACT FROM AUTHOR]

Dilated cardiomyopathy is a heart disease characterized by both left ventricular dilatation and left ventricular systolic dysfunction, leading to cardiac remodeling and ultimately heart failure. We aimed to investigate the effect of dilated cardiomyopathy on the pump performance and myocardial wall mechanics using patient-specific finite element analysis. Results evinced pronounced end-systolic wall stress on left ventricular wall of patients with dilated cardiomyopathy as compared to that of normal hearts. In dilated cardiomyopathy, both end-diastolic and end-systolic pressure-volume relationships of left ventricle and right ventricle were shifted to the right compared to controls, suggesting reduced myocardial contractility. We hereby propose that finite element analysis represents a useful tool to assess the myocardial wall stress and cardiac work, which are responsible for progressive left ventricular deterioration and poor clinical course. [ABSTRACT FROM AUTHOR]

We report two cases of cardiac transplantation of donor hearts with left anterior descending (LAD) myocardial bridging (MB). In the first case, the diagnosis was done only days after transplant. In the second case, a pre-operative angiography showed evidence of LAD myocardial bridging and the organ was used for a marginal recipient. Both patients tolerated the procedure very well and did not have peri-operative cardiac complications. In this study, MB is discussed and its relationship to rejection of donor hearts is evaluated. In light of the growing demand for donated hearts, and in consideration of the relatively high and often undiagnosed occurrence of MB, a liberalized approach to acceptance of this anatomic variant could be adopted in the selection of donor hearts. Identification of MB in the prospective donor heart should not be an absolute contraindication for transplantation.