298 research outputs found

    Myocardial fibrosis as a key determinant of left ventricular remodeling in idiopathic dilated cardiomyopathy: a contrast-enhanced cardiovascular magnetic study

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    In idiopathic dilated cardiomyopathy, there are scarce data on the influence of late gadolinium enhancement (LGE) assessed by cardiovascular magnetic resonance on left ventricular (LV) remodeling

    Sequence of penalties method to study excited states using VQE

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    We propose an extension of the Variational Quantum Eigensolver (VQE) that leads to more accurate energy estimations and can be used to study excited states. The method is based on the introduction of a sequence of increasing penalties in the cost function. This approach does not require circuit modifications and thus can be applied with no additional depth cost. Through numerical simulations, we show that we are able to produce variational states with desired physical properties, such as total spin and charge. We assess its performance both on classical simulators and on currently available quantum devices, calculating the potential energy curves of small molecular systems in different physical configurations. Finally, we compare our method to the original VQE and to another extension, obtaining a better agreement with exact simulations for both energy and targeted physical quantities.Comment: 11 pages, 9 figures, accepted in IOP Quantum Science and Technolog

    Leiomyosarcoma of the inferior vena cava in a patient with Budd-Chiari syndrome.

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    A 65-year-old man with no history of cardiovascular disease was admitted because of abdominal pain, nausea and lower limb edema. At clinical examination he presented hepatomegaly, ascites and laboratory evidence of liver failure. The echocardiogram (Figure 1A) showed preserved biventricular function, but a large irregular mass was visible in the right atrium (arrow; Supplementary data, Movie 1 and 2). Computed tomography (Figure 1B) showed patchy contrast uptake and positron emission tomography (Figure 1C) showed pathological uptake of 18-fluoro-deoxyglucose in the mass (arrow), extending along the inferior vena cava (arrowheads), suggesting a neoplastic nature. At cardiovascular magnetic resonance (Figure 1D and E; Supplementary data, Movie 3 and 4) the mass involved the right atrium (arrow) and extended into the inferior vena cava (arrowheads); moreover, it presented irregular contours and signal characteristics typical of a neoplastic mass

    Restrictive cardiomyopathy: definition and diagnosis

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    Restrictive cardiomyopathy (RCM) is a heterogeneous group of diseases characterized by restrictive left ventricular pathophysiology, i.e. a rapid rise in ventricular pressure with only small increases in filling volume due to increased myocardial stiffness. More precisely, the defining feature of RCM is the coexistence of persistent restrictive pathophysiology, diastolic dysfunction, non-dilated ventricles, and atrial dilatation, regardless of ventricular wall thickness and systolic function. Beyond this shared haemodynamic hallmark, the phenotypic spectrum of RCM is wide. The disorders manifesting as RCM may be classified according to four main disease mechanisms: (i) interstitial fibrosis and intrinsic myocardial dysfunction, (ii) infiltration of extracellular spaces, (iii) accumulation of storage material within cardiomyocytes, or (iv) endomyocardial fibrosis. Many disorders do not show restrictive pathophysiology throughout their natural history, but only at an initial stage (with an evolution towards a hypokinetic and dilated phenotype) or at a terminal stage (often progressing from a hypertrophic phenotype). Furthermore, elements of both hypertrophic and restrictive phenotypes may coexist in some patients, making the classification challenge. Restrictive pathophysiology can be demonstrated by cardiac catheterization or Doppler echocardiography. The specific conditions may usually be diagnosed based on clinical data, 12-lead electrocardiogram, echocardiography, nuclear medicine, or cardiovascular magnetic resonance, but further investigations may be needed, up to endomyocardial biopsy and genetic evaluation. The spectrum of therapies is also wide and heterogeneous, but disease-modifying treatments are available only for cardiac amyloidosis and, partially, for iron overload cardiomyopathy

    Valvular heart disease in patients with cardiac amyloidosis

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    : Cardiac amyloidosis (CA) is an underdiagnosed condition caused by the deposition of misfolded proteins, namely immunoglobulin light chains and transthyretin, in the extracellular spaces of the heart. Any cardiovascular structure can be affected by amyloid infiltration, including the valves. Amyloid accumulation within the cardiac valves may lead to their structural and functional impairment, with a profound impact on patients' prognosis and quality of life. The most common forms of valvular disease in CA are aortic stenosis (AS), mitral regurgitation (MR), and tricuspid regurgitation (TR). CA and AS share similar risk factors, disease mechanisms, and remodeling patterns, which make their diagnosis particularly challenging. Patients with both CA and AS experience worse outcomes than CA or AS alone, and transcatheter aortic valve replacement may represent a useful therapeutic strategy in this population. Data on MR and TR are quite limited and mainly coming from case reports or small series. This review paper will summarize our current understanding on the epidemiology, disease mechanisms, echocardiographic features, clinical implications, and therapeutic options of AS, MR, and TR in patients with CA
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