Publications by authors named "H Turto"

Background And Aim Of The Study: Myocardial fibrosis predisposes to heart failure in aortic valve stenosis. The study aim was to determine the value of: (i) circulating collagen metabolites as biomarkers of left ventricular fibrosis and heart failure in aortic stenosis; and (ii) myocardial fibrosis as a predictor of postoperative outcome.

Methods: Among a total of 132 patients (mean age 68 +/- 10 years) with severe aortic stenosis, measurements were made of circulating N-terminal propeptide of procollagen I (PINP), C-terminal telopeptide of collagen I (CITP) and N-terminal propeptide of procollagen III (PIIINP).

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Apelin is a newly discovered inotropic peptide tentatively linked up with the pathophysiology of heart failure (HF). To further assess the role of apelin in HF, we measured its transcardiac arteriovenous gradients in patients with left ventricular pressure overload with or without HF and in patients with structurally normal hearts. Blood samples from the aortic root and coronary sinus were drawn from 49 adult patients undergoing preoperative cardiac catheterization for severe aortic valve stenosis (AS).

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The pathogenesis of aortic valve stenosis (AS) is characterized by the accumulation of LDL-derived cholesterol in the diseased valves. Since LDL particles also contain plant sterols, we investigated whether plant sterols accumulate in aortic valve lesions. Serum samples were collected from 82 patients with severe AS and from 12 control subjects.

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Aims: In aortic stenosis (AS), adverse remodelling of the valves may depend on altered local regulation of pro- and antifibrotic systems. We have recently shown that angiotensin-converting enzyme (ACE), which generates profibrotic angiotensin II and inactivates antifibrotic bradykinin (BK), is upregulated in stenotic aortic valves. Here, we analyse the expression of neutral endopeptidase (NEP), another profibrotic and BK-degrading enzyme, and of BK receptors in aortic valves in AS.

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Objective: To examine the role of the complement system, a source of powerful proinflammatory mediators, in aortic valve stenosis (AS).

Methods And Results: Stenotic aortic valves (n=24) were obtained at valve replacement surgery, and non-stenotic (n=12) and early sclerotic (n=4) valves at cardiac transplantations. The terminal complement complex C5b-9 was stained by immunohistochemistry.

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