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BACKGROUND Myocardial fibrosis is a hallmark of hypertrophic cardiomyopathy and a proposed substrate for arrhythmias and heart failure. In animal models, profibrotic genetic pathways are activated early, before hypertrophic remodeling. Data showing early profibrotic responses to sarcomere-gene mutations in patients with hypertrophic cardiomyopathy are(More)
Changes in the composition of cardiac tissue develop in arterial hypertension and lead to structural remodeling of the myocardium. Structural remodeling is the consequence of a number of pathologic processes, mediated by mechanical, neurohormonal and cytokine routes, occurring in the cardiomyocyte and the noncardiomyocyte compartments of the heart. One of(More)
This study was designed to evaluate the association between circulating biomarkers of collagen metabolism and elevated left-sided filling pressures (FPs), as assessed from elevated estimated pulmonary capillary wedge pressure (ePCWP), in hypertensive patients with heart failure with normal ejection fraction. Echocardiography was performed and ePCWP was(More)
OBJECTIVE This study was designed to investigate whether plasma concentration of cardiotrophin-1 (CT-1), a cytokine that induces cardiomyocyte hypertrophy and stimulates cardiac fibroblasts, is related to hypertensive heart disease, as defined by the presence of echocardiographically assessed left ventricular hypertrophy (LVH). METHODS The study was(More)
A lterations of the structure and composition of cardio-myocyte and noncardiomyocyte compartments of the myocardium appear to play a central role in the pathogenesis of heart failure (HF) associated with a number of cardiac diseases. Among these alterations, changes in the quantity and quality of the extracellular matrix, including the collagen network,(More)
BACKGROUND This study was designed to investigate whether myocardial collagen content is related to myocardial stiffness in patients with essential hypertension. METHODS AND RESULTS The study was performed in 34 patients with hypertensive heart disease. Nineteen of these patients were also evaluated after 12 months of treatment with losartan. Transvenous(More)
The heart is a remarkably adaptive organ, capable of increasing its minute output and overcoming short-term or prolonged pressure overload. The structural response, in addition to the foregoing functional demands, is that of myocardial hypertrophy. Then, why should an adaptive response increase cardiovascular risk in hypertensive patients with left(More)
Because of its dynamic nature, the composition and structure of the myocardial collagen network can be reversibly modified to adapt to transient cardiac injuries. In response to persistent injury, however, irreversible, maladaptive changes of the network occur leading to fibrosis, mostly characterized by the excessive interstitial and perivascular(More)
PURPOSE OF REVIEW The potential contribution of alterations in matrix metalloproteinase activity to the development of myocardial fibrosis in hypertensive heart disease is reviewed. RECENT FINDINGS A number of experimental and clinical studies provide information on alterations in the balance between matrix metalloproteinase-1 or collagenase and tissue(More)
OBJECTIVE We investigated whether regression of left ventricular hypertrophy (LVH) in response to antihypertensive treatment is associated with plasma cardiotrophin-1 (CT-1) in hypertensive patients. METHODS The study was performed in 47 patients with mild to moderate essential hypertension, and LVH was assessed echocardiographically. The family doctor(More)