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MR studies of left ventricular remodeling
Magma: Magnetic Resonance Materials in Physics, Biology, and Medicine, 1998Already during the last century, the importance of structurally remodeled tissue has been recognized. In recent animal studies, it has convincingly been shown that large myocardial infarction which causes left ventricular dysfunction is followed by a remodeling process of the left ventricle.
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Surgical methods to reverse left ventricular remodeling
Current Heart Failure Reports, 2007Heart transplantation remains the gold standard treatment for "end-stage" dilated cardiomyopathy. However, its epidemiologic impact on the heart failure problem continues to be small due to limited donor organ availability and contraindications. Therefore, several "conventional" surgical procedures have been developed to reverse the vicious cycle of ...
DE BONIS , MICHELE, ALFIERI , OTTAVIO
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Left ventricular remodeling: clinical significance and therapy
Basic Research in Cardiology, 1997Myocardial infarction (MI) is a major cause of morbidity and mortality in developed countries. However, significant advances have been made over the past 25 years decreasing its in-hospital and long term death rate and complications. The routine use of thrombolysis, aspirin, and beta blockers has led to significant improvement in the prognosis of ...
A, Rosado, G A, Lamas
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[Left ventricular remodelling].
Cardiologia (Rome, Italy), 1991An acute myocardial infarction, particularly one that is large and transmural, can produce expansion and alterations in the topography of both the infarcted and non-infarcted regions or the ventricle. This remodelling can importantly affect the function of the ventricle and the prognosis. Side-to-side slippage of myocytes in the myocardium occurring in
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Nitrates and Left Ventricular Remodeling
The American Journal of Cardiology, 1998Left ventricular remodeling is the major mechanism leading to cardiac enlargement, failure, and death after myocardial infarction. It is associated with early disruption of collagen matrix and expansion of the infarct zone (IZ) followed by progressive global ventricular dilation, hypertrophy of the noninfarct zone (NIZ), and further global dysfunction.
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Drugs for Left Ventricular Remodeling in Heart Failure
The American Journal of Cardiology, 2005Left ventricular (LV) remodeling (ie, enlargement and functional deterioration occurring over time) is among the main mechanisms of progression in heart failure (HF). LV dilatation and dysfunction are major negative prognostic markers in patients with HF.
Maria, Frigerio, Elena, Roubina
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The genetics of left ventricular remodeling in competitive athletes
Journal of Cardiovascular Medicine, 2006Left ventricular (LV) remodeling in competitive athletes is a complex phenomenon, in which genetic and environmental determinants are implicated. In recent years, several investigations have demonstrated an association between LV remodeling and the angiotensin-converting enzyme (ACE I/D) and/or angiotensinogen (AGT M/T) polymorphism, with athletes with
Antonio, Pelliccia, Paul D, Thompson
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Left ventricular remodeling in chronic aortic regurgitation
The International Journal of Cardiac Imaging, 1993Left ventricular (LV) shape in chronic volume overload due to aortic regurgitation is commonly described as rounder than in normal subjects. This statement derives from observations of qualitative nature or based on the measure of eccentricity index. We analyzed LV shape and function in 16 normal subjects (N) and in 24 patients with chronic pure aortic
G. BARLETTA +4 more
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Stretch-activated pathways and left ventricular remodeling
Journal of Cardiac Failure, 2002Stretch of cardiomyocytes in vivo occurs in response to a number of stimuli, including pressure or volume overload, but it is most clearly seen following relatively large, acute myocardial infarctions. It is in this setting that stretch is most clearly related to the pathogenesis of heart failure.
Thomas, Force +3 more
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Gp130-mediated pathway and left ventricular remodeling
Journal of Cardiac Failure, 2002The binding of ligands to gp130 activates the JAK/STAT pathway, where STAT3 plays a central role in transmitting signals from the membrane to the nucleus. Cardiac-specific disruption of gp130 was shown to present heart failure in response to mechanical stress accompanied by an increase in apoptosis.
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