نتایج جستجو برای: myocardial hypertrophy
تعداد نتایج: 194363 فیلتر نتایج به سال:
Background Structural myocardial changes accompany myocardial pathologies such as myocardial ischemia, myocarditis, hypertrophy (HCM) and myocardial remodeling. These changes affect T2 relaxation times which can noninvasively be detected by cardiovascular magnetic resonance imaging (CMR). Since the interpretation of T2 weighted images remains a “risky business” due to subjectivity, the purpose ...
Background—Diet-induced obesity is associated with metabolic heart disease characterized by left ventricular hypertrophy and diastolic dysfunction. Polyphenols such as resveratrol and the synthetic flavonoid derivative S17834 exert beneficial systemic and cardiovascular effects in a variety of settings including diabetes mellitus and chronic hemodynamic overload. Methods and Results—We characte...
Postinfarct cardiac hypertrophy is an independent risk factor for heart failure and sudden death. Regression of cardiac hypertrophy has emerged as a promising strategy in the treatment of myocardial infarction (MI). Here we hypothesized that frizzled1 (FZD1), a receptor of the canonical Wnt signaling pathway, is a novel mediator of ischemia-associated cardiac hypertrophy. MI was induced in mice...
The aim of this study was to analyze the effect of indapamide and its combination with ACE inhibitor (captopril) and antioxidant (Provinols™) on both myocardial hypertrophy and fibrosis. Wistar rats were treated with L-NAME (40 mg/kg/day, L); L-NAME plus indapamide (1 mg/kg/day), or captopril (10 mg/kg/day), or Provinols™ (40 mg/kg/day), or combination of indapamide with captopril, and indapami...
Angiotensin II (AII) is a major determinant of arterial pressure and volume homeostasis, mainly because of its vascular action via the AII type 1 receptor (AT1R). AII has also been implicated in the development of cardiac hypertrophy because angiotensin I-converting enzyme inhibitors and AT1R antagonists prevent or regress ventricular hypertrophy in animal models and in human. However, because ...
Stem cell antigen (Sca) 1, a glycosyl phosphatidylinositol-anchored protein localized to lipid rafts, is upregulated in the heart during myocardial infarction and renovascular hypertension-induced cardiac hypertrophy. It has been suggested that Sca-1 plays an important role in myocardial infarction. To investigate the role of Sca-1 in cardiac hypertrophy, we performed aortic banding in Sca-1 ca...
Alterations in TR [thyroid hormone (TH) receptor]1 isoform expression have been reported in models of both physiologic and pathologic cardiac hypertrophy as well as in patients with heart failure. In this report, we demonstrate that TH induces hypertrophy as a direct result of binding to the TRalpha1 isoform and, moreover, that overexpression of TRalpha1 alone is also associated with a hypertro...
BACKGROUND S100B, a 20-kDa, Ca2+-binding dimer, is a putative intrinsic negative regulator of myocardial hypertrophy expressed after myocardial infarction. S100B-overexpressing transgenic (TG) and S100B-knockout (KO) mice have been generated to assess the consequences of S100B expression and altered hypertrophy after infarction. METHODS AND RESULTS We compared 21 wild-type (WT), 20 TG, and 24...
Systemic amyloidosis is a group of diseases associated with extracellular deposition fibrillar proteins, resulting in the loss normal organ structure and function. AL-amyloidosis occurs when amyloid deposited, consisting full-length lambda or kappa immunoglobulin light chains, fragments thereof. This article describes complexity timely diagnosis systemic predominant heart lesion absence myocard...
OBJECTIVE To characterize the follow-up of an experimental model of left ventricular hypertrophy (LVH) induced by supravalvular ascending aortic stenosis in young rats. METHODS Wistar rats were submitted to thoracotomy and aortic stenosis was created by placing a clip on the ascending aorta (AoS group, n=12). Age-matched control animals underwent a sham operation (C group, n=12). Cardiac func...
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