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Träfflista för sökning "WFRF:(Caidahl K) ;pers:(Hamsten A)"

Search: WFRF:(Caidahl K) > Hamsten A

  • Result 1-8 of 8
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  • Eriksson, SV, et al. (author)
  • Diastolic and systolic function as predictors of exercise capacity after myocardial infarction in young Men
  • 1998
  • In: Cardiology. - : S. Karger AG. - 0008-6312 .- 1421-9751. ; 90:1, s. 8-12
  • Journal article (peer-reviewed)abstract
    • We evaluated the power of measurements of left ventricular (LV) systolic and diastolic function for predicting exercise capacity in 97 young male survivors of a myocardial infarction. The patients were evaluated with M-mode echocardiography, a symptom-limited exercise test and coronary and LV angiography. In univariate analyses, maximum exercise workload was most closely related to the atrial emptying index, an index of diastolic function (r = 0.37, p < 0.005), but not to LV ejection fraction (r = 0.001, NS). This relationship was stronger in the 42 patients without signs of ischemia during exercise (r = 0.51, p < 0.005). Multivariate analyses indicated that the atrial emptying index (p < 0.005) provided independent contribution to the prediction of maximum exercise capacity. LV diastolic function but not LV systolic function was related to exercise capacity in young survivors of myocardial infarction.
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  • Maegdefessel, L, et al. (author)
  • miR-24 limits aortic vascular inflammation and murine abdominal aneurysm development
  • 2014
  • In: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 5, s. 5214-
  • Journal article (peer-reviewed)abstract
    • Identification and treatment of abdominal aortic aneurysm (AAA) remain among the most prominent challenges in vascular medicine. MicroRNAs (miRNAs) are crucial regulators of cardiovascular pathology and represent intriguing targets to limit AAA expansion. Here we show, by using two established murine models of AAA disease along with human aortic tissue and plasma analysis, that miR-24 is a key regulator of vascular inflammation and AAA pathology. In vivo and in vitro studies reveal chitinase 3-like 1 (Chi3l1) to be a major target and effector under the control of miR-24, regulating cytokine synthesis in macrophages as well as their survival, promoting aortic smooth muscle cell migration and cytokine production, and stimulating adhesion molecule expression in vascular endothelial cells. We further show that modulation of miR-24 alters AAA progression in animal models, and that miR-24 and CHI3L1 represent novel plasma biomarkers of AAA disease progression in humans.
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  • Result 1-8 of 8

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