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Vascular (dys)function in the failing heart
No full textHeart failure (HF) is not confined to contractile failure of cardiomyocytes or myocardial fibrosis. Coronary and systemic vascular dysfunction contributes to the initiation and progression of HF with or without reduced ejection fraction. Furthermore, HF compromises vascular function, creating and sustaining a vicious cycle with deranging effects on coronary blood flow, cardiac metabolism and cardiac function. In HF, systemic arterial dysfunction, characterized by increased arterial stiffness and resistance, raises cardiac afterload and impedes myocardial contractile function. Reduced coronary blood flow impairs myocardial oxygen delivery and consequently cardiomyocyte metabolism and function. Coronary microvascular dysfunction is heterogeneous in its pathogenesis and manifestations, complicating the diagnosis and management across different HF phenotypes. Understanding the alterations in function in different segments of the vasculature, from the aorta to the capillary level, offers mechanistic insights into disease drivers and therapeutic interventions. Interventional approaches can improve vascular haemodynamics, whereas established and emerging pharmacotherapies target the neurohumoral axis and reduce extravascular compression, inflammation, and oxidative stress, thereby improving vascular function and HF-related outcomes. In this Review, we provide a mechanistic framework of vascular dysfunction in the pathogenesis of HF with or without reduced ejection fraction, pointing towards integrated therapies that consider the vascular implications of contemporary HF management across HF phenotypes
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Inotropic therapy of heart failure - Editorial comments on: Vasodilation and mechanoenergetic inefficiency dominates the effect of the "Ca2+ sensitizer" MCI-154 in intact pigs
No full textEffects of chonotropic and inotropic stimulation on the coronary pressure-flow relation in the pressure-overload hypertrophied left ventricle: Contributions to exercise-induced alternations.
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Endothelial nitric oxide synthase and cardiac remodelling: location, location, location?
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Prior exercise improves survival, infarct healing, and left ventricular function after myocardial infarction
No full textde Waard MC, Duncker DJ. Prior exercise improves survival, infarct healing, and left ventricular function after myocardial infarction. J Appl Physiol 107: 928-936, 2009; doi:10.1152/japplphysiol.91281.2008.-We investigated the effects of voluntary wheel running before an acute myocardial infarction (MI) on survival, left ventricular (LV) remodeling and dysfunction and whether exercise before and after MI provides superior protection compared with either exercise intervention alone. After 2 wk of voluntary wheel running or sedentary housing, MI was induced in C57B1/6 mice, after which exercise was stopped (EX-MI-SED and SED-MI-SED groups, where EX is exercise and SED is sedentary) or continued (EX-MI-EX and SED-MI-EX groups) for a period of 8 wk. Exercise after MI in SED-MI-EX mice had no effect on survival, the area of infarction, and global LV remodeling, but attenuated fibrosis and apoptosis in the remote myocardium and blunted LV dysfunction and pulmonary congestion compared with SED-MI-SED mice. Exercise before MI in both EX-MI-SED and EX-MI-EX mice decreased post-MI mortality compared with both SED-MI-SED and SED-MI-EX mice. Furthermore, in both pre-MI exercise groups, the infarct area was thicker, whereas interstitial fibrosis and apoptosis in the remote LV myocardium were blunted. In contrast, the ameliorating effects of either pre-MI or post-MI exercise alone on LV dysfunction were lost in EX-MI-EX mice, which may in part be related to the increased daily exercise distance in the first week post-MI in EX-MI-EX versus SED-MI-EX mice. In conclusion, exercise before or after MI blunted LV dysfunction, whereas only exercise before MI improved survival. These findings suggest that even when regular physical activity fails to prevent an acute MI, it can still act to improve cardiac function and survival after MI
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