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The Role of Arterial Stiffness and Central Hemodynamics in Heart Failure
Weber Thomas 대한심부전학회 2020 International Journal of Heart Failure Vol.2 No.4
Whereas traditional understanding of left ventricular afterload was focused on a steady-state circulation model with continuous pressures and flow, a more realistic concept is emerging, taking the pulsatile nature of the heart and the arterial system into account. The most simple measure of pulsatility is brachial pulse pressure, representing the pulsatility fluctuating around the mean blood pressure level. Brachial pulse pressure is widely available, fundamentally associated with the development and treatment of heart failure (HF), but its analysis is often confounded in patients with established HF. The next step of analysis consists of arterial stiffness, central (rather than brachial) pressures, and of wave reflections. The latter are closely related to left ventricular late systolic afterload, ventricular remodeling, diastolic dysfunction, exercise capacity, and, in the long term, the risk of new-onset HF. Wave reflection may also evolve as a suitable therapeutic target for HF with preserved and reduced ejection fraction. A full understanding of ventricular-arterial coupling, however, requires dedicated analysis of time-resolved pressure and flow signals. This review provides a summary of current understanding of pulsatile hemodynamics in HF.
Pulsatile Hemodynamics and Coronary Artery Disease
Hack-Lyoung Kim,Thomas Weber 대한심장학회 2021 Korean Circulation Journal Vol.51 No.11
Coronary artery disease (CAD) is the leading cause of human death and has a high prevalence throughout the world. Therefore, it is important to detect CAD early and to apply individualized therapy according to the patients' risk. There is an increasing interest in pulsatile arterial hemodynamics in the cardiovascular area. Widely used measurements of arterial pulsatile hemodynamics include pulse pressure, pulse wave velocity and augmentation index. Here, we will review underlying pathophysiology linking the association of arterial pulsatile hemodynamics with CAD, and the usefulness of the measurements of pulsatile hemodynamics in the prediction of future cardiovascular events of CAD patients. Clinical and therapeutic implications will be also addressed.
Fabian Stögbauer,Johanna Weigert,Markus Neumeier,Josef Wanninger,Daniela Sporrer,Markus Weber,Andreas Schäffler,Carlos Enrich,Peta Wood,Thomas Grewal,Charalampos Aslanidis,Christa Buechler 생화학분자생물학회 2009 Experimental and molecular medicine Vol.41 No.7
Adiponectin stimulates cholesterol efflux in macrophages and low adiponectin may in part contribute to disturbed reverse cholesterol transport in type 2 diabetes. Monocytes express high levels of annexin A6 that could inhibit cholesterol efflux and it was investigated whether the atheroprotective effects of adiponectin are accompanied by changes in annexin A6 levels. Adiponectin reduces annexin A6 protein whereas mRNA levels are not affected. Adiponectin-mediated activation of peroxisome proliferator-activated receptor α (PPARα) and AMP-activated protein kinase (AMPK) does not account for reduced annexin A6 expression. Further, fatty acids and lipopolysaccharide that are elevated in obesity do not influence annexin A6 protein levels. Annexin A6 in monocytes from overweight probands or type 2 diabetic patients is significantly elevated compared to monocytes of normal- weight controls. Monocytic annexin A6 positively correlates with body mass index and negatively with systemic adiponectin of the blood donors. Therefore, the current study demonstrates that adiponectin reduces annexin A6 in monocytes and thereby may enhance cholesterol efflux. In agreement with these in vitro finding an increase of monocytic annexin A6 in type 2 diabetes monocytes was observed. Adiponectin stimulates cholesterol efflux in macrophages and low adiponectin may in part contribute to disturbed reverse cholesterol transport in type 2 diabetes. Monocytes express high levels of annexin A6 that could inhibit cholesterol efflux and it was investigated whether the atheroprotective effects of adiponectin are accompanied by changes in annexin A6 levels. Adiponectin reduces annexin A6 protein whereas mRNA levels are not affected. Adiponectin-mediated activation of peroxisome proliferator-activated receptor α (PPARα) and AMP-activated protein kinase (AMPK) does not account for reduced annexin A6 expression. Further, fatty acids and lipopolysaccharide that are elevated in obesity do not influence annexin A6 protein levels. Annexin A6 in monocytes from overweight probands or type 2 diabetic patients is significantly elevated compared to monocytes of normal- weight controls. Monocytic annexin A6 positively correlates with body mass index and negatively with systemic adiponectin of the blood donors. Therefore, the current study demonstrates that adiponectin reduces annexin A6 in monocytes and thereby may enhance cholesterol efflux. In agreement with these in vitro finding an increase of monocytic annexin A6 in type 2 diabetes monocytes was observed.