533Does targeting the site of maximal electrical delay result in the optimal haemodynamic improvement; results from an international multi-centre registry

EP Europace ◽  
2018 ◽  
Vol 20 (suppl_1) ◽  
pp. i103-i104
Author(s):  
B Sieniewicz ◽  
J Behar ◽  
M Sohal ◽  
S Claridge ◽  
B Porter ◽  
...  
2014 ◽  
Vol 111 (01) ◽  
pp. 154-164 ◽  
Author(s):  
Su-Emmanuelle Degirmenci ◽  
Fatiha Zobairi ◽  
Asael Berger ◽  
Grégory Meyer ◽  
Mélanie Burban ◽  
...  

SummaryCirculating microparticles play a pro-inflammatory and procoagulant detrimental role in the vascular dysfunction of septic shock. It was the objective of this study to investigate mechanisms by which a pharmacological modulation of microparticles could affect vascular dysfunction in a rat model of septic shock. Septic or sham rats were treated by activated protein C (aPC) and resuscitated during 4 hours. Their microparticles were harvested and inoculated to another set of healthy recipient rats. Haemodynamic parameters were monitored, circulating total procoagulant microparticles assessed by prothrombinase assay, and their cell origin characterised. Mesenteric resistance arteries, aorta and heart were harvested for western blotting analysis. We found that a) the amount and phenotype of circulating microparticles were altered in septic rats with an enhanced endothelial, leucocyte and platelet contribution; b) aPC treatment significantly reduced the generation of leucocyte microparticles and norepinephrine requirements to reach the mean arterial pressure target in septic rats; c) Microparticles from untreated septic rats, but not from aPC-treated ones, significantly reduced the healthy recipients’ mean arterial pressure; d) Microparticle thromboxane content and aPC activity were significantly increased in aPC-treated septic rats. In inoculated naïve recipients, microparticles from aPC-treated septic rats prompted reduced NF-κB and cyclooxygenase-2 arterial activation, blunted the generation of pro-inflammatory iNOS and secondarily increased platelet and endothelial microparticles. In conclusion, in this septic shock model, increased circulating levels of procoagulant microparticles led to negative haemodynamic outcomes. Pharmacological treatment by aPC modified the cell origin and levels of circulating microparticles, thereby limiting vascular inflammation and favouring haemodynamic improvement.


2015 ◽  
Vol 10 (1) ◽  
pp. 39 ◽  
Author(s):  
Dagmar M Ouweneel ◽  
Bimmer E Claessen ◽  
Krischan D Sjauw ◽  
José PS Henriques ◽  
◽  
...  

The experience and usage of percutaneous cardiac assist devices in cardiogenic shock as well as high-risk percutaneous coronary intervention have increased over the years. Nonetheless, there is still little evidence of clinical benefit of these devices other than immediate haemodynamic improvement. Despite the fact that these devices are used to treat a rather complex patient population, clinical testing remains important in order to evaluate their true impact on clinical outcome before being adopted into clinical practice. Therefore, this review shows an overview of the current experience and evidence of the available percutaneous cardiac assist devices.


2019 ◽  
Vol 15 (4) ◽  
pp. 497-498 ◽  
Author(s):  
Aleksander Araszkiewicz ◽  
Stanisław Jankiewicz ◽  
Sylwia Sławek-Szmyt ◽  
Aneta Klotzka ◽  
Marek Grygier ◽  
...  

Author(s):  
Sophie Vergnaud ◽  
David Dobarro ◽  
John Wort

A 16-year-old girl with a diagnosis of diffuse cutaneous systemic sclerosis is referred to a specialist pulmonary hypertension centre with a history of progressive breathlessness, reduced exercise tolerance, and raised pulmonary pressures on transthoracic echocardiogram. She is found to have pulmonary arterial hypertension on right cardiac catheterization and is started on sildenafil, a phosphodiesterase-5 inhibitor, which stabilizes her condition. An endothelin receptor antagonist is added, which provides some initial symptomatic improvement. She continues to deteriorate over a period of 5 years, ultimately requiring intravenous prostanoids, the only treatment to provide a real symptomatic and haemodynamic improvement. This chapter explores the physiology and pathophysiology of pulmonary arterial hypertension, its classification, the means of investigation and diagnosis, who to refer to specialist centres, and the concepts behind current and future treatment strategies.


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