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Yung-Kuo Lin, Yao-Chang Chen, Yi-Ann Chen, Jen-Hung Huang, Shih-Ann Chen, Yi-Jen Chen
INTRODUCTION: Calcium overload increases the risk of atrial fibrillation (AF). Levosimendan, a calcium sensitizer, increases myofilament contractility. Clinical reports suggested that levosimendan might increase AF occurrence, but the electrophysiological effects of levosimendan on AF substrates and triggers (pulmonary veins, PVs) are not clear. METHODS AND RESULTS: Conventional microelectrodes were used to record action potentials (APs) in isolated rabbit PVs, sinoatrial nodes (SANs), the left atrium (LA), and right atrium (RA) before and after application of different concentrations of levosimendan with or without milrinone (a phosphodiesterase [PDE] III inhibitor), and glibenclamide (an ATP-sensitive potassium channel [KATP ] inhibitor)...
May 7, 2018: Journal of Cardiovascular Electrophysiology
Michael Hessler, Philip-Helge Arnemann, Sebastian Rehberg, Christian Ertmer
There is increasing evidence in the literature that preoperative treatment with levosimendan optimizes cardiopulmonary haemodynamics in patients scheduled for the implantation of a Left Ventricular Assist Device (LVAD). The present case report describes changes in sublingual microcirculation using incident dark field video microscopy in a patient, who received a continuous infusion of 0.5 mg/h levosimendan 12 h before LVAD implantation. Despite no evident macrohaemodynamic or metabolic changes, there was a dramatic reduction in total vessel density and perfused vessel density suggesting a deterioration of microcirculation according to the consensus conference criteria in vessels smaller than 20 μm in diameter...
2018: Clinical Hemorheology and Microcirculation
Juergen Konczalla, Jan Mrosek, Stefan Wanderer, Patrick Schuss, Erdem Guresir, Volker Seifert, Hartmut Vatter, Johannes Platz
Levosimendan is a novel calcium sensitizer that is an established treatment for congestive heart failure. In coronary vessels, levosimendan has a vasorelaxant, endothelium-independent effect and an antagonistic effect on endothelin-1 (ET-1). There is also some data for a neuroprotective effect in a traumatic brain injury model, and levosimendan can prevent the reduction of the luminal area of the basilar artery. We considered that patients who suffer heart attack after subarachnoid hemorrhage (SAH) might respond well to levosimendan, which might also be useful to induce hypertension in patients with cerebral vasospasm...
May 2013: Current Neurovascular Research
G V Lobacheva, A V Khar'kin, A F Manerova, E R Dzhobava
After cardiosurgical interventions, the incidence of low cardiac output syndrome (LCOS) is 3-10% depending on age and surgery. The basis for management of patients with LCOS and high pulmonary hypertension is to maintain low total peripheral vascular resistance and to exclude volume overload. Due to the fact that the Russian Federation lacked phosphodiesterase (PDE) III inhibitors that are basic intensive care drugs in pediatric surgery in the West, levosimendan was used as an inodilator in the complex intensive care for postoperative LCOS in 75 infants aged 3 days to 2 years 10 months in October to December 2007...
September 2010: Anesteziologiia i Reanimatologiia
A A Eremenko, P E Kolpakov, M A Babaev, G V Revunenkov, M V Fominykh
The impact of administration of the calcium sensitizer levosimendan on hemodynamic parameters, dose of intraoperative and postoperative cardiotonic maintenance, length of intensive care unit stay, and hospital mortality was studied in cardiosurgical patients with dilated cardiomyopathy, second-fourth degree mitral valve insufficiency, or NYHA Class IV circulatory insufficiency. Levosimendan was administered to 25 patients 3-5 days prior to surgery. A control group of 22 patients did not receive levosimendan...
March 2010: Anesteziologiia i Reanimatologiia
Fabien Despas, Charlotte Trouillet, Nicolas Franchitto, Marc Labrunee, Michel Galinier, Jean-Michel Senard, Atul Pathak
Levosimendan is a new inodilatory agent with calcium sensitizing activity. A major concern regarding the use of inotropic agent in heart failure is their effect on the sympathetic tone. This effect could explain increase in short term mortality with other inotropes. We aimed to assess the effect of levosimendan on sympathetic tone measured directly by microneurogra-phy. In a group of acute decompensated heart failure patients, we assessed cardiac performance by digital plethysmography measurement. Sympathetic tone was assessed through recording of muscle sympathetic nerve activity (MSNA) by micro-neurography...
March 2010: Acute Cardiac Care
Nadine Gauthier, Anjali H Anselm, Haissam Haddad
PURPOSE OF REVIEW: Hospitalization and mortality rates associated with heart failure are persistently high. This is due partly to aging of the population but mostly to delayed progress in the pharmacological treatment of decompensated heart failure. We will review the current recommendations and most recent advancement in the pharmacological treatment of acute decompensated heart failure while providing a systematic approach to the management of this prevalent condition. RECENT FINDINGS: Loop diuretics, nitrates and inotropes such as dobutamine and milrinone are the current mainstay of acute heart failure management although their associated morbidity and possible mortality have raised serious concerns...
March 2008: Current Opinion in Cardiology
Oguzhan Yildiz
Levosimendan, a novel agent developed for the treatment of acute and decompensated heart failure, exerts potent positive inotropic action and peripheral vasodilatory effects. The mechanism of vasodilation by levosimendan may involve reduction of Ca2+ sensitivity of contractile proteins in vascular smooth muscle, the lowering of intracellular free Ca2+, the potential inhibition of phosphodiesterase (PDE) III, and an opening of K+ channels. Although the importance and relative contribution of each of these mechanisms of vasorelaxation is unclear and may be different in various vessels and dependent on the dose of levosimendan, the important roles of K+-channel opening and Ca2+ desensitization in vascular smooth muscle are obvious, whereas the role of PDE inhibition remains to be defined...
May 2007: Journal of Pharmacological Sciences
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