[Levosimendan in heart failure].

Laura Scelsi; Carlo Campana; Stefano Ghio; Lorenzo Monti; Cristina Opasich; Stefania De Feo; Franco Cobelli; Mario Orlandi; Giuseppe Di Pasquale; Luigi Tavazzi

PubMed · 15303549

[Levosimendan in heart failure].

Laura Scelsi·Carlo Campana·Stefano Ghio·Lorenzo Monti·Cristina Opasich·Stefania De Feo·Franco Cobelli·Mario Orlandi·Giuseppe Di Pasquale·Luigi Tavazzi

View original source ↗Export metadata ↓

Abstract

Clinical trials investigating traditional inotropic agents in patients with heart failure demonstrated an increased mortality rate (odds ratio 1.50; IC=0.51-3.92), high incidence of discontinuation of infusion therapy (odds ratio 0.46; IC=0.083-2.29) due to major side effects and, most of all, a limited clinical benefit (odds ratio 0.75; IC=1.42-0.08). On this background a new class of inotropic drugs, the calcium-sensitisers, have been developed. The safety and efficacy of levosimendan (Simdax) has been recently demonstrated in trials (LIDO e RUSSLAN) in patients with heart failure due to ischemic and not ischemic disease. Twenty-six patients with decompensated heart failure of different etiology have been treated with 24 hour infusion of levosimendan. In this experience the levosimendan improved the clinical status and the left ventricular ejection fraction.

Explore related subjects

Calcium Channel Agonists Cardiotonic Agents Clinical Trials as Topic Heart Failure Humans Hydrazones Infusions, Intravenous Myocardial Ischemia Pyridazines Simendan Stroke Volume Treatment Outcome Journal Article Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

Laura Scelsi, Carlo Campana, Stefano Ghio, Lorenzo Monti, Cristina Opasich, Stefania De Feo, Franco Cobelli, Mario Orlandi, Giuseppe Di Pasquale, Luigi Tavazzi. [Levosimendan in heart failure].. https://pubmed.ncbi.nlm.nih.gov/15303549/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2005

Investigation into the structure-activity relationship of novel concentration dependent, dual action T-type calcium channel agonists/antagonists.

This paper describes the synthesis and biological evaluation of a series of straight chain analogs of a compound (1) that was previously synthesized in our research program. These compounds, which are T-type calcium channel antagonists, exhibits potent anti-proliferative activity against a variety of cancer cells. A structure-activity relationship of these analogs against a variety of cancer cells has provided insight into a logical pharmacophore for this series of compounds. Furthermore, this series of compounds has presented itself as a set of novel, concentration dependent, dual action agonists/antagonists for the T-type calcium channel.

Calcium Channel Agonists↗

PubMed2004

Slow calcium oscillations in human spermatozoa.

We have used single-cell imaging to investigate intracellular Ca2+ signalling in human spermatozoa stimulated with progesterone (3 microM). In approx. 9% of cells progesterone caused the activation of slow repetitive [Ca2+]i (intracellular Ca2+ concentration) oscillations, with a period of 1-4 min, which persisted for the duration of recording (20-30 min). Pretreatment with nifedipine, which blocks T- and L-type voltage-operated Ca2+ channels in spermatogenic cells, did not modify the characteristics of the oscillations, but reduced the proportion of cells in which they were observed. Stimulation with Bay K 8644 or FPL64176 induced [Ca2+]i oscillations in 5-10% of cells, but their frequency was low (period, 4-5 min). Application of valinomycin (1 microM) to clamp membrane potential at E(K) (equilibrium potential for potassium) did not modify activity in oscillating cells, showing that plasma membrane potential and activation of voltage-operated conductances are not involved in the mechanism by which sperm [Ca2+]i oscillations are generated.

Calcium Channel Agonists↗

PubMed2003

Ca2+ channel characteristics in neuroendocrine tumor cell cultures analyzed by color contour plots.

Neuroendocrine tumor (NET) cells express several voltage-operated Ca2+ channels (VOCCs). To address the question, if clinically distinct entities of NETs could be associated by specific patterns of VOCC expression, electrophysiological properties of NET primary cultures derived from consecutive surgical resections and permanent NET cell cultures were determined and analyzed by a color-coding contour diagram method. Using whole-cell patch-clamp technique, electrophysiological data were obtained from human pancreatic (foregut) BON and mouse intestinal (midgut) STC-1 cells as well as from human primary cultivated NET cells from fore- and midgut tumors or liver metastasis. To describe definite Ca2+ channel characteristics, we suggested a color-coding method to depict the contours of time- and voltage-dependence. In this study, we could demonstrate specific Ca2+ channel properties in NET cells from midgut tumors which were not found in NET cells from foregut location. This may be important functionally in respect of different cell biological functions of NET cells such as release of bioamines and neuropeptides. In addition, definite differences between the effect of specific and unspecific Ca2+ channel modulators on NET cells were detected. Although most of this information can be obtained by superimposing current-voltage curves at different times after the onset of the voltage step, the color-coding contour diagrams clearly provides a better visual summary, and hence might be generally quite useful.

Calcium Channel Agonists↗