Document Detail


Acute heart failure with low cardiac output: can we develop a short-term inotropic agent that does not increase adverse events?
MedLine Citation:
PMID:  20625945     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Acute heart failure represents an increasingly common cause of hospitalization, and may require the use of inotropic drugs in patients with low cardiac output and evidence of organ hypoperfusion. However, currently available therapies may have deleterious effects and increase mortality. An ideal inotropic drug should restore effective tissue perfusion by enhancing myocardial contractility without causing adverse effects. Such a drug is not available yet. New agents with different biological targets are under clinical development. In particular, istaroxime seems to dissociate the inotropic effect exerted by digitalis (inhibition of the membrane sodium/potassium adenosine triphosphatase) from the arrhythmic effect and to ameliorate diastolic dysfunction (via sarcoendoplasmic reticulum calcium adenosine triphosphatase activation). Additionally, the myosin activator omecamtiv mecarbil appears to have promising characteristics, while genetic therapy has been explored in animal studies only. Further investigations are needed to confirm and expand the effectiveness and safety of these agents in patients with acute heart failure and low cardiac output.
Authors:
Umberto Campia; Savina Nodari; Mihai Gheorghiade
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Current heart failure reports     Volume:  7     ISSN:  1546-9549     ISO Abbreviation:  Curr Heart Fail Rep     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-07-19     Completed Date:  2010-10-29     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101196487     Medline TA:  Curr Heart Fail Rep     Country:  United States    
Other Details:
Languages:  eng     Pagination:  100-9     Citation Subset:  IM    
Affiliation:
Center for Cardiovascular Quality and Outcomes, Northwestern University Feinberg School of Medicine, 645 North Michigan Avenue, Suite 1006, Chicago, IL 60611, USA.
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MeSH Terms
Descriptor/Qualifier:
Acute Disease
Animals
Cardiac Output / physiology*
Cardiotonic Agents / adverse effects,  pharmacology*
Clinical Trials as Topic
Digoxin / adverse effects,  pharmacology
Dobutamine / adverse effects,  pharmacology
Etiocholanolone / adverse effects,  analogs & derivatives,  pharmacology
Gene Therapy / methods
Heart Failure / drug therapy*,  epidemiology,  physiopathology
Humans
Hydrazones / adverse effects,  pharmacology
Pyridazines / adverse effects,  pharmacology
Ryanodine Receptor Calcium Release Channel / drug effects
Sarcoplasmic Reticulum Calcium-Transporting ATPases / drug effects
Sodium-Potassium-Exchanging ATPase / antagonists & inhibitors
Urea / analogs & derivatives,  pharmacology
Chemical
Reg. No./Substance:
0/3-((2-aminoethoxy)imino)androstane-6,17-dione; 0/Cardiotonic Agents; 0/Hydrazones; 0/Pyridazines; 0/Ryanodine Receptor Calcium Release Channel; 0/omecamtiv mecarbil; 131741-08-7/simendan; 20830-75-5/Digoxin; 34368-04-2/Dobutamine; 53-42-9/Etiocholanolone; 57-13-6/Urea; EC 3.6.3.8/Sarcoplasmic Reticulum Calcium-Transporting ATPases; EC 3.6.3.9/Sodium-Potassium-Exchanging ATPase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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