Document Detail


Placental ischemia and cardiovascular dysfunction in preeclampsia and beyond: making the connections.
MedLine Citation:
PMID:  19018690     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hypertensive disorders of pregnancy continue to be a significant source of maternal and fetal morbidity and mortality, and recent evidence suggests that the incidence of preeclampsia (PE) is increasing. Recent epidemiological studies indicate that the effects of PE may persist long after pregnancy, in both the mother and the offspring, as increased incidence of cardiovascular disease. The last decade has produced new insights into the pathogenesis of PE. The initiating event in PE appears to be impaired placental perfusion and subsequent placental ischemia, which results in the elaboration of numerous factors. Factors such as soluble fms-like tyrosine kinase-1, soluble endoglin and the angiotensin II type-1 receptor autoantibodies contribute to maternal endothelial and cardiovascular dysfunction, marked by increased reactive oxygen species and decreased bioavailable VEGF, nitric oxide and prostacyclin. However, the importance of the various endothelial and humoral factors that mediate these changes during PE remain to be elucidated.
Authors:
Jeffrey S Gilbert; Mark J Nijland; Penny Knoblich
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Expert review of cardiovascular therapy     Volume:  6     ISSN:  1744-8344     ISO Abbreviation:  Expert Rev Cardiovasc Ther     Publication Date:  2008 Nov 
Date Detail:
Created Date:  2008-11-21     Completed Date:  2009-02-02     Revised Date:  2013-09-02    
Medline Journal Info:
Nlm Unique ID:  101182328     Medline TA:  Expert Rev Cardiovasc Ther     Country:  England    
Other Details:
Languages:  eng     Pagination:  1367-77     Citation Subset:  IM    
Affiliation:
Department of Physiology and Pharmacology, University of Minnesota Medical School-Duluth and Duluth Medical Research Institute, Duluth, MN 55812, USA. jgilbert@d.umn.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Anoxia / physiopathology
Cardiovascular Diseases / etiology
Disease Models, Animal
Female
Fetal Diseases / etiology
Humans
Ischemia / complications,  epidemiology,  physiopathology*
Placenta / blood supply,  physiopathology*
Pre-Eclampsia / epidemiology,  etiology,  physiopathology*
Pregnancy
Pregnancy Complications, Cardiovascular / physiopathology
Grant Support
ID/Acronym/Agency:
F32 HL090269-01/HL/NHLBI NIH HHS; HD21350/HD/NICHD NIH HHS; HL90269/HL/NHLBI NIH HHS; P01 HD021350/HD/NICHD NIH HHS; P01 HD021350-159002/HD/NICHD NIH HHS; P01 HD021350-16A10003/HD/NICHD NIH HHS; P01 HD021350-16A16263/HD/NICHD NIH HHS
Comments/Corrections

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