title: Pathophysiology of lower extremity edema in acute heart failure revisited.
abstract: BACKGROUND
  The pathophysiology and key determinants of lower extremity edema in patients with acute heart failure are poorly investigated.
  
  
  METHODS
  We prospectively enrolled 279 unselected patients presenting to the Emergency Department with acute heart failure. Lower extremity edema was quantified at predefined locations. Left ventricular ejection fraction, central venous pressure quantifying right ventricular failure, biomarkers to quantify hemodynamic cardiac stress (B-type natriuretic peptide), and the activity of the arginine-vasopressin system (copeptin) also were recorded.
  
  
  RESULTS
  Lower extremity edema was present in 218 (78%) patients and limited to the ankle in 22%, reaching the lower leg in 40%, reaching the upper leg in 11%, and was generalized (anasarca) in 3% of patients. Patients in the 4 strata according to the presence and extent of lower leg edema had comparable systolic blood pressure, left ventricular ejection fraction, central venous pressure, and B-type natriuretic peptide levels, as well as copeptin and glomerular filtration rate (P=NS for all). The duration of dyspnea preceding the presentation was longer in patients with more extensive edema (P=.006), while serum sodium (P=.02) and serum albumin (P=.03) was lower.
  
  
  CONCLUSIONS
  Central venous pressure, hemodynamic cardiac stress, left ventricular ejection fraction, and the activity of the arginine-vasopressin system do not seem to be key determinants of the presence or extent of lower extremity edema in acute heart failure.
authors.affiliation: Department of Internal Medicine, University Hospital, Basel, Switzerland.
authors.forename: Tobias
authors.initials: T
authors.lastname: Breidthardt
authors.forename: Affan
authors.initials: A
authors.lastname: Irfan
authors.forename: Theresia
authors.initials: T
authors.lastname: Klima
authors.forename: Beatrice
authors.initials: B
authors.lastname: Drexler
authors.forename: Cathrin
authors.initials: C
authors.lastname: Balmelli
authors.forename: Nisha
authors.initials: N
authors.lastname: Arenja
authors.forename: Thenral
authors.initials: T
authors.lastname: Socrates
authors.forename: Rebekka
authors.initials: R
authors.lastname: Ringger
authors.forename: Corinna
authors.initials: C
authors.lastname: Heinisch
authors.forename: Ronny
authors.initials: R
authors.lastname: Ziller
authors.forename: Jürg
authors.initials: J
authors.lastname: Schifferli
authors.forename: Christophe
authors.initials: C
authors.lastname: Meune
authors.forename: Christian
authors.initials: C
authors.lastname: Mueller
mesh_terms: D000208:Acute Disease; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D002496:Central Venous Pressure; D004487:Edema / Q000209:etiology / Q000503:physiopathology*; D005260:Female; D006020:Glycopeptides / Q000097:blood*; D006333:Heart Failure / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D007010:Hyponatremia / Q000209:etiology; D035002:Lower Extremity; D008297:Male; D020097:Natriuretic Peptide, Brain / Q000097:blood*; D011446:Prospective Studies; D013318:Stroke Volume; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: D015415:Biomarkers; D006020:Glycopeptides; C048197:copeptins; D020097:Natriuretic Peptide, Brain