title: Ventricular dysfunction and dilation in severe sepsis and septic shock: relation to endothelial function and mortality.
abstract: OBJECTIVE
  The aim of this study was to evaluate echocardiography-based indices of myocardial function and markers of vascular inflammation and endothelial dysfunction in the early phases of severe sepsis.
  
  
  METHODS
  Forty-five adult patients (67% women; age 51 ± 18 years; Acute Physiology and Chronic Health Disease Classification System II score, 23 ± 7) admitted to the intensive care unit up to 24 hours after fulfilling criteria for severe sepsis or septic shock were studied. Clinical, laboratorial (endothelin 1 [ET1], vascular cellular adhesion molecule 1), and echocardiographic data were collected within the first 24 hours and again 72 hours and 7 days after admission.
  
  
  RESULTS
  Intrahospital mortality was 33% (15 deaths). Left ventricular (LV) dysfunction (LV ejection fraction <55%) was identified in 15 (33%) patients, whereas right ventricular (RV) dysfunction (RV tissue Doppler peak systolic velocity [RV-Sm] <12 cm/s) was present in 14 (30%) patients. LogET1 was increased in patients with LV dysfunction (2.3 ± 0.6 vs 1.8 ± 0.4 pg/mL; P = .01) and RV dysfunction (2.5 ± 0.5 vs 1.8 ± 0.4 pg/mL; P < .001) and had negative correlations with LV ejection fraction (r = -0.50; P = .002) and RV-Sm (r = -0.67; P < .001). Left ventricular end-diastolic diameter, RV-Sm, and diastolic dysfunction were able to discriminate survivors from nonsurvivors, and the combination of these parameters identified groups of very low and high risk.
  
  
  CONCLUSIONS
  Both LV and RV systolic dysfunctions are prevalent in severe sepsis, being directly associated with markers of endothelial dysfunction. Left ventricular nondilation, RV dysfunction, and diastolic dysfunction seem related to poor prognosis in this scenario.
authors.affiliation: Cardiology and Cardiovascular Sciences, Medical School from Rio Grande doSul Federal University, Brasil.
authors.forename: Thiago
authors.initials: T
authors.lastname: Furian
authors.forename: Cyntia
authors.initials: C
authors.lastname: Aguiar
authors.forename: Karen
authors.initials: K
authors.lastname: Prado
authors.forename: Roberto Vanin Pinto
authors.initials: RV
authors.lastname: Ribeiro
authors.forename: Leandro
authors.initials: L
authors.lastname: Becker
authors.forename: Nidiane
authors.initials: N
authors.lastname: Martinelli
authors.forename: Nadine
authors.initials: N
authors.lastname: Clausell
authors.forename: Luis Eduardo
authors.initials: LE
authors.lastname: Rohde
authors.forename: Andréia
authors.initials: A
authors.lastname: Biolo
mesh_terms: D015415:Biomarkers / Q000097:blood; D001938:Brazil / Q000453:epidemiology; D002311:Cardiomyopathy, Dilated / Q000000981:diagnostic imaging / Q000209:etiology*; D004452:Echocardiography; D019332:Endothelin-1 / Q000097:blood; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D018805:Sepsis / Q000150:complications* / Q000175:diagnosis / Q000401:mortality*; D012772:Shock, Septic / Q000150:complications / Q000175:diagnosis / Q000401:mortality; D015996:Survival Rate; D018754:Ventricular Dysfunction / Q000000981:diagnostic imaging / Q000209:etiology*
chemical_list: D015415:Biomarkers; D019332:Endothelin-1; D018799:Intercellular Adhesion Molecule-1