title: Left ventricular systolic function is associated with sympathetic nervous activity and markers of inflammation in cirrhosis.
abstract: An accurate evaluation of cardiac function in patients with cirrhosis remains a challenge. We used robust echocardiographic indices to characterize left ventricular (LV) systolic function and its relationship to activation of the sympathetic nervous system and inflammation in 59 patients with cirrhosis and 59 age-matched controls. Additionally, in 11 patients we withdrew beta-blockers and diuretics and used phenylephrine and albumin infusion to evaluate the response to acute afterload and preload changes (interventional substudy). Measures of systolic LV function such as the ejection intraventricular pressure difference (EIVPD) and the systolic strain rate were higher in patients with cirrhosis than in controls (median [1st-3rd quartile], 4.0 [3.1-5.1] versus 2.9 [2.4-3.6] mm Hg and -1.3 [-1.6 to -1.1] versus -1.2 [-1.6 to -1.1)] s-1, respectively; P < 0.05 for both). EIVPD was related to the severity of liver disease (Model for End-Stage Liver Disease, rho = 0.45, P < 0.001), the degree of sympathetic nervous system activation (noradrenaline, rho = 0.26, P = 0.05; heart rate variability, rho = -0.43, P = 0.003), and treatment with beta-blockers (P = 0.001). In the interventional substudy, EIVPD was higher in patients with ascites (6.5 [5.4-8.5] versus 4.0 [3.9-5.1] mm Hg, P = 0.045). The decrease in EIVPD induced by phenylephrine was inversely related to baseline systolic function (P < 0.05) and associated with markers of systemic vasodilatation (nitric oxide, rho = -0.66, P = 0.06; diastolic blood pressure, rho = 0.68, P = 0.04) and inflammation (interleukin-1beta, rho = -0.80, P = 0.009).
  
  
  
  LV systolic function is enhanced in cirrhosis due to augmented adrenergic tone and modulated by treatment with beta-blockers; acute afterload stress induces a deeper impairment of systolic function in patients with more advanced degrees of vasodilatation and inflammation; these changes in LV function related to cirrhosis can be assessed using robust echocardiographic methods. (Hepatology 2017;65:2019-2030).
authors.affiliation: Department of Cardiology and CIBERCV, Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria Gregorio Marañón, and Facultad de Medicina, Universidad Complutense, Madrid, Spain.
authors.forename: Raquel
authors.initials: R
authors.lastname: Yotti
authors.affiliation: Department of Digestive Diseases and CIBEREHD, Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria Gregorio Marañón, and Facultad de Medicina, Universidad Complutense, Madrid, Spain.
authors.forename: Cristina
authors.initials: C
authors.lastname: Ripoll
authors.affiliation: Department of Cardiology and CIBERCV, Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria Gregorio Marañón, and Facultad de Medicina, Universidad Complutense, Madrid, Spain.
authors.forename: Yolanda
authors.initials: Y
authors.lastname: Benito
authors.affiliation: Department of Digestive Diseases and CIBEREHD, Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria Gregorio Marañón, and Facultad de Medicina, Universidad Complutense, Madrid, Spain.
authors.forename: Maria Vega
authors.initials: MV
authors.lastname: Catalina
authors.affiliation: Department of Cardiology and CIBERCV, Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria Gregorio Marañón, and Facultad de Medicina, Universidad Complutense, Madrid, Spain.
authors.forename: Jaime
authors.initials: J
authors.lastname: Elízaga
authors.affiliation: Department of Digestive Diseases and CIBEREHD, Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria Gregorio Marañón, and Facultad de Medicina, Universidad Complutense, Madrid, Spain.
authors.forename: Diego
authors.initials: D
authors.lastname: Rincón
authors.affiliation: Department of Cardiology and CIBERCV, Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria Gregorio Marañón, and Facultad de Medicina, Universidad Complutense, Madrid, Spain.
authors.forename: Francisco
authors.initials: F
authors.lastname: Fernández-Avilés
authors.affiliation: Department of Cardiology and CIBERCV, Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria Gregorio Marañón, and Facultad de Medicina, Universidad Complutense, Madrid, Spain.
authors.forename: Javier
authors.initials: J
authors.lastname: Bermejo
authors.affiliation: Department of Digestive Diseases and CIBEREHD, Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria Gregorio Marañón, and Facultad de Medicina, Universidad Complutense, Madrid, Spain.
authors.forename: Rafael
authors.initials: R
authors.lastname: Bañares
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D001794:Blood Pressure / Q000502:physiology; D016022:Case-Control Studies; D016001:Confidence Intervals; D004452:Echocardiography / Q000379:methods; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D008103:Liver Cirrhosis / Q000150:complications* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D015588:Observer Variation; D011379:Prognosis; D012016:Reference Values; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging* / Q000188:drug therapy / Q000209:etiology*; D016277:Ventricular Function, Left / Q000502:physiology
chemical_list: D000319:Adrenergic beta-Antagonists; D018836:Inflammation Mediators