Left ventricular systolic function is associated with sympathetic nervous activity and markers of inflammation in cirrhosis

Raquel Yotti, Cristina Ripoll, Yolanda Benito, Maria Vega Catalina, Jaime Elízaga, Diego Rincón, Francisco Fernández-Avilés, Javier Bermejo, Rafael Bañares
Hepatology: Official Journal of the American Association for the Study of Liver Diseases 2017, 65 (6): 2019-2030

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).

CONCLUSION: 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).

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