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Left ventricular systolic function is associated with sympathetic nervous activity and markers of inflammation in
Raquel Yotti1, Cristina Ripoll2, Yolanda Benito1
1Department of Cardiology and CIBERCV, Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria Gregorio Marañón, and Facultad de Medicina, Universidad Complutense, Madrid, Spain.
Insights
Cardiac function in cirrhosis patients is enhanced due to sympathetic nervous system activation. Echocardiography effectively assesses these changes, which are influenced by inflammation and vasodilatation.
Area of Science:
- Cardiology
- Hepatology
- Physiology
Background:
- Accurate assessment of cardiac function in cirrhosis patients is challenging.
- Cirrhosis is associated with complex cardiovascular changes, including alterations in sympathetic nervous system activity and inflammation.
Purpose of the Study:
- To characterize left ventricular (LV) systolic function in cirrhosis patients using echocardiography.
- To investigate the relationship between LV systolic function, sympathetic nervous system activation, and inflammation in cirrhosis.
- To evaluate the response of LV systolic function to acute afterload and preload changes in a subset of patients.
Main Methods:
- Echocardiographic indices, including ejection intraventricular pressure difference (EIVPD) and systolic strain rate, were used to assess LV systolic function in 59 cirrhosis patients and 59 controls.
- Sympathetic nervous system activation was assessed via noradrenaline levels and heart rate variability.
- An interventional substudy in 11 patients evaluated the response to phenylephrine and albumin infusion after withdrawal of beta-blockers and diuretics.
Main Results:
- Patients with cirrhosis exhibited enhanced LV systolic function compared to controls, indicated by higher EIVPD and systolic strain rate.
- EIVPD was positively correlated with the severity of liver disease (Model for End-Stage Liver Disease score) and negatively with heart rate variability.
- In the interventional substudy, patients with ascites showed higher EIVPD, and phenylephrine-induced decrease in EIVPD was linked to systemic vasodilatation and inflammation markers.
Conclusions:
- Left ventricular systolic function is enhanced in cirrhosis, likely due to augmented adrenergic tone and modulated by beta-blocker treatment.
- Acute afterload stress reveals impaired systolic function in patients with advanced vasodilatation and inflammation.
- Robust echocardiographic methods can effectively assess these cirrhosis-related changes in LV function.
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).
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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