Key result
Cirrhosis was associated with higher ejection intraventricular pressure difference compared to controls (median 4.0 vs 2.9 mm Hg, P<0.05), reflecting enhanced left ventricular systolic function.
Why the study?
Is left ventricular systolic function altered in patients with cirrhosis, and how does it relate to sympathetic nervous activity and inflammation?
Case-Control (n=118)
Is left ventricular systolic function altered in patients with cirrhosis, and how does it relate to sympathetic nervous activity and inflammation?
Absolute Event Rate: 4% vs 2.9%
p-value: p=<0.05
Left ventricular systolic function is enhanced at baseline in cirrhosis due to augmented adrenergic tone, but acute afterload stress unmasks systolic impairment in patients with advanced vasodilatation and inflammation.
Enhanced LV systolic function in cirrhosis detectable by EIVPD/strain; leaves open role in guiding beta-blockers or prognosis.
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. (H epatology 2017;65:2019‐2030).
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Yotti et al. (2017) conducted a case-control in Cirrhosis (n=118). Cirrhosis vs. Age-matched controls was evaluated on Ejection intraventricular pressure difference (EIVPD) (p=<0.05). Cirrhosis was associated with higher ejection intraventricular pressure difference compared to controls (median 4.0 vs 2.9 mm Hg, P<0.05), reflecting enhanced left ventricular systolic function.
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