Key result
Severe hepatic steatosis and fibrosis in patients with metabolic syndrome were associated with a 3.6-fold and 8-fold increased risk of left ventricular diastolic dysfunction, respectively (P<0.0001).
Why the study?
Metabolic syndrome components increase the risk for cardiovascular disease and NAFLD, but the correlation between liver fibrosis, steatosis, and left ventricular dysfunction in these patients required investigation.
Is there an association between liver steatosis and fibrosis and subclinical left ventricular dysfunction in patients with metabolic syndrome?
Case-Control (n=300)
Is there an association between liver steatosis and fibrosis and subclinical left ventricular dysfunction in patients with metabolic syndrome?
Relative Risk: 3.6
p-value: p=<0.0001
In patients with metabolic syndrome, the presence and severity of hepatic steatosis and fibrosis are significantly associated with subclinical left ventricular systolic and diastolic dysfunction.
May warrant closer LV monitoring in MS with severe steatosis/fibrosis; leaves open causality and need for prospective validation.
PURPOSE: The components of metabolic syndrome (MS) are risk factors for developing both cardiovascular disease (CVD) and non-alcoholic fatty liver disease (NAFLD). Strain (SI) and strain‑rate imaging (SRI) are able to recognize early changes in cardiac function. Vibration-controlled transient elastography (VCTE) and controlled attenuation parameter (CAP) detect and quantify liver fibrosis and steatosis. We aimed to assess whether there is any correlation between liver fibrosis and steatosis and left ventricular (LV) dysfunction in MS patients. PATIENTS AND METHODS: A total of 150 adults with MS were registered in the study. They were compared with a control group of 150 age- and sex-matched adults without MS. After the classic echocardiographic assessment of LV function, two-dimensional speckle echocardiography (2D-STE) was used to evaluate LV peak systolic strain (S) and peak systolic strain rate (SR), while liver steatosis and fibrosis were evaluated by VCTE and CAP. RESULTS: LV diastolic dysfunction was significantly more frequent among the patients with MS. We found significant differences between the two groups regarding the presence of subtle LV systolic dysfunction, detected by reduced values of S and SR. The risk for LV diastolic dysfunction was 3.6 times higher in MS with severe steatosis and 8 times higher in patients with severe fibrosis, P<0.0001. The risk for LV systolic dysfunction was double in MS with severe steatosis and 1.7 times higher in MS with severe fibrosis, P<0.0001. CONCLUSION: In MS patients with normal LV ejection fraction, conventional echocardiography parameters identified diastolic LV dysfunction, while SI and SRI identified subtle impairment of systolic LV dysfunction. The presence of hepatic steatosis and fibrosis increases significantly the risk for cardiac dysfunction in MS patients (P<0.0001).
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Vitel et al. (2020) conducted a case-control in Metabolic syndrome (n=300). Liver steatosis and fibrosis vs. Absence of severe steatosis and fibrosis was evaluated on Left ventricular diastolic dysfunction (RR 3.6, p=<0.0001). Severe hepatic steatosis and fibrosis in patients with metabolic syndrome were associated with a 3.6-fold and 8-fold increased risk of left ventricular diastolic dysfunction, respectively (P<0.0001).
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