What this Trial Is About

1. Background Handgrip strength , a core indicator of muscle function, has been confirmed to be significantly associated with the clinical prognosis of patients with liver cirrhosis. However, no studies have explored its correlation with portal venous hemodynamics. 2. Objective The purpose of the study is to examine the effects of Handgrip strength on portal vein and left gastric vein pressure, blood flow velocity and direction in patients with liver cirrhosis, as well as its hemodynamic impact on gastroesophageal varices. 3. Method Study Design: Interventional study. Detection Timing: Hemodynamic indices were measured simultaneously after patients achieved their maximum handgrip strength. Participants were divided into three groups based on the assessment methods. Group 1 (Portal Pressure Measurement Group): Before the placement of TIPS, the pressures of the portal vein and left gastric vein were measured, both before and after the handgrip strength test. Group 2 (Doppler Ultrasound Measurement Group): Measurements of portal flow velocity and direction were taken before and after the handgrip strength test, based on Doppler ultrasound. Group 3 (Endoscopic Ultrasound Measurement Group): Measurements of blood flow volume and direction in esophagogastric varices were conducted before and after the handgrip strength test, based on endoscopic ultrasonography. The inclusion and exclusion criteria were described. 4. Elaboration of the Research Hypothesis 4.1. Core Hypothesis The handgrip strength level in patients with liver cirrhosis is correlated with portal venous system hemodynamic indices. Specifically, enhanced handgrip strength may affect portal hypertension and the hemodynamics of varicose veins by improving systemic muscle function or circulatory status. 4.2. Speculation on potential mechanisms Association between muscle function and circulation: As a representative of systemic muscle function, increased handgrip strength may reflect an increase in cardiac output or changes in splanchnic vascular resistance, thereby influencing portal venous hemodynamics. Effects on varicose veins: Improved handgrip strength may reduce blood flow velocity or diameter of esophagogastric varices by decreasing splanchnic congestion or regulating local vascular tension, thus lowering the risk of variceal rupture and bleeding. Role of compensatory mechanisms: Muscle wasting is common in decompensated cirrhosis. Patients with higher handgrip strength may have better compensatory capacity, and the degree of hemodynamic disorder in their portal venous system may be less severe. Conclusion This study uses a multi-method grouping design to first explore the association between handgrip strength and portal venous hemodynamics in cirrhotic patients. The hypothesis is based on the potential regulatory role of muscle function in the circulatory system, which is expected to provide a new non-invasive indicator for clinical assessment of portal hypertension risk.

Effect of Handgrip Strength on Portal Vein Hemodynamics in Patients With Liver Cirrhosis