Exciting findings exploring different cardiac output states in patients undergoing #TTVR, roping together the role of the liver, kidneys, splanchnic circulation. We were able to gain more insights in this intriguing pathophysiology: bit.ly/3iFlxMZ -explainer thread below 
1/5 By analyzing n=132 patients who underwent #TTVR in severe #TR, we assessed Cardiac Output states, hemodynamics, liver and kidney function to understand which mechanisms are triggered and sustained by TR, but also to observe changes made in these organ systems after treatment.
2/5 Tricuspid regurgitation-related backward failure increases central venous pressures, causes liver congestion and dysfunction with portal hypertension and reduced washout of vasoactive substances.
3/5 Splanchnic and peripheral vasodilation alongside with renal congestion results in RAAS activation and sympathetic overactivation, leading to fluid retention and blood volume shifting from splanchnic to central circulation, leading to ascites and intestinal dysfunction.
4/5 Sympathetic overdrive and volume retention lead to capacitance depletion and volume overload, eventually resulting in a high cardiac output state, with limited preload reduction and poor prognostic benefit following TTVR.
5/5 A better understanding of the underlying pathophysiology allows us to approach TR in a multimodal fashion, paving the way for further exciting research. A very special thank you to all contributors @KP_Kresoja @PhilippLurz @kp_rommel @thiele_holger @maorban @mvonroeder
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