Cardiac output states in patients with severe functional tricuspid regurgitation: impact on treatment success and prognosis. (28th July 2021) - Unterhuber, Matthias
Abstract : Aims: To investigate whether there is evidence for distinct cardiac output (CO) based phenotypes in patients with chronic right heart failure associated with severe tricuspid regurgitation (TR) and to characterize their impact on TR treatment and outcome. Methods and results: A total of 132 patients underwent isolated transcatheter tricuspid valve repair (TTVR) for functional TR at two centres. Patients were clustered according to k‐means clustering into low [cardiac index (CI) < 1.7 L/min/m 2 ], intermediate (CI 1.7–2.6 L/min/m 2 ) and high CO (CI > 2.6 L/min/m 2 ) clusters. All‐cause mortality and clinical characteristics during follow‐up were compared among different CO clusters. Mortality rates were highest for patients in a low (24%) and high CO state (42%, log‐rank P < 0.001). High CO state patients were characterized by larger inferior vena cava diameters ( P = 0.003), reduced liver function, higher incidence of ascites ( P = 0.006) and markedly reduced systemic vascular resistance ( P < 0.001) as compared to TTVR patients in other CO states. Despite comparable procedural success rates, the extent of changes in right atrial pressures ( P = 0.01) and right ventricular dimensions ( P < 0.001) per decrease in regurgitant volume following TTVR was less pronounced in high CO state patients as compared to other CO states. Successful TTVR was associated with the smallest prognostic benefit among low and high CO state patients. Conclusions: Patients with chronic right heart failure and severe TR display distinct CO states. The high CO state is characterized by advanced congestive hepatopathy, a substantial decrease in peripheral vascular tone, a lack of response of central venous pressures to TR reduction, and worse prognosis. These data are relevant to the pathophysiological understanding and management of this important clinical syndrome. Abstract : Proposed mechanism of hypercirculatory tricuspid regurgitation. Tricuspid regurgitation related backward failure causes liver congestion and dysfunction with portal hypertension and reduced washout of vasoactive substances. Consequent splanchnic and peripheral vasodilatation alongside with reduced renal blood flow results in renin–angiotensin–aldosterone system (RAAS) activation and sympathetic overactivation. The sympathetic drive and volume retention lead to further capacitance depletion and volume overload, eventually resulting in a high cardiac output state, with limited preload reduction and prognostic benefit following transcatheter tricuspid valve repair. The alterations in the graph should be interpreted as simultaneous interaction rather than a timeline. Continuous lines indicate findings in the present study. Dashed lines express currently accepted mechanistical considerations. AP, alkaline phosphatase; γGT, gamma‐glutamyl‐transferase; RA, right atrium; RV, right ventricle.