Acute haemodynamic instability after transcatheter tricuspid valve replacement: insights from pressure-volume loops

A 63-year-old male was admitted for dyspnoea and ascites. Seven years ago he suffered an inferior wall infarction with right ventricular (RV) involvement, and was known for an isolated torrential secondary tricuspid regurgitation (TR) with now RV dysfunction. After being declined for any surgical treatment (including transplantation) he underwent a compassionate transcatheter tricuspid valve replacement (TTVR) preceded by low-dose inotropes prehabilitation. At the time of the intervention, RV pressure-volume loops showed a decrease in RV end-systolic single beat elastance (Ees) combined with an increase in effective arterial elastance (Ea), consistent with RV/pulmonary artery (PA) coupling worsening, from 0.78 to 0.34. Within 48 h, the patient presented with fever and significant elevation in leucocytes (11.2 g/l) and ultra-sensitive C-reactive protein (54 mg/l), associated with hypotension, oliguria and acute kidney injury. On Day 3 he developed symptomatic bradycardia requiring pacemaker implantation, and remained unstable despite heart rate optimization. In this setting of a previously infarcted RV, with presumed no contractile reserve, the uncoupling was primarily driven by its inability to adapt to the increased forward flow after TR treatment, resulting in a mismatch between Ees and Ea. However, this phenomenon alone likely does not fully account for the acute haemodynamic instability (AHI). A ‘second hit’ appears plausible—either an inflammatory response or a lack of preload recruitment due to a chronically dilated and functionally exhausted RV. Conversely to most TTVR patients, advanced computed tomography (CT)-derived RV systolic metrics did not improve.1 Post TTVR–AHI remains complex and the ongoing registry (NCT06954792) should help to refine our understanding of it.