OBJECTIVES: Right heart failure is a major cause of morbidity and mortality after left ventricular assist device implantation and is still hard to predict. This study investigated the haemodynamic effect of a modified Glenn shunt on induced right ventricular (RV) failure. METHODS: Isolated RV failure was induced by coronary ligation in 11 pigs. A modified Glenn shunt was established by a superior vena cava to pulmonary artery connection. Haemodynamic data were obtained at baseline, RV failure, and RV failure and open shunt. Myocardial biopsies were taken to ascertain established heart failure. RESULTS: RV failure defined as right atrial pressure ≥20 mmHg was achieved in all 11 animals. A reduction in cardiac output (CO) from 3.7 (3.5-4.2) to 2.3 l/min (2.0-2.6) and mean arterial pressure (MAP) from median 72.7 (70.1-82.2) to 55.9 mmHg (52.6-59.8) was seen during heart failure. The median flow in the shunt was 681 ml. Right atrial pressures decreased from 20.3 (19.6-21.1) to 13.4 mmHg (12.7-14.0), and RV pressures decreased from 18.1 (16.4-20.1) to 13.6 mmHg (13.5-14.2) with open shunt (P = 0.001 for both). CO increased to 2.9 l/min (2.4-3.3) when the shunt was in use. Mixed venous oxygen saturation increased with the shunt from 32 (27-38) to 49% (45-56), P = 0.001. Genes associated with heart failure were upregulated during heart failure. CONCLUSIONS: A modified Glenn shunt improved haemodynamics by reduced right atrial pressure, increased CO, MAP and mixed venous oxygen saturation in an experimental model of induced RV failure.
OBJECTIVES: Right heart failure is a major cause of morbidity and mortality after left ventricular assist device implantation and is still hard to predict. This study investigated the haemodynamic effect of a modified Glenn shunt on induced right ventricular (RV) failure. METHODS: Isolated RV failure was induced by coronary ligation in 11 pigs. A modified Glenn shunt was established by a superior vena cava to pulmonary artery connection. Haemodynamic data were obtained at baseline, RV failure, and RV failure and open shunt. Myocardial biopsies were taken to ascertain established heart failure. RESULTS:RV failure defined as right atrial pressure ≥20 mmHg was achieved in all 11 animals. A reduction in cardiac output (CO) from 3.7 (3.5-4.2) to 2.3 l/min (2.0-2.6) and mean arterial pressure (MAP) from median 72.7 (70.1-82.2) to 55.9 mmHg (52.6-59.8) was seen during heart failure. The median flow in the shunt was 681 ml. Right atrial pressures decreased from 20.3 (19.6-21.1) to 13.4 mmHg (12.7-14.0), and RV pressures decreased from 18.1 (16.4-20.1) to 13.6 mmHg (13.5-14.2) with open shunt (P = 0.001 for both). CO increased to 2.9 l/min (2.4-3.3) when the shunt was in use. Mixed venous oxygen saturation increased with the shunt from 32 (27-38) to 49% (45-56), P = 0.001. Genes associated with heart failure were upregulated during heart failure. CONCLUSIONS: A modified Glenn shunt improved haemodynamics by reduced right atrial pressure, increased CO, MAP and mixed venous oxygen saturation in an experimental model of induced RV failure.