OBJECTIVES: Right ventricular failure after left ventricular assist device implantation is a serious complication with high rates of mortality and morbidity. It has been demonstrated in experimental settings that volume exclusion of the right ventricle with a modified Glenn shunt can improve haemodynamics during ischaemic right ventricular failure. However, the concept of a modified Glenn shunt is dependent on a normal pulmonary vascular resistance, which can limit its use in some patients. The aim of this study was to explore the effects of volume exclusion with a modified Glenn shunt during right ventricular failure due to pulmonary banding, and to study the alterations in genetic expression in the right ventricle due to pressure and volume overload. METHODS: Experimental right ventricular failure was induced in pigs (n = 11) through 2 h of pulmonary banding. The pigs were randomized to either treatment with a modified Glenn shunt and pulmonary banding (n = 6) or solely pulmonary banding (n = 5) as a control group. Haemodynamic measurements, blood samples and right ventricular biopsies for genetic analysis were sampled at baseline, at right ventricular failure (i.e. 2 h of pulmonary banding) and 1 h post-right ventricular failure in both groups. RESULTS: Right atrial pressure increased from 10 mmHg (9.0-12) to 18 mmHg (16-22) (P < 0.01) and the right ventricular pressure from 31 mmHg (26-35) to 57 mmHg (49-61) (P < 0.01) after pulmonary banding. Subsequent treatment with the modified Glenn shunt resulted in a decrease in right atrial pressure to 13 mmHg (11-14) (P = 0.03). In the control group, right atrial pressure was unchanged at 19 mmHg (16-20) (P = 0.18). At right heart failure, there was an up-regulation of genes associated with heart failure, inflammation, angiogenesis, negative regulation of cell death and proliferation. CONCLUSIONS: Volume exclusion with a modified Glenn shunt during right ventricular failure reduced venous congestion compared with the control group. The state of right heart failure was verified through genetic expressional changes.
OBJECTIVES:Right ventricular failure after left ventricular assist device implantation is a serious complication with high rates of mortality and morbidity. It has been demonstrated in experimental settings that volume exclusion of the right ventricle with a modified Glenn shunt can improve haemodynamics during ischaemic right ventricular failure. However, the concept of a modified Glenn shunt is dependent on a normal pulmonary vascular resistance, which can limit its use in some patients. The aim of this study was to explore the effects of volume exclusion with a modified Glenn shunt during right ventricular failure due to pulmonary banding, and to study the alterations in genetic expression in the right ventricle due to pressure and volume overload. METHODS: Experimental right ventricular failure was induced in pigs (n = 11) through 2 h of pulmonary banding. The pigs were randomized to either treatment with a modified Glenn shunt and pulmonary banding (n = 6) or solely pulmonary banding (n = 5) as a control group. Haemodynamic measurements, blood samples and right ventricular biopsies for genetic analysis were sampled at baseline, at right ventricular failure (i.e. 2 h of pulmonary banding) and 1 h post-right ventricular failure in both groups. RESULTS: Right atrial pressure increased from 10 mmHg (9.0-12) to 18 mmHg (16-22) (P < 0.01) and the right ventricular pressure from 31 mmHg (26-35) to 57 mmHg (49-61) (P < 0.01) after pulmonary banding. Subsequent treatment with the modified Glenn shunt resulted in a decrease in right atrial pressure to 13 mmHg (11-14) (P = 0.03). In the control group, right atrial pressure was unchanged at 19 mmHg (16-20) (P = 0.18). At right heart failure, there was an up-regulation of genes associated with heart failure, inflammation, angiogenesis, negative regulation of cell death and proliferation. CONCLUSIONS: Volume exclusion with a modified Glenn shunt during right ventricular failure reduced venous congestion compared with the control group. The state of right heart failure was verified through genetic expressional changes.
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