Dobutamine stress in patients with a Fontan circulation significantly augmented aortopulmonary collateral flow (P<0.001) and decreased pulmonary vascular resistance (P<0.01) compared to rest.
Observational (n=10)
How does dobutamine stress affect pulmonary vascular resistance, collateral flow, and ventricular function in patients with a Fontan circulation compared to rest?
In Fontan patients, dobutamine stress enhances pulmonary flow via aortopulmonary collaterals and decreases pulmonary vascular resistance, but reveals decreased diastolic compliance as a key component of ventricular dysfunction.
BACKGROUND: The role, interplay, and relative importance of the multifactorial hemodynamic and myocardial mechanisms causing dysfunction of the Fontan circulation remain incompletely understood. METHODS AND RESULTS: Using an MRI catheterization technique, we performed a differential analysis of pulmonary vascular resistance and aortopulmonary collateral blood flow in conjunction with global ventricular pump function, myocontractility (end-systolic pressure-volume relation), and diastolic compliance (end-diastolic pressure-volume relation) in 10 patients with a Fontan circulation at rest and during dobutamine stress. Pulmonary and ventricular pressures were measured invasively and synchronized with velocity-encoded MRI-derived pulmonary and aortic blood flows and cine MRI-derived ventricular volumes. Pulmonary vascular resistance and end-systolic and end-diastolic pressure-volume relations were then determined. Aortopulmonary collateral flow was calculated as the difference between aortic and pulmonary flow. Compared to rest, dobutamine caused a small increase in mean pulmonary pressures (P<0.05). Collateral flow was significantly augmented (P<0.001) and contributed importantly to an increase in pulmonary flow (P<0.01). Pulmonary vascular resistance decreased significantly (P<0.01). Dobutamine did not increase stroke volumes significantly despite slightly enhanced contractility (end-systolic pressure-volume relation). Active early relaxation (τ) was inconspicuous, but the end-diastolic pressure-volume relation shifted upward, indicating reduced compliance. CONCLUSIONS: In patients with a Fontan circulation, aortopulmonary collateral flow contributes substantially to enhanced pulmonary flow during stress. Our data indicate that pulmonary vascular response to augmented cardiac output was adequate, but decreased diastolic compliance was identified as an important component of ventricular dysfunction.
Schmitt et al. (Thu,) conducted a observational in Fontan circulation (n=10). Dobutamine stress vs. Rest was evaluated on Pulmonary vascular resistance, aortopulmonary collateral blood flow, and ventricular function. Dobutamine stress in patients with a Fontan circulation significantly augmented aortopulmonary collateral flow (P<0.001) and decreased pulmonary vascular resistance (P<0.01) compared to rest.