Key result
Dobutamine stress in post-Fontan HLHS reveals blunted cardiac index response vs controls, driven by preload limitation.
Why the study?
Exercise limitation is common post-Fontan in patients with hypoplastic left heart syndrome, and haemodynamic response to stress in this population is not well characterized.
What is the haemodynamic response to dobutamine stress and inhaled nitric oxide in symptomatic children with hypoplastic left heart syndrome post-Fontan compared to healthy controls?
Observational (n=13)
What is the haemodynamic response to dobutamine stress and inhaled nitric oxide in symptomatic children with hypoplastic left heart syndrome post-Fontan compared to healthy controls?
In symptomatic children with HLHS post-Fontan, cardiac output at peak stress is blunted due to preload limitation that does not respond to inhaled pulmonary vasodilators.
Answers are grounded in this paper and cite their sources.
May explain exertional intolerance in HLHS post-Fontan; leaves open whether preload-targeted interventions improve reserve.
AIMS: Exercise limitation is common post-Fontan. Hybrid X-ray and magnetic resonance imaging (XMR) catheterization allows haemodynamic assessment by means of measurement of ventricular volumes and flow in major vessels with simultaneous invasive pressures. We aim to assess haemodynamic response to stress in patients with hypoplastic left heart syndrome (HLHS) post-Fontan. METHODS AND RESULTS: Prospective study of 13 symptomatic children (NHYA 2) with HLHS post-Fontan using XMR catheterization. Three conditions were applied: baseline (Stage 1), dobutamine at 10 µg/kg/min (Stage 2), and dobutamine at 20 µg/kg/min (Stage 3). Seven consecutive patients received inhaled nitric oxide (iNO) at peak stress. Control MRI data were from normal healthy adults. In the HLHS patients, baseline mean pulmonary vascular resistance (PVR) was 1.51 ± 0.59 WU m(2) and aortopulmonary collateral flow was 17.7 ± 13.6% of systemic cardiac output. Mean right ventricular end-diastolic pressure was 6.7 ± 2.5 mmHg which did not rise with stress. Cardiac index (CI) increased at Stage 2 in HLHS (40%) and controls (61%) but continued to increase at Stage 3 only in controls (19%) but not in HLHS. The blunted rise in CI in HLHS was due to a continuing fall in end-diastolic volume throughout stress, with no significant change in PVR or CI at peak stress in response to iNO. CONCLUSION: Cardiac output post-Fontan in HLHS at peak stress is blunted due to a limitation in preload which is not responsive to inhaled pulmonary vasodilators in the setting of normal PVR.
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Pushparajah et al. (2015) conducted an observational in Hypoplastic left heart syndrome (HLHS) post-Fontan (n=13). Dobutamine stress and inhaled nitric oxide vs. Healthy adult controls was evaluated on Increase in cardiac index at Stage 2 dobutamine stress. Dobutamine stress testing in children with HLHS post-Fontan revealed a blunted cardiac index response at peak stress compared to healthy controls, driven by a limitation in preload.
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