Abstract 15538: Heart Rate Reserve in Fontan and Pulmonary Hypertension Patients: Chronotropic Incompetence or Chronotropic Protection?
Introduction: Patients with pulmonary hypertension or a Fontan circulation are said to have an impaired heart rate (HR) response to exercise. However, it is yet to be determined whether the impaired HR response in these patients is a primary disorder of chronotropic responsiveness or a consequence of changes in cardiac load.
Hypothesis: We hypothesized that patients with chronic thromboembolic pulmonary hypertension (CTEPH) or a Fontan circulation would have a normal HR response relative to exercise intensity, but an attenuated maximal HR due to decreased systemic ventricular filling.
Methods: 40 subjects (20 controls, 10 CTEPH and 10 Fontan) underwent cardiac magnetic resonance imaging with simultaneous invasive pressure recording during supine bicycle exercise to near maximal exertion. Adjusted HR reserve (HRR) was determined as the change from rest to peak exercise HR divided by the difference of age-predicted maximal heart rate (220 - age) and resting HR.
Results: Adjusted HHR was lower in Fontan and CTEPH patients than in controls (P=0.001). In contrast, increases in HR relative to workload or oxygen consumption (VO2) were higher than in controls (Figure). The lower HRR in CTEPH and Fontans was associated with failure to maintain left ventricular end-diastolic and stroke volume index (SVi) during exercise (P<0.001 for interaction). Thus, whereas the change in cardiac index (CI) relative to the change in VO2 (ΔCI/ΔVO2) was similar between groups, CTEPH and Fontan patients had higher ΔHR/ΔVO2 and lower ΔSVi/ΔVO2 than controls (both P<0.01).
Conclusions: At any given exercise intensity, chronotropic responsiveness is preserved in CTEPH and Fontan patients, indicating normal sino-atrial function. However, exercise capacity and peak HR are attenuated and this occurs in association with reduced systemic ventricular filling. This raises the possibility that the attenuated peak heart rate may be a consequence as much as a cause of abnormal exercise hemodynamics.
Author Disclosures: G. Claessen: None. A. La Gerche: None. A. Van De Bruaene: None. M. Claeys: None. J. Bogaert: None. P. Claus: None. W. Budts: None. M. Delcroix: None. H. Heidbuchel: None. M. Gewillig: None.
- © 2016 by American Heart Association, Inc.