Abstract 4139170: Relationship between hemodynamics and oxygen consumption in hypertrophic cardiomyopathy during maximal stress testing

Background: Hypertrophic cardiomyopathy (HCM) is a global heart disease with great variability in disease severity, which can lead to significant impairment of exercise capacity. In healthy populations, oxygen consumption is related to cardiac output and arteriovenous oxygen difference. We sought to determine the relationship between hemodynamics (cardiac output and stroke volume) and oxygen consumption in HCM compared to healthy controls during maximal stress testing. Aims: To evaluate associations between the trajectories of hemodynamic function and oxygen consumption in HCM compared to healthy controls. Methods: Twenty individuals with HCM (51±15 years old, body mass index (BMI): 28±3 kg/m 2 , females, n=4) and 16 healthy controls (66±7 years old, 27±6 kg/m 2 , females, n=6) were included in the present study. Participants completed a maximal-graded stress test coupled with non-invasive hemodynamic bioreactance (cardiac output, stroke volume) and gas exchange (oxygen consumption, VO 2 ) measurements. Data were analyzed in quartiles (exercise only) and phases (rest, pre-pedalling, exercise and recovery) of the maximal-graded stress test. Results: In HCM, cardiac output declined in the fourth quartile of the exercise phase of the stress test (-0.39 L/min, p <0.001) whilst VO 2 increased (3.86 ml/kg/min, p <0.001). There was a significant difference in the gradient of cardiac output between HCM and controls in the final quartile of the test (-1.6 vs. 18.1 L/min, p<0.001). In coherence, stroke volume declined in the fourth quartile of the test (-18.4 ml, p <0.01) in response to increasing VO 2 in HCM. The rates of recovery were faster in HCM compared to the control group for VO 2 (-4.3 vs -2.6 mL/second, p<0.001), cardiac output (-0.03 vs -0.02 L/second, p<0.001), heart rate (-0.17 vs -0.10 beats/second, p<0.001), and stroke volume (-0.18 vs -0.07 L/second, p<0.001). Conclusions: In HCM, cardiac output declined during the later stages of maximal stress testing whereas in controls it continued to rise, indicating impaired maximal cardiac output responses to exercise. These findings have implications for exercise prescription and training regimens in HCM suggesting avoidance of maximal exercise levels.