In hypertrophic cardiomyopathy (HCM), cardiopulmonary exercise testing (CPET) is considered the gold standard for assessing exercise tolerance, with O 2 -pulse commonly used as a surrogate for stroke volume (SV). However, because SV reduction can be masked by increased oxygen extraction, direct non-invasive measurement of SV is valuable. This study involved 102 HCM patients (mean age 53 ± 16 years, 78% male), predominantly with a non-obstructive phenotype (74%), who underwent CPET with SV measurement using Physioflow (PF). Abnormal O 2 -pulse kinetics were observed in 12 patients, all confirmed by abnormal SV trends with PF. Additionally, PF identified another 28 patients with altered SV kinetics. Abnormal SV trends were associated with higher peak VE/VO 2 ratios (42.6 37.4–47.5 vs. 38.0 33.6–41.3) and lower end-tidal CO 2 values (31.8 ± 4.9 vs. 34.3 ± 5.6 mmHg, p < 0.05). Patients with greater SV growth during the final 25% of exercise showed improved anaerobic threshold VO 2 (49.8 ± 12.3% vs. 43.9 ± 15.2% predicted peak VO 2 ), VO 2 /work slope (10.2 ± 2.0 vs. 9.3 ± 1.3 mL/min/Watt), and peak PetCO 2 (34.5 ± 5.6 vs. 32.3 ± 5.2 mmHg), alongside a lower VE/VCO 2 slope (28.7 24.9–31.0 vs. 31.3 27.3–34.2, p < 0.05). Integrating PF and CPET may enhance the detection of abnormal SV kinetics, which are associated with reduced functional capacity in HCM patients.
Mapelli et al. (Tue,) studied this question.