Cardiopulmonary exercise testing in athletes and non-athletes with hypertrophic cardiomyopathy

Cardiopulmonary exercise testing (CPET) in hypertrophic cardiomyopathy (HCM) is useful for risk stratification and symptom evaluation. Current guidelines recommend serial CPET testing in this subgroup. Data comparing CPET testing in athletes versus non-athletic individuals with HCM is inexistent.

The main objective of this study was to compare CPET variables in athletes and non-athletes with HCM.

HCM patients consecutively referred for CPET were included. HCM diagnosis included those with a) unexplained LV maximal wall thickness (LVMWT) of ≥ 15mm or b) LVMWT 12-15 mm with supporting features (FH of HCM, abnormal ECG, abnormal MV morphology, scar, genotype positive). Those with concomitant cardiovascular disease were excluded. Individuals who engaged in ≥4hrs of moderate-high intensity physical activity weekly (within the previous year) were placed in the athletic group.

39 HCM patients were included (mean age at diagnosis 48 ± 15 years, 92.3% male, 69.2% non-athletes, 87.2% Caucasian, mean BMI 28.4 kg/m2 ± 4.3, median follow up 36 months). A fourth (6/26, 23.1%) had a FH of HCM, 9/25 (36.0%) had a FH of SCD. Some (43.6%) were on a beta blocker. Most were asymptomatic (66.7%). A few (10.2%) had evidence of LVOT obstruction. Most (76.9%) had ECG features typical of HCM. A fourth (17.9%) had a device implanted (n=6 ICD, n=1 ILR). 44.0% (11/25) were genotype positive. Nearly a third (28.2%) had a maximal LV wall thickness of >20mm. Septal HCM was the most common phenotype (61.5%), followed by apical (20.5%), apical/septal (12.8%) and other (5.1%). The mean HCM 5-year SCD risk score was 2.3% ± 1.5%.

Non-athletic patients were more symptomatic (44.4% vs 9.1%, p=0.034). The RV was also larger in the athletic group (p=0.048). All other baseline characteristics where similar in both groups. LV size, RV/LV function, replacement fibrosis, left atrial size and maximal LV wall thickness on ECHO and CMR were also similar.

CPET was a maximal test in the majority (92.3%). Half (53.8%) had a reduced aerobic exercise capacity (%VO2MAX). VO2MAX was significantly lower in individuals on beta blockers (19.1±5.2 vs 25.1±6.4 mls/kg/min, p=0.003). A third (30.8%) had a reduced O2/Pulse, some (15.4%) and/or abnormal O2/pulse response. Most had a reduced PETCO2 at peak (71.8%). VO2/WR was reduced in 64%. A third (38.5%) had ventricular arrhythmias, 10.3% had an inappropriate blood pressure response, 23.1% had an abnormal heart rate recovery.

Athletes with HCM performed better compared to non-athletes. Athletes had higher aerobic exercise capacity and more favourable CPET parameters (Table 1). Athletes were also less likely to have ≥2 abnormal CPET variables that would suggest a cardiac limitation (41.7% vs 81.5%, p=0.01).

Athletes with HCM performed better during CPET compared to non-athletes. This suggests that athletic remodelling may enable athletic individuals with HCM to cope better during exercise.