Introduction: The clinical course of hypertrophic cardiomyopathy (HCM) is very heterogeneous and the development of heart failure (HF) is difficult to predict. Exercise echocardiography can provide information about potential mechanisms involved in the occurrence of HF symptoms: development of intraventricular obstruction, increase in mitral regurgitation (MR) severity, impaired left ventricular (LV) and left atrial (LA) function.
Objective: To analyse the changes in LV and LA function during exercise and to identify the main correlates of exercise capacity in patients (pts) with HCM, in si-nus rhythm and with normal LV ejection fraction.
Methods: We have prospectively enrolled 32 patients (48±17 years, 15 men) with HCM and no obstruction at rest. A symptom limited exercise echocardiogram was performed in all patients using a table ergometer (Ergoline). Maximum LV wall thickness (LVWT), indexed left atrial volume (LAVi), septal E’, E/septal E’ ratio, were measured at rest (r) and during exercise (e). Global longitudinal LV strain (GLS) and left atrial strain (LAere assessed by speckle tracking echocardiography at rest and during exercise. The peak LV outflow tract gradient, systolic pulmonary artery pressure (PAP), and MR degree were recorded at rest and during exercise. Exercise-related symptoms, peak exercise heart rate (HR) and exercise capacity calculated in metabolic equivalents (METs) were also recorded.
Results: T he mean value of achieved METs was 5.9±1.4, the peak HR was 124±25 bpm, representing 72±12% of maximal HR, during a mean of 8.5±2.5 minutes of exercise. Thirteen patients developed LV gra-dients>30 mmHg. Fifteen patients were asymptomatic, while 17 patients reported dyspnea during exercise. There were no significant differences between patients with and without symptoms regarding: age, rE’, rE/E’, rGLS, rLA, rPAP, LAVi, eE/e’, eGLS, eMR, ePAP (p>0.05 for all). Symptomatic patients had lower values for eE’ (p=0.01), eLA p=0.03) and tended to have higher values for LVWT (p=0.06) and a higher prevalence of eLV outflow tract obstruction (p=0.13) compared to asymptomatic patients. In symptomatic group of patients, E’ (p=0.004), PAP (p<0.001) and GLS (p=0.04) significantly increased and LAended to decrease (p=0.18) during exercise. Age (r=-0.44, p=0.01), rE’ (r=0.40, p=0.02), eE’ (r=0.46, p=0.01), ePAP (r=-0.35, p=0.04) and LVWT (r=-0.32, p=0.07) significantly correlated with achieved METs in HCM patients overall. In multivariate analysis, eE’ (β=0.60, 95% CI 0.122 to 0.009, p=0.003) was the only parameter independently correlated with exercise capacity (expressed in METs).
Conclusions: Symptomatic patients had a worse LV diastolic function (as expressed by E’) and a severe LA longitudinal dysfunction (as expressed by LAuring exercise. E’ during exercise was the only parameter in-dependently correlated with exercise capacity in patients with HCM. These suggest that a detailed analysis of LV and LA function during exercise could provide additional information to predict the occurrence of HF in HCM patients.