Abstract

Background: Exercise intolerance occurs in patients with hypertrophic cardiomyopathy (HCM) in part due to impaired augmentation of stroke volume (SV reserve) and diastolic dysfunction. Systolic-diastolic (S-D) coupling characterizes how systolic contraction of the left ventricle (LV) primes efficient elastic recoil during diastole. S-D coupling declines with age and is further reduced in patients with heart failure. Impaired S-D coupling may contribute to impaired cardiac response to exercise in patients with HCM. Hypothesis: We hypothesized that S-D coupling is associated with peak oxygen uptake (peak VO 2 ) and peak cardiac output (Qc) patients with HCM. Methods: Patients with HCM (HCM: n=25, age=46 ± 8.9 years) and healthy, sedentary adults (CON: n=115, age=50 ± 9.7 years) underwent cardiopulmonary exercise testing and resting echocardiography. S-D coupling is the relationship between LV longitudinal excursion of the mitral annulus during systole (S exc ) and early diastole (ED exc ) measured with tissue Doppler imaging. Peak VO 2 (Douglas bag), peak Qc (C 2 H 2 rebreathe), and SV reserve were assessed during maximal treadmill exercise. Linear regression was performed between S-D coupling and peak VO 2 , peak Qc, and SV reserve and multivariate regression with age as a covariate. Results: S-D coupling was reduced in HCM (HCM: 0.56±0.10, CON: 0.63±0.08, p <0.001). In CON, S-D coupling was independently associated with age (r = 0.52, p <0.001), but not peak VO 2 (r = 0.26, p = 0.473) or peak Qc (r = 0.04, p = 0.538). In HCM, S-D coupling was associated with peak VO 2 (r = 0.46 p = 0.019) and peak Qc (r = 0.56, p = 0.003) with a trend in SV reserve (r = 0.36, p = 0.071) (Figure), independent of age (VO 2 p = 0.020, Qc p = 0.004). Conclusion: Impaired systolic-diastolic coupling is associated with fitness and the cardiac response to exercise in patients with HCM. Inefficient S-D coupling may link insufficient stroke volume generation, diastolic dysfunction, and exercise intolerance in HCM.

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