Impaired left ventricular mechanics and functional reserve are associated with reduced exercise capacity in patients with hypertrophic cardiomyopathy

Abstract

Background: Reduced metabolic equivalents (METs) are an indicator of exercise intolerance, which predicts poor prognosis in hypertrophic cardiomyopathy (HCM) patients. We sought to evaluate the changes in left ventricular (LV) mechanics and functional reserves, as well as their association with functional capacity in HCM patients.Methods: Seventy HCM patients and thirty controls were included in this study. LV mechanics were evaluated at rest and during exercise by echocardiography and twodimensional speckle-tracking imaging to obtain parameters of functional reserve, LV global longitudinal strain (LVGLS), strain rate (SR), and circumferential strain.Results: Hypertrophic cardiomyopathy (HCM) patients had lower LVGLS, systolic SR, early and late diastolic SR at rest and during exercise, and reduced absolute and relative systolic and diastolic reserve compared to controls. LV circumferential strain was significantly higher at rest but lower during exercise in HCM patients. Exercise capacity was markedly reduced in HCM patients, and peak exercise LVGLS (LVGLS-exe) significantly correlated with exercise capacity. Multivariate regression analyses showed that LVGLS-exe, LV filling pressure during exercise (E/e'-exe), and LV mass index (LVMI) were independent predictors of exercise capacity. Moreover, LVGLSexe displayed incremental predictive value over E/e'-exe and LVMI for exercise intolerance. Receiver operating characteristic curve analysis showed LVGLS-exe had optimal accuracy for predicting exercise intolerance in HCM patients. Conclusions:Hypertrophic cardiomyopathy (HCM) patients have reduced LV mechanics at rest and during exercise and impaired mechanical reserve. LVGLS-exe is associated with exercise capacity and is an optimal predictive value for reduced exercise capacity in HCM patients. K E Y W O R D Sexercise stress echocardiography, functional reserve, hypertrophic cardiomyopathy, speckletracking imaging | 267 WU et al.

Application of non‐invasive bioreactance to assess hemodynamic function in patients with hypertrophic cardiomyopathy

“…It is primarily influenced by central (cardiac) and peripheral factors (skeletal muscle function) (del Buono et al, 2019 ; van Wezenbeek et al, 2019 ). Reduced exercise capacity (i.e., peak exercise O 2 consumption <22 mL/kg/min) reported in the present study is consistent with previous studies (Saberi et al, 2017 ; Wu et al, 2019 ). Reduced cardiac output rather than arterio‐venous oxygen difference was the main factor responsible for lower exercise tolerance in this study.…”

“…Whilst this assumption supports our findings under resting conditions, beta‐blockers have been reported to attenuate blood pressure response to exercise (Chen et al, 1999 ). Wu et al, 2019 ; however, reported reduced exercise capacity even after withdrawal of beta blocker medication. Earlier studies suggest that peak exercise cardiac output appears to be a major determinant of peak exercise capacity in patients with hypertrophic cardiomyopathy, which is dependent primarily on stroke volume augmentation (Lele et al, 1995 ; Re et al, 2013 ).…”

The Diagnostic and Prognostic Value of Echocardiographic Strain

“…Abnormal GLS (defined by a cutoff value of −16%) was independently associated with a composite of adverse events at a median follow-up time of 22 months, with incremental risk stratification benefit over standard clinical and echocardiographic parameters . A recent study has shown patients with HCM have impaired LV GLS at rest and exercise, and lower absolute LV GLS during exercise is associated with patient exercise intolerance . These data underscore the potential role of strain in improved risk stratification of patients with HCM.…”

Impaired longitudinal systolic–diastolic coupling and cardiac response to exercise in patients with hypertrophic cardiomyopathy

“…Twist mechanics and the longitudinal motion of the LV in patients with HCM are abnormal in those with both obstructive and nonobstructive HCM and are associated with reduced fitness and adverse outcomes in HCM. 4,[29][30][31] Potential causes of impaired myocardial mechanics in HCM include LVOT obstruction, regional fibrosis, and abnormal myocardial perfusion. 9,32,33 Prior studies have evaluated S-D coupling as a function of the twist-untwist relationship in the ventricle and found associations with intra-ventricular pressure gradients which drive blood into the ventricle during diastole.…”