Lisa Van Ryckeghem1,2, Charly Keytsman3,4, Elvire Verbaanderd5, Ines Frederix4,6,7,8, Elise Bakelants6,9, Thibault Petit6,10, Siddharth Jogani6, Sarah Stroobants6, Paul Dendale4,6, Virginie Bito4, Jan Verwerft6, Dominique Hansen3,4,6. 1. REVAL-Rehabilitation Research Centre, Faculty of Rehabilitation Sciences, Hasselt University, Agoralaan, Building A, 3590, Diepenbeek, Belgium. lisa.vanryckeghem@uhasselt.be. 2. BIOMED-Biomedical Research Centre, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium. lisa.vanryckeghem@uhasselt.be. 3. REVAL-Rehabilitation Research Centre, Faculty of Rehabilitation Sciences, Hasselt University, Agoralaan, Building A, 3590, Diepenbeek, Belgium. 4. BIOMED-Biomedical Research Centre, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium. 5. Physical Activity, Sport & Health Research Group, Faculty of Movement Sciences, KU Leuven, Leuven, Belgium. 6. Department of Cardiology, Virga Jessa Hospital, Heart Centre Hasselt, Hasselt, Belgium. 7. Faculty of Medicine & Health Sciences, Antwerp University, Antwerp, Belgium. 8. Department of Cardiology, Antwerp University Hospital, Edegem, Belgium. 9. Hôpitaux Universitaires de Genève (HUG), Genève, Switzerland. 10. Department of Cardiology, Hospital Oost-Limburg, Genk, Belgium.
Abstract
BACKGROUND AND PURPOSE: The development of myocardial fibrosis is a major complication of Type 2 diabetes mellitus (T2DM), impairing myocardial deformation and, therefore, cardiac performance. It remains to be established whether abnormalities in longitudinal strain (LS) exaggerate or only occur in well-controlled T2DM, when exposed to exercise and, therefore, cardiac stress. We therefore studied left ventricular LS at rest and during exercise in T2DM patients vs. healthy controls. METHODS AND RESULTS: Exercise echocardiography was applied with combined breath-by-breath gas exchange analyses in asymptomatic, well-controlled (HbA1c: 6.9 ± 0.7%) T2DM patients (n = 36) and healthy controls (HC, n = 23). Left ventricular LS was assessed at rest and at peak exercise. Peak oxygen uptake (V̇O2peak) and workload (Wpeak) were similar between groups (p > 0.05). Diastolic (E, e's, E/e') and systolic function (left ventricular ejection fraction) were similar at rest and during exercise between groups (p > 0.05). LS (absolute values) was significantly lower at rest and during exercise in T2DM vs. HC (17.0 ± 2.9% vs. 19.8 ± 2% and 20.8 ± 4.0% vs. 23.3 ± 3.3%, respectively, p < 0.05). The response in myocardial deformation (the change in LS from rest up to peak exercise) was similar between groups (+ 3.8 ± 0.6% vs. + 3.6 ± 0.6%, in T2DM vs. HC, respectively, p > 0.05). Multiple regression revealed that HDL-cholesterol, fasted insulin levels and exercise tolerance accounted for 30.5% of the variance in response of myocardial deformation in the T2DM group (p = 0.002). CONCLUSION: Myocardial deformation is reduced in well-controlled T2DM and despite adequate responses, such differences persist during exercise. TRIAL REGISTRATION: NCT03299790, initially released 09/12/2017.
BACKGROUND AND PURPOSE: The development of myocardial fibrosis is a major complication of Type 2 diabetes mellitus (T2DM), impairing myocardial deformation and, therefore, cardiac performance. It remains to be established whether abnormalities in longitudinal strain (LS) exaggerate or only occur in well-controlled T2DM, when exposed to exercise and, therefore, cardiac stress. We therefore studied left ventricular LS at rest and during exercise in T2DM patients vs. healthy controls. METHODS AND RESULTS: Exercise echocardiography was applied with combined breath-by-breath gas exchange analyses in asymptomatic, well-controlled (HbA1c: 6.9 ± 0.7%) T2DM patients (n = 36) and healthy controls (HC, n = 23). Left ventricular LS was assessed at rest and at peak exercise. Peak oxygen uptake (V̇O2peak) and workload (Wpeak) were similar between groups (p > 0.05). Diastolic (E, e's, E/e') and systolic function (left ventricular ejection fraction) were similar at rest and during exercise between groups (p > 0.05). LS (absolute values) was significantly lower at rest and during exercise in T2DM vs. HC (17.0 ± 2.9% vs. 19.8 ± 2% and 20.8 ± 4.0% vs. 23.3 ± 3.3%, respectively, p < 0.05). The response in myocardial deformation (the change in LS from rest up to peak exercise) was similar between groups (+ 3.8 ± 0.6% vs. + 3.6 ± 0.6%, in T2DM vs. HC, respectively, p > 0.05). Multiple regression revealed that HDL-cholesterol, fasted insulin levels and exercise tolerance accounted for 30.5% of the variance in response of myocardial deformation in the T2DM group (p = 0.002). CONCLUSION:Myocardial deformation is reduced in well-controlled T2DM and despite adequate responses, such differences persist during exercise. TRIAL REGISTRATION: NCT03299790, initially released 09/12/2017.
Entities:
Keywords:
Exercise tests; Left ventricular longitudinal strain; Stress echocardiography; Type 2 diabetes mellitus
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