Eighty-seven MetS patients were enrolled in a 6 month lifestyle intervention program based on dietary management and increased physical activity, and compared with 44 aged and sex-matched healthy controls. MetS individuals were allocated to different groups randomized (computer-generated randomization) on exercise modalities (high-intensity dominant resistance or aerobic training, and moderate-intensity of both modes). EAT was measured by transthoracic echocardiography and LV longitudinal strains and strain rates were obtained using vector velocity imaging. Blood chemistry allowed assessments of adipocytokines (TNF-α: tumor necrosis factor α, PAI active: active plasminogen activator inhibitor-1 and adiponectin) and glucose tolerance markers.
Regardless of exercise training modalities, lifestyle intervention improved significantly LV strains and strain rates (p < 0.001) as well as metabolic and inflammatory profiles. Stepwise multiple regression analyses revealed EAT (β = 0.73, p < 0.01), log adiponectin (β = − 0.13, p < 0.05) and log TNF-α (β = 0.15, p < 0.05) as independent predictors of LV longitudinal strain (R2 = 0.74, p < 0.001) while myocardial function improvement consecutive to lifestyle intervention was explained by EAT changes only (R2 = 0.54, p < 0.001).
The mechanisms through which regional myocardial function is impaired in MetS and improved consecutive to intervention involved EAT, possibly via paracrine effects of adipocytokines. EAT should be considered as a future therapeutic target of interest in the treatment of metabolic-related cardiac diseases.