Left ventricular systolic dysfunction in obesity: a meta-analysis of speckle tracking echocardiographic studies

Background: Obesity is a risk factor for left ventricular hypertrophy (LVH) and diastolic dysfunction. Available evidence on impaired myocardial deformation in obese patients without apparent systolic dysfunction assessed by LV ejection fraction (LVEF) is based on single studies. The aim of the present meta-analysis was to provide a comprehensive and updated information on this issue. Methods: The PubMed, OVID-MEDLINE, and Cochrane library databases were analysed to search English-language articles published from the inception up to 31 December 2023. Studies were identified by using MeSH terms and crossing the following search items: 'myocardial strain', 'left ventricular mechanics', 'longitudinal global strain', 'speckle tracking echocardiography', 'systolic dysfunction', 'left ventricular ejection fraction', and 'obesity'. Results: Twenty-four studies including 5792 obese and 5518 nonobese individuals from different clinical settings were considered for the analysis. LV global longitudinal strain (GLS) was significantly impaired in the obese group [standard means difference (SMD): -0.86 ± 0.08; confidence interval (CI) -1.02 to -0.69, P < 0.0001] and this was paralleled by a significant difference in pooled LVEF between obese and controls (SMD -0.27 ± 0.06; CI -0.40 to -0.15, P < 0.0001). Unlike GLS, however, the majority of the selected studies failed to show statistically significant differences in LVEF. Furthermore, in patients with advanced obesity (BMI > 35 kg/m2, data from six studies), LV systolic dysfunction was more significantly detected by GLS (SMD -1.24 ± 0.19, CI -1.61/-0.87, P < 0.0001) than by LVEF (SMD -0.54 ± 0.27, CI -1.07 to -0.01, P = 0.046). Conclusion: The present meta-analysis suggests that GLS may unmask systolic dysfunction often undetected by conventional LVEF in the obese setting; thus, this parameter should be incorporated into routine work-up aimed to identify obesity-mediated subclinical cardiac damage.