Key result
In obese subjects, the presence of left ventricular hypertrophy was associated with significantly reduced left ventricular ejection fraction (p<0.001) and increased cardiometabolic comorbidities.
Why the study?
Obesity-associated changes in cardiac structure and ventricular function involve hemodynamic and non-hemodynamic alterations, but the prevalence of LVH and its effect on systolic and diastolic function needed evaluation in obese patients.
Cross-Sectional (n=319)
p-value: p=< .001
Obese patients with LVH represent a distinct phenotype characterized by higher cardiometabolic risk, lower adiponectin levels, and early left ventricular systolic dysfunction.
Obese patients with LVH may warrant closer cardiometabolic monitoring; hypothesis-generating for prospective studies on systolic outcomes.
Background: It has been reported that changes in cardiac structure and ventricular function associated with obesity have to be attributable to hemodynamic and non-hemodynamic alterations. Accordingly, the aim of this was to evaluate left ventricular hypertrophy (LVH) prevalence and its effect on left ventricular systolic and diastolic function in a cohort of obese patients.Materials and Methods: LV internal diameter (LVID), left ventricular mass (LVM) and LVM/height2.7(LVMI), relative wall thickness (RWT), LV ejection fraction (LVEF), E/A ratio, isovolumic relaxation time, deceleration time of E velocity by echocardiography and pulsed-wave Doppler and total circulating adiponectin (ADPN) by radioimmunoassay were measured in 319 obese subjects with and without LVH.Results: Increased values of BMI, WHR, SBP, DBP, MBP LVID, LVM, LVMI, IVST (p < .001), increased prevalence of subjects with LVEF< 50%,(p < .001), central fat distribution (p < .001), hypertension (p < .001), diabetes (p < .001), metabolic syndrome (p < .02), and reduced value of ADPN (p < .0001) and LVEF (p < .001) were detected in LVH obese subjects than controls without LVH. No significant differences in diastolic parameters were observed between the two groups. LVEF correlated directly with ADPN (p < .0001) and inversely with age (p < .01), BMI (p < .01), WHR (p < .001), MBP (p < .01) MetS (p < .02) and LVMI (p < .001). WHR, MBP, LVMI and ADPN were independently associated with LVEF.Conclusions: In conclusion, our data indicate that obese subjects with LVH might be considered a distinct phenotype of obesity, characterised by LVH, increased prevalence of cardiometabolic comorbidities, central fat distribution, hypoadiponectinemia and early left ventricular systolic dysfunction.
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Chiara et al. (2019) conducted a cross-sectional in Obesity (n=319). Left ventricular hypertrophy (LVH) vs. Obese subjects without LVH was evaluated on Left ventricular systolic and diastolic function (including LVEF) (p=< .001). In obese subjects, the presence of left ventricular hypertrophy was associated with significantly reduced left ventricular ejection fraction (p<0.001) and increased cardiometabolic comorbidities.
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