Abstract

Abstract Aim To evaluate effect of body mass index on left ventricle electromechanical delay among adults with no history of cardiac disease. Obesity is a complex disorder involving an excessive amount of body fat. Being extremely obese increases the risk of diseases and health problems, such as heart disease, type 2 diabetes mellitus, hypertension and premature death. The assessment of LV dyssynchrony has been gaining interest because it is increasingly considered to indicate the risk of progression to heart failure in various populations. Ventricular electromechanical delay can be measured from the onset of the QRS complex on electrocardiogram to the onset or peak of ventricular contraction determined by tissue Doppler imaging. Methods 66 subjects divided into three groups with 22 subjects for each group with age range (≥18 years and < 60 years old) of either sex with no history of cardiac disease were classified according to BMI into three group; Group A: subjects with normal BMI (18.5 – 24.9 kg/m2|), Group B: overweight subjects with BMI (25-29.9 kg/m2), Group C: obese subjects with BMI (≥ 30 kg/m2). The study groups were age, gender and risk factors matched. The time from the beginning of the QRS complex (on electrocardiogram) to the onset of systolic velocities in the septum and lateral wall were assessed and the time from the beginning of the QRS complex (on electrocardiogram) to the peak of systolic velocities in the septum and lateral wall were assessed using the pulsed wave Tissue Doppler Imaging (PW-TDI) by placing the sample volume in the middle of the basal portions of the LV septal and lateral walls in the apical four-chamber view at end-expiratory at a sweep speed of 100 mm/s, The difference between time recorded from septal and that recorded from lateral walls was referred as the lateral-to-septal delay. Results There was significant difference between the three groups regarding (lateral to septal delay) from onset of QRS to onset of S'(23.36±7.6 ms vs. 24.05±5.9ms vs. 35.18±9.3ms respectively, P < 0.0001), also there was a significant difference between study groups regarding (lateral to septal delay) from onset of QRS to peak of S'(39.41±9 ms vs. 48±10.4ms vs. 62.82±15.3ms respectively, P < 0.0001). There was a direct correlation between BMI and (lateral to septal delay) onset of QRS to peak of S' (r = 0.633, P < 0.0001) as well as (lateral to septal delay) onset of QRS to onset of S'(r = 0.64, P < 0.0001). Conclusion We present an interesting finding of left ventricular electromechanical delay in asymptomatic obese subjects with sinus rhythm and no history of cardiac disease. It would be speculative to say that the intraventricular dyssynchrony seen in asymptomatic obese individuals is related to cardiac electrical remodeling occurs with obesity and gives a proposal to understand pathophysiology of heart failure occurring in obese patients.

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