Early abnormalities of LV longitudinal systolic deformation were found both in pre-HT and HT, together with a mild LV diastolic dysfunction. In both groups this early cardiac systolic and diastolic dysfunction is associated to insulin resistance, systolic pressure load, and cardiac remodeling.
Background: The aim of this study was to evaluate the relationship between insulin resistance and preclinical abnormalities of the left ventricular structure and function detected in severe obesity by Color Doppler Myocardial Imaging (CDMI). Forty-eight consecutive severely obese patients (Group O) (11 males, 37 females, mean age 32.877 years) were enrolled. Forty-eight sexand age-matched non-obese healthy subjects were also recruited as controls (Group C). All subjects underwent conventional 2D-Color Doppler echocardiography and CDMI. The homeostasis model assessment insulin resistance index (HOMA-IR) was used to assess insulin resistance results. Obese subjects had a greater left ventricular mass index (by height) (58.8714 g/m 2.7 ) than controls (3778 g/m 2.7 ) (Po0.0001), owing to compensation response to volume overload caused by a greater cardiac output (Po0.02). Preload reserve was increased in obese subjects, as demonstrated by a significant increase in left atrial dimension (Po0.0001). Obese patients had a slightly reduced LV diastolic function (transmitral E/A ratio: Group O, 1.170.8 vs Group C, 1.5 70.5; Po0.002). Cardiac deformation assessed by regional myocardial systolic strain and strain rate (SR) values was significantly lower (abnormal) in obese patients than in controls, both at the septum and lateral wall level. These strain and SR abnormalities were significantly related to body mass index. In addition, the early phase of diastolic function, evaluated using SR, was compromised in obese patients (Po0.001). The HOMA-IR values in obese patients were significantly higher (3.0971.6) than those determined in the control group (0.9270.5) (Po0.0001). The HOMA-IR values, in the obese group, were significantly related to systolic strain and SR values sampled at the septum level (Po0.0001). Conclusion: In conclusion, this study has demonstrated that obese patients pointed out systolic structural and functional abnormalities at a preclinical stage, in particular through strain and SR analysis; on the other hand, those altered CDMI parameters well distinguish obese subjects as compared with the control group. Furthermore, another main finding of the study was that myocardial deformation (systolic strain) could have a correlation with insulin resistance level.
The present study demonstrated that active acromegalic patients had early impairment of systolic function and increased cardiac fibrosis; increased fibrosis may precede LV hypertrophy; these changes are related to the activity of disease and might improve during treatment with SMSA.
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