Original articleImprovements in systemic metabolism, anthropometrics, and left ventricular geometry 3 months after bariatric surgery
Section snippets
Subject Selection
We offered participation to consecutive patients, of any race/ethnicity, from the University of Texas, Houston Bariatric Surgery Center, who met the candidacy requirements for bariatric surgery, as outlined previously [10]. In brief, they included a body mass index (BMI) >40 kg/m2 (or ≥35 kg/m2 with significant obesity-related co-morbidities), normal psychological evaluation findings, a history of multiple failed medically managed weight loss attempts, and an absence of any genetic or
Baseline Characteristics
The baseline clinical and demographic characteristics are shown in Table 1. The mean age ± SEM and BMI was 44 ± 2.1 years and 46.8 ± 1.4 kg/m2, respectively. The mean resting heart rate and blood pressure were normal. All patients met the criteria for abdominal obesity as determined from the waist circumference. The abdominal VAT area was 232 ± 18.5 cm2 at baseline, an area that has been demonstrated to predict for significant cardiovascular risk in women [23]. Even though only slightly greater
Discussion
In this prospective, longitudinal study after bariatric surgery, we have demonstrated improvements in systemic metabolism and profound decreases in weight and VAT during the first 3 postoperative months. Concurrent with these changes was a decrease in LV hypertrophy, but no change in LV contractile function, at 3 months postoperatively.
The causes of LV hypertrophy include obesity, activation of the sympathetic nervous system [26], and derangements in glucose and insulin metabolism [27]. We have
Conclusion
The results of this study have shown that the early phase of weight loss after bariatric surgery produces favorable changes in LV geometry that are associated with changes in glucose metabolism. The improvement in anthropometric measures and decreases in sympathetic tone, as a consequence of weight loss, may also play a role in decreased LV hypertrophy.
Acknowledgments
We thank E. Jane Meyers for her administrative support and Mark Punyanitya for his technical assistance with the MRI analysis; we also acknowledge Roxy Tate for her technical and editorial assistance.
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Supported in part from the National Institutes of Health, National Heart, Lung, and Blood Institute (5RO1 HL073162-02) to H. Taegtmeyer; American Society of Bariatric Surgeons Research grant to E. B. Wilson; and University of Texas Houston General Clinical Research Center (grant M01RR002558)