Clinical research study
Progressive Regression of Left Ventricular Hypertrophy Two Years after Bariatric Surgery

https://doi.org/10.1016/j.amjmed.2009.11.020Get rights and content

Abstract

Background

Obesity is a systemic disorder associated with an increase in left ventricular mass and premature death and disability from cardiovascular disease. Although bariatric surgery reverses many of the hormonal and hemodynamic derangements, the long-term collective effects on body composition and left ventricular mass have not been considered before. We hypothesized that the decrease in fat mass and lean mass after weight loss surgery is associated with a decrease in left ventricular mass.

Methods

Fifteen severely obese women (mean body mass index [BMI]: 46.7 ± 1.7 kg/m2) with medically controlled hypertension underwent bariatric surgery. Left ventricular mass and plasma markers of systemic metabolism, together with body mass index (BMI), waist and hip circumferences, body composition (fat mass and lean mass), and resting energy expenditure were measured at 0, 3, 9, 12, and 24 months.

Results

Left ventricular mass continued to decrease linearly over the entire period of observation, while rates of weight loss, loss of lean mass, loss of fat mass, and resting energy expenditure all plateaued at 3 months (P <.001 for all). Parameters of systemic metabolism normalized by 9 months, and showed no further change at 24 months after surgery.

Conclusions

Even though parameters of obesity, including BMI and body composition, plateau, the benefits of bariatric surgery on systemic metabolism and left ventricular mass are sustained. We propose that the progressive decrease of left ventricular mass after weight loss surgery is regulated by neurohumoral factors, and may contribute to improved long-term survival.

Section snippets

Subjects

Fifteen consecutive women with clinically severe obesity (BMI 46.7 kg/m2, mean age: 49.1 ± 2.1 years; 10 white, 4 black, 1 Hispanic) underwent bariatric surgery at the University of Texas Medical School at Houston Bariatric Surgery Center. The subjects met inclusion criteria published previously.14 Exclusion criteria were: age <18 years, pregnancy, coronary artery disease, ischemic cardiomyopathy, severe peripheral vascular disease, or a current history of smoking. The study was approved by the

Clinical Data

Significant physical and metabolic changes were observed as early as 1 month post surgery (Figure 1) and continued to be present throughout the entire 2-year period. The clinical, hemodynamic, and metabolic data are summarized in the Table.

All patients were severely obese at the start of the study (BMI 46.7 kg/m2) and experienced significant weight reduction (from 126.7 to 86.8 kg), yet remained clinically obese at 24 months following surgery (BMI 32.4 kg/m2) (Figure 1A). More specifically, the

Discussion

We made the following observations: weight decreased early after weight loss surgery, but plateaued when patients were still obese; left ventricular mass decreased progressively, and continued to decrease at a linear rate for at least 24 months after weight-loss surgery; left ventricular mass was overall insensitive to body composition, suggesting that the heart continued to remodel even after body weight had reached a new plateau; and systemic metabolism normalized by 3 months, and remained so

Conclusions

Even though parameters of obesity, including BMI and body composition, plateau, the benefits of bariatric surgery on metabolism and left ventricular mass are sustained. We propose that the decrease of left ventricular mass after weight loss surgery is regulated by neurohumoral factors. No matter what the mechanism, the decrease in left ventricular mass is likely to contribute to the improved long-term survival of patients following weight loss surgery.

Acknowledgments

We wish to thank Dr. Eddy Barasch for his insightful suggestions, and Mrs. Roxy Tate for her expert editorial assistance.

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    Funding: This study was supported by The National Heart, Lung, and Blood Institute of the US Public Health Service (R01HL073162), and Grant # M01RR002558 for the Center for Clinical Research, University of Texas Medical School at Houston.

    Conflict of Interest: None of the authors of this work have any financial conflicts of interest to disclose.

    Authorship: Mohamed F. Algahim and Thomas R. Lux contributed equally to the manuscript. All authors had access to the data and a role in writing the manuscript.

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