Author + information
- Shishir Sharma, MD,
- Laura A. Colangelo, MS,
- João Lima, MD,
- Kiang Liu, PhD,
- Chintan Desai, MD,
- Satoru Kishi, MD,
- Jared Reis, PhD and
- Philip Greenland, MD∗ ()
- ↵∗Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, 680 North Lake Shore Drive, Suite 1400, Chicago, Illinois 60611
Relative weight, often characterized as body mass index (BMI), is a factor associated with left ventricular (LV) mass and geometry. Cross-sectional studies in middle-aged adults showed higher BMI was associated with higher LV mass and volumes (1). Longitudinal data in another middle-aged cohort showed higher initial BMI was associated with greater increase in LV mass (2).
The goal of this study was to determine whether BMI was associated with changing cardiac structure and function over the next 20 years and whether maintaining a stable BMI was associated with less change in cardiac structure and function.
The CARDIA (Coronary Artery Risk Development in Young Adults Study) study recruited 5,115 Caucasian and African American men and women, 18 to 30 years of age, in 4 U.S. centers in 1985 (year 1). We stratified participants by year 5 (initial) BMI (kg/m2): 18.5 to 24.9, 25 to 29.9, 30 to 34.9, ≥35. We further stratified participants by BMI change between years 5 and 25: increasing BMI (>2), stable BMI (≤2), and fluctuating BMI (>2 at interim exam but ≤2 by year 25 exam). Blind rereading of echocardiograms to assess inter-reader variability, intrareader variability, and intra-patient variability showed LV mass coefficients of variability were <8% (3). LV mass index (LVMi) = LV mass/height1.7. Year 25 minus year 5 differences in risk factor-adjusted (age, sex, race, systolic blood pressure, antihypertensive use, heart rate, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, diabetes, tobacco and alcohol use) echocardiographic variables were examined using an analysis of covariance, treating initial (year 5) BMI group and BMI change group as the main effects.
At year 5, the LVMi cohort was 51% white and 45% male with mean age of 30 years. There was no interaction between initial BMI and BMI change. Initial BMI was associated with change in LVMi (p = 0.02) and left ventricular ejection fraction (LVEF) (p = 0.009). BMI change was associated with change in LVMi (p < 0.0001), relative wall thickness (RWT) (p = 0.006), and LV end-diastolic volume index (LVEDVi) (p < 0.0001). Table 1 displays changes in LVMi and LVEF. RWT only changed in participants with increasing BMI (0.011 ± 0.003; p = 0.0005). LVEDVi only changed in participants with increasing (–10 ± 1 ml/m2; p < 0.0001) and fluctuating (–12 ± 2 ml/m2; p < 0.0001) BMI. In the increasing BMI group, for each adjusted 1 kg/m2 increase in BMI, LVMi increased 0.9 ± 0.1 g/m1.7 (p < 0.0001) and LVEDVi decreased –0.4 ± 0.2 ml/m2 (p = 0.02).
Higher initial BMI was associated with greater increase in LVMi, which is consistent with previous studies (2). We showed the novel finding that BMI stability over 20 years was associated with increased LVMi. Long-term exposure to pathologic changes of obesity, without further weight gain may be sufficient to cause this increase. As a result, BMI stability may not be an adequate goal for overweight individuals. Fluctuating BMI was associated with a lower increase in LVMi than increasing BMI, suggesting transient increases in BMI may not be as harmful as long as the individual eventually loses weight.
The current study supports the idea that obesity increases wall thickness more than it increases cavity size. We found increasing BMI was associated with concentric remodeling (LVMi and RWT increased). However, we also showed the novel finding that stable and fluctuating BMI were associated with eccentric remodeling (LVMi increased but RWT did not). This may reconcile how obesity was previously believed to be associated with eccentric remodeling.
We showed the novel finding that higher initial BMI was associated with greater decrease in LVEF over 20 years. Compensatory cardiac remodeling may maintain LVEF in the short term, as seen in cross-sectional studies, but cannot do so in the setting of persistently elevated BMI over the long term follow-up conducted in this study.
In summary, in this prospective, longitudinal study of young adults, we showed that both higher initial BMI and increases in BMI were associated with adverse changes over 20 years in LV structure and function. Even participants with stable but high BMI developed adverse LV change. These observations support the need to maintain lower BMI from an early age to prevent adverse LV remodeling over time and eventual decrease in LVEF.
Please note: The CARDIA study is supported by contracts HHSN268201300025C, HHSN268201300026C, HHSN268201300027C, HHSN268201300028C, HHSN268201300029C, and HHSN268200900041C from the National Heart, Lung, and Blood Institute (NHLBI), the Intramural Research Program of the National Institute on Aging (NIA), and an interagency agreement between the NIA and NHLBI (AG0005). All authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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