Impact of obesity on cardiac geometry and function in a population of adolescents: the Strong Heart Study

Abstract

Objectives: The goal here was to examine left ventricular (LV) geometry and function in a large, unselected group of adolescents with different degrees of abnormal body build, and verify whether possibly higher LV mass is compensatory for increased cardiac workload.

Background: There is little information on how much the excess of body weight impacts LV geometry and function in populations of adolescents.

Methods: Anthropometric, laboratory, and Doppler echocardiographic parameters of cardiac geometry and function were obtained in 460 adolescent participants (age 14 to 20 years, 245 female participants, 27 hypertensive, 10 with diabetes) from the Strong Heart Study. Body build was classified based on 85th and 95th percentiles of body mass index (BMI)-for-age charts.

Results: Range of BMI was 16.3 to 56.5 kg/m2 (28.8 +/- 8.3 kg/m2); 114 participants (24.9%) fell within the 85th percentile of BMI distribution (normal weight [NW]), 113 (24.6%) fell between 85th and 95th percentile (overweight [OW]), and 223 (48.5%) fell above the 95th percentile (obese [OB]). Obese participants were older than OW and NW subjects (p < 0.01), without differences in heart rate. Both OW and OB had greater LV diameter and mass than NW (all p < 0.05). Left ventricular hypertrophy was more prevalent in the OB (33.5%) and OW (12.4%), as compared with NW participants (3.5%; p < 0.001), largely compensating increased cardiac workload. However, OB subjects had four-fold higher probability of carrying an LV mass exceeding values compensatory for their cardiac workload (p < 0.001), a feature associated with lower ejection fraction, myocardial contractility, and greater force developed by left atrium to complete LV filling (all p < 0.05).

Conclusions: While in OW adolescents increased levels of LV mass are appropriate to compensate their higher hemodynamic load, in OB increase in LV mass exceeds this need and is associated with mildly reduced LV myocardial performance and increased left atrial force to contribute to LV filling.