The results of this study indicate that obesity is positively related to LV mass and volume in a large, community-based multiethnic population. Using multiple measures of obesity (BMI, WC, WHR, and FM), LV mass increased to a greater extent than LV volume. We observed 1) increasing levels of obesity were associated with concentric LV remodeling, expressed by increased LV M/V ratio; 2) the increased M/V ratio was due to a greater increase in LV mass relative to LV end-diastolic volume; 3) the relationships between obesity measures and LV mass and M/V ratio were generally greater in Hispanic and Caucasian men compared with other subgroups; 4) global ventricular systolic function (assessed by ejection fraction) was insensitive to myocardial changes associated with obesity.
Obesity has been considered as a state of chronic volume overload because the heart is required to circulate blood through the large and relatively low resistance depot of adipose tissue. Early studies had suggested that obesity was associated with eccentric LV remodeling. The results of this CMR study and other echocardiography studies instead now consistently show that both LV cavity size and wall thickness may be increased in obese subjects with wall thickness increased to a greater extent than cavity size (concentric LV remodeling) (3
). Several studies have found that LV ejection fraction is normal to increased in the majority of obese subjects (14
Multiple biological mechanisms have been implicated in explaining the impact of excess adiposity on LV geometry and function. Visceral fat, which has been shown to be the metabolically active compartment of fat deposits, may mediate the increased LV mass by secreting a variety of bioactive molecules such as angiotensin II and inflammatory cytokines. A previous MESA study has reported that pathways related to inflammation might, at least partially, explain the association between obesity and chronic heart failure (18
). Hyperinsulinemia and insulin resistance, which are also closely related to abdominal obesity, may induce myocardial hypertrophy by growth-stimulating effect of insulin or increasing blood volume (19
). Typically, higher systolic blood pressures, even if they are not in the hypertensive range, have an additive effect on concentric myocardial remodeling. Finally, obstructive sleep apnea could contribute to LV hypertrophy by exacerbation of daytime and nighttime hypertension, increased sympathetic tone, and chronic hypoxemia (19
Iacobellis and Sharma (20
) proposed “uncomplicated obesity” as those individuals with elevated BMI but with normal fasting glucose, glucose tolerance, systolic and diastolic blood pressures, lipid profile, resting electrocardiogram, and thyroid function, without history of metabolic, cardiovascular, respiratory disease, and clinically significant abnormalities on physical examination. They reported that indexed LV mass and LV geometry in subjects with uncomplicated obesity (n = 75) were not significantly different from a lean control group (n = 60) (17
). In the present study, only 1.8% (89/5,004) of participants were obese and without hypertension, impaired glucose tolerance/diabetes, dyslipidemia, and major electrocardiographic changes. Therefore, the concept of uncomplicated obesity was not useful in our study population due to the rare occurrence of this phenotype.
Determining the relationship between obesity and cardiac size is confounded by the known positive relationship of body size to LV mass and volume. Body surface area is the most common index for cardiac size but has been suggested to underestimate the impact of obesity on LV mass and geometry (21
). Alternatively, indexing LV mass to the 2.7 power of height has been reported to be appropriate for but has unknown applicability for CMR. For the MESA population, LV mass indexed to the 2.7 power of height resulted in a higher proportion of LV hypertrophy for shorter participants compared with taller participants (data not shown), raising questions regarding the validity of this approach for our data.
To overcome this difficulty, we looked at multiple measures of obesity (BMI, WC, and WHR) and also examined the association of FM with LV size after controlling for fat-free mass. In addition, LV M/V ratio and ejection fraction allow ventricular geometry and function, respectively, to be assessed without the need for further body size adjustment. With all measures of obesity, ejection fraction showed no consistent change in relation to in- creased obesity levels.
Selection of participants in MESA was designed to minimize biases typically associated with studies of volunteers. Because all our participants were free of clinically apparent cardiovascular disease at baseline, participants represent a relatively healthy population-based sample. Severely obese participants (>300 pounds) had to be excluded because of CMR bore-diameter and table weight limits. Estimation of FM from weight-height models allowed only an approximate evaluation of FM amount.