DALLAS, TX — Even a small amount of weight gain in healthy, young individuals is associated with worsening concentric left ventricular remodeling and cardiac function, posing a greater risk for future heart failure, a Dallas Heart Study analysis suggests[1].
“I was a little surprised that at just 5% weight gain, which is right at the clinical threshold of what we think is important, there was certainly an association with these changes,” said senior author Dr Ian Neeland (University of Texas Southwestern Medical Center, Dallas).
“What was also surprising was that there was an association with obesity status, so people who were not obese at baseline and gained weight had a greater negative impact on their cardiac structure and function than people who were obese already.”
The research was published online July 17, 2017 in the Journal of the American Heart Association.
Commenting to theheart.org | Medscape Cardiology, Dr Chiadi Ndumele (Johns Hopkins University School of Medicine, Baltimore, MD) said that there are already a lot of data with single measures of adiposity showing a very significant association between excess adiposity and myocardial dysfunction.
“We know that that’s there, but what this basically demonstrates is that even for those without that much adiposity at baseline, increasing weight over time still has an adverse effect on myocardial function, which broadly supports the idea of weight management across the weight spectrum,” Ndumele said. “I think it supports the importance of weight management basically for everybody.”
The 1262 participants (57% women) were free of coronary artery disease at baseline, but both Neeland and Ndumele said the results are likely to be applicable to those with established CVD.
Neeland noted that the Dallas Heart Study is also a more racially diverse (44% black) and younger (mean age 44 years) cohort than prior studies, and that they used multiple indices of adiposity as well as MRI, a more precise method than echocardiography, to assess cardiac structure.
Over a median follow-up of 6.8 years, 41% of participants gained clinically significant weight (>5%) and 15% lost clinically significant weight.
After adjustment for relevant confounders, increasing weight was associated with significantly higher LV mass (β=0.10; P<0.0001), wall thickness (β=0.10; P<0.0001), and concentricity (β=0.06; P=0.002).
The effect of increasing weight was more modest on end-diastolic volume (β=0.04; P=0.044) and ejection fraction (β=0.05; P=0.046), which is consistent with the literature including the Multi-Ethnic Study of Atherosclerosis (MESA) study, in which obesity in older adults was associated with concentric remodeling without much impact on ejection fraction, Neeland said.
In addition, increases in central adiposity over time, defined by waist circumference, index of central obesity, and visceral adiposity index, were also associated with concentric remodeling but not with volume or ejection fraction.
“The results suggest that concentric remodeling is the predominant phenotype with regard to obesity,” he said.
Neeland explained that obese persons were originally thought to have larger hearts and bigger volumes because the fat mass required more bloodflow, which increased cardiac output and led to changes in heart structure over time. The thinking has shifted in recent years, however, to concentric remodeling, characterized by a larger heart mass but a greater wall thickness, which causes a smaller rather than larger cavity size.
“As the mass goes up, the volume may go down or not change, which increases the concentricity. So that ends up with a relatively smaller, very thick chamber, which can lead to diastolic dysfunction and heart failure, especially with preserved ejection fraction,” he said.
It’s estimated that over 80% of people with heart failure with preserved ejection fraction are overweight or obese―more than twice the general population.
“Unfortunately, there’s nothing specifically we have in terms of our medical armamentarium to treat this beyond just good blood pressure control and diuretics, but it’s possible that targeting adiposity, body fatness, may be one way to treat heart failure with preserved ejection fraction in the future if this link does turn out to improve with therapy. Because what we saw is that if you lose weight, these changes can improve,” Neeland said.
“The heart is very plastic, very dynamic. It’s not like an MI where once the damage is done, it’s done,” he added.
Indeed, any amount of weight loss among the participants was associated with a decrease in concentricity, while any weight gain up to 20% was associated with greater concentricity.
Ndumele commented that the study is “a very helpful addition to the literature,” but that there’s more work to be done.
“We need to have a better understanding of the mechanisms that underlie this relationship and make some individuals more prone to myocardial changes in the setting of excess weight,” he said.
“I think we need additional data as well on the effects of long-term weight management and intentional weight loss through lifestyle modification on these measures of cardiac remodeling as well as on subsequent heart failure risk.”
The Dallas Heart Study was supported by a grant from the Reynolds Foundation and National Center for Advancing Translational Sciences of the National Institutes of Health. Neeland was supported by a grant from the National Institute of Diabetes and Digestive and Kidney Diseases, and by the Dedman Family Scholarship in Clinical Care from UT Southwestern. Ndumele reported no relevant financial relationships.
Follow Patrice Wendling on Twitter: @pwendl. For more from theheart.org | Medscape Cardiology, follow us on Twitter and Facebook.
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