A Spahillari1, K J Mukamal2, C DeFilippi3, J R Kizer4, J S Gottdiener5, L Djoussé6, M F Lyles7, T M Bartz8, V L Murthy9, R V Shah10. 1. Division of Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Electronic address: aspahill@bidmc.harvard.edu. 2. Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Electronic address: kmukamal@bidmc.harvard.edu. 3. Division of Cardiovascular Medicine, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA. Electronic address: cdefilip@medicine.umaryland.edu. 4. Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York, NY, USA. Electronic address: jorge.kizer@einstein.yu.edu. 5. Department of Medicine, University of Maryland Medical School, Baltimore, MD, USA. Electronic address: jgottdie@medicine.umaryland.edu. 6. Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA. Electronic address: ldjousse@partners.org. 7. Department of Medicine, Section on Gerontology and Geriatrics, Wake Forest School of Medicine, Winston-Salem, NC, USA. Electronic address: mlyles@wakehealth.edu. 8. Department of Biostatistics, University of Washington, Seattle, WA, USA. Electronic address: bartzt@uw.edu. 9. Frankel Cardiovascular Center and Department of Medicine (Cardiovascular Medicine Division), University of Michigan, Ann Arbor, MI, USA. Electronic address: vlmurthy@med.umich.edu. 10. Department of Medicine (Division of Cardiology), Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: rvshah@partners.org.
Abstract
BACKGROUND AND AIMS: Understanding contributions of lean and fat tissue to cardiovascular and non-cardiovascular mortality may help clarify areas of prevention in older adults. We aimed to define distributions of lean and fat tissue in older adults and their contributions to cause-specific mortality. METHODS AND RESULTS: A total of 1335 participants of the Cardiovascular Health Study (CHS) who underwent dual-energy x-ray absorptiometry (DEXA) scans were included. We used principal components analysis (PCA) to define two independent sources of variation in DEXA-derived body composition, corresponding to principal components composed of lean ("lean PC") and fat ("fat PC") tissue. We used Cox proportional hazards regression using these PCs to investigate the relationship between body composition with cardiovascular and non-cardiovascular mortality. Mean age was 76.2 ± 4.8 years (56% women) with mean body mass index 27.1 ± 4.4 kg/m2. A greater lean PC was associated with lower all-cause (HR = 0.91, 95% CI 0.84-0.98, P = 0.01) and cardiovascular mortality (HR = 0.84, 95% CI 0.74-0.95, P = 0.005). The lowest quartile of the fat PC (least adiposity) was associated with a greater hazard of all-cause mortality (HR = 1.24, 95% CI 1.04-1.48, P = 0.02) relative to fat PCs between the 25th-75th percentile, but the highest quartile did not have a significantly greater hazard (P = 0.70). CONCLUSION: Greater lean tissue mass is associated with improved cardiovascular and overall mortality in the elderly. The lowest levels of fat tissue mass are linked with adverse prognosis, but the highest levels show no significant mortality protection. Prevention efforts in the elderly frail may be best targeted toward improvements in lean muscle mass.
BACKGROUND AND AIMS: Understanding contributions of lean and fat tissue to cardiovascular and non-cardiovascular mortality may help clarify areas of prevention in older adults. We aimed to define distributions of lean and fat tissue in older adults and their contributions to cause-specific mortality. METHODS AND RESULTS: A total of 1335 participants of the Cardiovascular Health Study (CHS) who underwent dual-energy x-ray absorptiometry (DEXA) scans were included. We used principal components analysis (PCA) to define two independent sources of variation in DEXA-derived body composition, corresponding to principal components composed of lean ("lean PC") and fat ("fat PC") tissue. We used Cox proportional hazards regression using these PCs to investigate the relationship between body composition with cardiovascular and non-cardiovascular mortality. Mean age was 76.2 ± 4.8 years (56% women) with mean body mass index 27.1 ± 4.4 kg/m2. A greater lean PC was associated with lower all-cause (HR = 0.91, 95% CI 0.84-0.98, P = 0.01) and cardiovascular mortality (HR = 0.84, 95% CI 0.74-0.95, P = 0.005). The lowest quartile of the fat PC (least adiposity) was associated with a greater hazard of all-cause mortality (HR = 1.24, 95% CI 1.04-1.48, P = 0.02) relative to fat PCs between the 25th-75th percentile, but the highest quartile did not have a significantly greater hazard (P = 0.70). CONCLUSION: Greater lean tissue mass is associated with improved cardiovascular and overall mortality in the elderly. The lowest levels of fat tissue mass are linked with adverse prognosis, but the highest levels show no significant mortality protection. Prevention efforts in the elderly frail may be best targeted toward improvements in lean muscle mass.
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