Cardiac Structure and Function and Frailty in Subjects Aged 85 and 86 Years

David Leibowitz*, Jeremy M. Jacobs, Dan Gilon, Irit Lande-Stessman, Eliana Ein-Mor, Jochanan Stessman

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

Frailty is a biologic syndrome reflecting a state of decreased physiological reserve of increasing importance in cardiovascular disease given the aging of the population. The relation between frailty and indexes of cardiac structure and function remains unclear, particularly in the “oldest old.” The objective of this study was to examine the association between cardiac function and frailty in an age-homogenous, community-dwelling population of subjects aged 85 and 86 years. Subjects were recruited at ages 85 to 86 from the Jerusalem Longitudinal Cohort Study that has followed an age-homogenous cohort of Jerusalem residents. Subjects underwent echocardiography at their place of residence with standard assessment of cardiac structure and function. Frailty was defined according to the “phenotype of frailty” including at least 3 of the following: weakness, slowness, low physical activity level, exhaustion, and weight loss; 405 subjects (193 men and 212 women) were enrolled in the study. Subjects defined as frail had significantly lower ejection fraction compared with the non-frail group (53.7 ± 0.09% vs 56.4 ± 0.09%; p <0.04). In addition, frail subjects had increased LV mass index (130.6 ± 36.2 g/m2 vs 119.2 ± 31.1 g/m2; p <0.03) and LA volume index (41.9 ± 14.7 cm3/m2 vs 36.7 ± 13.1 cm3/m2; p <0.001). Indexes of diastolic function (E/e)' were not significantly different in the 2 groups (11.5 vs 11.8; p = NS). In this age-homogenous cohort of the oldest old, structural changes and indexes of systolic but not diastolic function were associated with frailty.

Original languageAmerican English
Pages (from-to)760-764
Number of pages5
JournalAmerican Journal of Cardiology
Volume118
Issue number5
DOIs
StatePublished - 2016

Bibliographical note

Publisher Copyright:
© 2016 Elsevier Inc.

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