Aging Alters Cardiac Cytoskeletal Properties

It is well established that the aging heart exhibits diastolic dysfunction, which has been attributed to the altered structure of the heart, particularly increased interstitial collagen. The objective of this study was to measure changes in cardiac cytoskeletal components in order to test the hypothesis that the mechanism mediating dysfunction in the aging heart resides, in part, in changes in the material properties of cardiac cells. In vivo cardiac function was measured by echocardiography in young (4 mos) (n=7) and old (30 mos) (n=7) Fischer 344 x Brown Norway F1 hybrid (F344xBN) rats. Significant (P<0.05) systolic dysfunction was seen with age where a 37% decrease in LV Percentage Fractional Shortening was measured (from 52.0 ± 1.5 % (n = 7) to 37.9 ± 2.4 % (n = 7)). Significant (P<0.05) diastolic dysfunction was also measured with a 48% increase in Isovolumic Relaxation Time (IVRT) (from 17.5 ± 1.3 msec (n = 7) to 25.9 ± 1.2 msec (n = 7)). Left Ventricular (LV) samples were collected for imunoblot (western) analyses. The western results indicate a significant (P<0.05) 41% decrease in the amount of the intermediate filament Desmin with aging (from 1.8 ± 0.1 arbitrary density units (ADU) (n = 7) to 1.1 ± 0.1 ADU (n = 7)) and a significant (P<0.05) increase in the amount of microtubules with aging with a 2.3 fold increase in α‐tubulin (from 1.3 ± 0.1 ADU (n = 7) to 4.1 ± 0.4 ADU (n = 7)) and 1.7 fold increase in β‐tubulin (from 1.5 ± 0.3 ADU (n = 7) to 4.1 ± 0.4 ADU (n = 7)). In conclusion, these data support the hypothesis that the mechanism mediating cardiac dysfunction with aging may also involve alterations in cytoskeletal proteins.