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1 Biophysics, Maastricht University, Maastricht, Netherlands; Bioengineering Institute, University of Auckland, Auckland, New Zealand
2 Physiology, Maastricht University, Maastricht, Netherlands
3 Biophysics, Maastricht University, Maastricht, Netherlands
4 Medicine, University of Auckland, Auckland, New Zealand
5 Bioengineering Institute, University of Auckland, Auckland, New Zealand
* To whom correspondence should be addressed. E-mail: j.lumens{at}fys.unimaas.nl.
With aging, structural and functional changes occur in the myocardium without obvious impairment of systolic LV function. Transmural differences in myocardial vulnerability for these changes may result in increase of transmural inhomogeneity in contractile myofiber function. Subendocardial fibrosis and impairment of subendocardial perfusion due to hypertension might change the transmural distribution of contractile myofiber function. The ratio of left ventricular (LV) torsion to endocardial circumferential shortening (torsion-to-shortening ratio; TSR) during systole reflects the transmural distribution of contractile myofiber function. We investigated whether the transmural distribution of systolic contractile myofiber function changes with age. Magnetic resonance tissue tagging (MRT) was performed to derive LV torsion and endocardial circumferential shortening. TSR was quantified in asymptomatic young [age 23.2 (SD 2.6) yrs, n = 15] and aged volunteers [age 68.8 (SD 4.4) yrs, n = 16]. TSR and its standard deviation were significantly elevated in the aged group [0.47 (SD 0.12) aged vs. 0.34 (SD 0.05) young; P = 0.0004]. In the aged, blood pressure and the ratio of LV wall mass to end-diastolic volume were mildly elevated, but could not be correlated to the increase in TSR. There were no significant differences in other indices of systolic LV function such as end-systolic volume (ESV) and ejection fraction (EF). The elevated systolic TSR in the asymptomatic aged subjects suggests that aging is associated with local loss of contractile myofiber function in the subendocardium relative to the subepicardium potentially caused by subclinical pathological incidents.
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