• Aging Clin Exp Res · Apr 2018

    Ventricular-arterial coupling in centenarians without cardiovascular diseases.

    • Andrea Sonaglioni, Massimo Baravelli, Michele Lombardo, Carmen Sommese, Claudio Anzà, Jonathan A Kirk, and Luigi Padeletti.
    • Department of Cardiology, Ospedale San Giuseppe Multimedica, Via San Vittore 12, 20123, Milan, Italy. sonaglioniandrea@gmail.com.
    • Aging Clin Exp Res. 2018 Apr 1; 30 (4): 367-373.

    BackgroundVentricular-arterial (VA) coupling is a central determinant of cardiovascular system performance and cardiac energetics. This index is expressed by the Ea/Ees ratio, where the effective arterial elastance (Ea) indicates the net arterial load exerted on the left ventricle and the left ventricular end-systolic elastance (Ees) is a load-independent measure of left ventricular chamber performance.MethodsThirty-three centenarians (100.6 ± 1.2 years, range 99-105 years, 10 M) without cardiovascular diseases underwent a complete echocardiographic evaluation and an instantaneous arterial blood pressure measurement, to characterize the Ea/Ees ratio and its two determinants indexed to body surface area.ResultsVA coupling was markedly reduced (Ea/Ees ratio 0.40 ± 0.1), reflecting a disproportionate increase in Ees index (8.5 ± 2.2 mmHg/ml/m2) compared with Ea index (3.2 ± 0.8 mmHg/ml/m2). Notably, the coupling ratio was significantly lower in women (0.37 ± 0.1) than in men (0.45 ± 0.1, p = 0.0003), due to an increase in Ees index significantly greater in women (9.4 ± 1.9 mmHg/ml/m2) than in men (6.5 ± 1.5 mmHg/ml/m2, p = 0.0002). Using multivariate regression analysis, only female gender (β coefficient -0.04, p = 0.01) and relative wall thickness (β coefficient -0.49, p < 0.0001) showed a significant inverse correlation to VA coupling.ConclusionsOur analysis in a population of centenarians without overt cardiovascular disease revealed very low values of VA coupling, especially in women. Both a LV structural remodeling as well as a high aortic elastance might have contributed to a secondary disproportionate increase in myocardial stiffness.

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