SYM-01: Bioengineering the Heart


June-Chiew Han, Denis Loiselle, Andrew Taberner

The University of Auckland, New Zealand

The heart is an engine. It consumes oxygen; it generates pressure-volume (or force-length) work; and it liberates heat. Any perturbation to its energy balance (such as from disease) will disturb its efficiency. If the perturbation is significant, the heart will fail.

Innovative experimental techniques and novel bioinstrumentation have allowed us to gain deeper insights into the energetics of the heart. In a basic-science experiment, the heart or its tissue strips are dissected from healthy or diseased animals. The preparation is mounted onto an apparatus with which to load it to various extents of pressure (or force), achieved by altering its volume (or length), under controlled experimental conditions. With such manoeuvres, the dependence of oxygen consumption (or heat), of work output, and of energy efficiency on pressure (or force) is revealed. These dependences of energy components change in the diseased heart. In the heart experiencing diabetes-induced left-ventricular hypertrophy, prolongation of the duration of contraction reduces the time for filling, resulting in reduced capability to work at high afterloads. Consequently, the dependence of efficiency on pressure (afterload) shifts leftward. Nevertheless, its peak efficiency, which occurs at a lower afterload, is unaffected. In contrast, in the systemic hypertension-induced left-ventricular hypertrophic heart, peak efficiency is compromised given lower work output arising from reduced ability both to produce force and to shorten.

The coupling between the ventricles of the heart is clinically significant and is hence of current interest. When the right ventricle is pressure overloaded, as in pulmonary hypertension, the left ventricle, in response, shrinks. Despite this effect, when the high pressure of the right ventricle is removed, the left ventricle can exhibit normal energetics, having a normal efficiency-afterload dependency. Understanding how the dependences of energy components change in the diseased heart, with respect to the healthy heart, is valuable for planning therapeutic strategy.

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