Heart failure was associated with an increased cell size throughout the left ventricle, but the form of the changes in electrophysiology and Ca2+ transient were dependent on the myocyte sub-type. In particular sub-endocardial cells displayed markedly different changes compared to the other myocyte sub-types.
There was enhanced shortening of APD and ventricular refractoriness in hypertrophied muscle during global ischaemia. This could increase the dispersion of repolarization and refractoriness between normal and ischaemic hypertrophied muscle during regional ischaemia which may explain the increased susceptibility of hypertrophied hearts to arrhythmias.
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