Myocyte contractile dysfunction with hypertrophy and failure: Relevance to cardiac surgery

As the number of patients with pre-existing myocardial hypertrophy and/or CHF increases, the elucidation of mechanisms that potentially contribute to LV dysfunction after cardiac surgery is warranted. The results from recently performed studies, some of which have been reviewed here, suggest that underlying contributory factors for the exacerbation of LV dysfunction in patients with pre-existing hypertrophy and/or failure in the postoperative cardiac setting are changes in ionic currents and Ca2+ homeostasis. Therefore strategies that are focused on these ionic defects in LV hypertrophy and/or failure may have therapeutic benefit in the cardiac surgical setting. For example, the induction of myocardial electrical quiescence and cardioplegic arrest has been successfully achieved through the use of potassium channel openers that maintain the negative resting membrane potential of the myocyte.55 In isolated myocyte systems, the use of potassium channel openers has been demonstrated to prevent intracellular Ca2+ accumulation during the cardioplegic arrest period, which translated into reduced cytosolic Ca2+ levels with reperfusion and rewarming.55 Furthermore, the use of potassium channel openers in the intact LV has been demonstrated to maintain indices of LV ejection performance with reperfusion and rewarming in the setting of cardiopulmonary bypass.155 Thus strategies that facilitate cardioplegic arrest without detrimental effects on ionic currents and intracellular Ca2+ dynamics may have important implications with pre-existing LV hypertrophy and/or failure.