Cardiac hypertrophy in response to systolic pressure overloading results in myocyte contractile dysfunction, the mechanisms for which have not been established. Stress loading increases the microtubules, which apparently is responsible for the cellular contractile dysfunction. These alterations in microtubules and contractile function have a specific association with increased ventricular wall stress. The linked microtubule and contractile abnormalities are persistent and the further increase of microtubules plays an important role in the deterioration of initially compensated cardiac hypertrophy into heart failure.
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