Key result
Pressure loading increased the microtubule component of the cardiac muscle cell cytoskeleton, causing persistent cellular contractile dysfunction in hypertrophied myocardium.
Systolic pressure loading increases the microtubule component of the cytoskeleton, leading to contractile dysfunction in hypertrophied myocardium, which may contribute to the progression to congestive heart failure.
Hypothesis-generating for cytoskeletal role in pressure-overload HF progression; leaves open microtubule targeting in patients.
Cardiac hypertrophy in response to systolic pressure loading frequently results in contractile dysfunction of unknown cause. In the present study, pressure loading increased the microtubule component of the cardiac muscle cell cytoskeleton, which was responsible for the cellular contractile dysfunction observed. The linked microtubule and contractile abnormalities were persistent and thus may have significance for the deterioration of initially compensatory cardiac hypertrophy into congestive heart failure.
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Tsutsui et al. (1993) studied Cardiac hypertrophy and contractile dysfunction. Pressure loading was evaluated on Microtubule component of the cardiac muscle cell cytoskeleton and cellular contractile dysfunction. Pressure loading increased the microtubule component of the cardiac muscle cell cytoskeleton, causing persistent cellular contractile dysfunction in hypertrophied myocardium.
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