titin extension during diastole is limited and protects the myocardium from being stretched too far beyond resting length. In experimental end-stage dilated cardiomyopathy, titin isoforms and distribution have been shown to change in a manner that confers an increase in stiffness. 21 Likewise, an increase in microtubule density and distribution has been shown in some forms of pressure overload to act as a viscous load and increase myocardial and cardiomyocyte viscoelastic stiffness. 7, 22–25 This change in diastolic function is reversible when microtubules are acutely depolymerized by chemical or physical agents. 7, 22–25