Dilated cardiomyopathy (DCM) is a frequently occurring heart disease characterized by dilation of the left or both ventricles, and systolic and diastolic dysfunctions leading to heart failure.

Considering that changes in the expression of titin have been reported to modulate the passive mechanical properties of myocardium and have been associated with human cases of DCM, this study was aimed at relating the passive mechanical properties of myofibrils to the expression of titin in the left ventricle of the Bio TO-2 hamster, a genetic animal model of human DCM, during the progression of the disease.

The results of this thesis suggest that a minor change in the expression of titin toward the stiffer N2B isoform occurs with disease progression in the left ventricle of the DCM hamster, but the change is too small to result in a measurable difference between the passive mechanical properties of the DCM and control myofibrils.