Chronic Heart Rate Reduction by Ivabradine Does Not Modify the Elastic Fiber Content in Post-Myocardial Infarction Scar of Middle-Aged Rats

A large myocardial infarction (MI) triggers progressive cardiac remodeling which results in left ventricular (LV) chamber dilatation and, as a consequence, in greater wall tension, particularly in the area of scar formation. Chronically elevated mechanical stress applied to fibroblasts and myofibroblasts within the scar has been known to stimulate the production of extracellular matrix proteins, predominantly collagen and elastin, that improves the tensile strength of the thinning LV wall. Considering that during a prolonged diastole the end-diastolic volume and, hence, the force and duration of mechanical signals transduced into the scar become even more augmented it is feasible to assume that any heart rate-lowering agent would promote further deposition of extracellular proteins by activated fibrogenic cells. Nevertheless, we have previously shown that chronic heart rate reduction (HRR) by ivabradine (IVA), a selective inhibitor of a pacemaker If current, did not alter the content of fibrillar collagen...