Cardiac fibrosis is a disease state characterized by excessive collagenous matrix accumulation within the myocardium that can lead to ventricular dilation and systolic failure. Current treatment options are severely lacking due in part to the poor understanding of the complexity of molecular pathways involved in cardiac fibrosis. To close this gap, in vitro model systems that recapitulate the defining features of the fibrotic cellular environment are in need. Type I collagen, a major cardiac ECM protein and the defining component of fibrotic depositions, is an attractive choice for a fibrosis model, but demonstrates poor mechanical strength due to solubility limits. However, plastic compression of collagen matrices has been shown to significantly increase its mechanical properties. Here, we utilized confined compression of oligomeric, type I collagen matrices to resemble defining hallmarks seen in fibrotic tissue such as increased collagen content, fibril thickness and bulk compressive modulus. Cardiomyocytes seeded on compressed matrices show a strong beating abrogation as observed in cardiac fibrosis. Gene expression analysis of selected fibrosis markers indicated fibrotic activation and cardiomyocyte maturation with regard to the existing literature. With these results, we present a promising first step towards a facile heart-on-chip model to study cardiac fibrosis.