Heart failure is one of the leading causes of death in an ageing population. Hallmarks are cardiac hypertrophy, fibrosis and inflammation. The molecular mechanisms, however, are poorly understood. Glycosylation is one of the most common posttranslational modifications of proteins, which can have important consequences for protein folding, function and turnover. We hypothesized that changes in glycoprotein abundance and glycosylation patterns may contribute to cardiac aging. Western Blot analysis suggests increased protein mannosylation in the aging heart. Glycoprotein pull-downs from heart lysates of young (3 months) and old (2 years) mice in combination with quantitative mass spectrometry support widespread alterations of the glycoproteome in aged hearts.