The extracellular matrix (ECM) includes structural proteins (e.g. collagen types 1 and 3 and elastin), adhesive proteins (e.g. fibronectin), and matrix metalloproteinases (MMPs; responsible for collagen degradation). MMP activity is regulated by endogenous inhibitors (TIMPs). Four TIMP isoforms (TIMP1-4) are known to be present in the heart. In the heart, the ECM is responsible for connecting myocytes, aligning contractile elements, transmitting force and preventing myocardial rupture. Although it is well known that there is a remodelling of the ECM in the working myocardium in heart failure (Graham et al., 2008), it is not known whether there is a similar remodelling in the sinoatrial node (SAN; pacemaker of the heart). The aim of the present study was to investigate the effect of heart failure on the ECM and the factors that control the ECM (e.g. transforming growth factor β1, TGFβ1, and tumour necrosis factor α, TNFα). Sprague-Dawley rats, aged five weeks, received a single subcutaneous injection of monocrotaline (60 mg/kg), which induced inflammation of the pulmonary artery and pulmonary arterial hypertension. After three weeks, the experiments were ended after the animals developed congestive heart failure as confirmed by echocardiography. All experiments were conducted in accordance with the Japanese Act on Welfare and Management of Animals (Act No. 105 of October 1, 1973). Quantitative PCR was used to measure the expression of transcripts in the SAN (and also the right atrium, RA, and right ventricle, RV). In the heart failure rats (as compared to control rats), mRNAs for collagen type 1 (constitutes 80% of total collagen) and elastin were significantly increased in the SAN, RA and RV; collagen type 3α mRNA was significant increased, but only in the RA and RV. Fibronectin mRNA was significantly increased in all three tissues. MMP2 mRNA was significantly increased in the RA only. TIMP-1 was significantly increased in all three tissues; TIMP2 did not show any changes; TIMP4 was significantly decreased in the SAN and RV. Fibroblasts synthesise collagen, and vimentin mRNA (a marker for fibroblasts) was significantly increased in all three tissues in the heart failure rats. TGFβ1 mRNA was significantly increased in all three tissues, although TNFα mRNA was significantly increased in the RA only. We conclude that, in this model of congestive heart failure, there is a remodelling of the ECM (fibrosis) in the SAN as well as the RA and RV. The remodelling may contribute to the SAN dysfunction that is known to occur in heart failure.