It has become increasingly clear that also on a cellular level, DMCMP presents as two distinct diseases with a HFrEF and HFpEF phenotype. Early evidence suggests that in the DMCMP HFpEF phenotype collagen and advanced glycation end-products (AGEs) deposition are increased. In contrast, cardiomyocytes in patients with the DMCMP HFrEF phenotype show an overall loss of sarcomeres.
Unfortunately, limited information is available on differences between DMCMP with HFrEF and HFpEF. Elucidating these differences will aid in our understanding of the underlying pathophysiological differences of DMCMP with HFrEF and HFpEF and provide for novel treatment targets. Additionally, it has become increasingly clear that particular DM medications might have beneficial effects in patients with HF. Results from the EMPA-REG trial showed that sGLT2 inhibitors might possible aid in reducing the number of HF hospital readmissions. Novel targets on DMCMP patients with HFrEF and HFpEF will aid in identifying HF patients potentially benefitting from existing treatment for DM.