The prevalence of diabetic cardiomyopathy is expected to increase in parallel with that of T2DM. In the US alone, an estimated 26 million adults are diagnosed with T2DM, 9.4 million adults have undiagnosed T2DM and 91.8 million adults have pre-diabetes (AHA 2021 update). Clinical trials show the prevalence of HF in patients with T2DM range from 19% to 26%. Conversely, T2DM is highly prevalent in those with HF, being reported in 25-40% of patients and associated with increased mortality.
Diabetic cardiomyopathy is associated with abnormalities of myocardial tissue structure affecting all cardiac chambers and all phases of cardiac function. Structural hallmarks include myocardial fibrosis and maladaptive changes in ventricular geometry including concentric left ventricular (LV) hypertrophy with potential LV dilatation in more advanced stages, with concomitant right ventricular (RV) involvement typified by early-onset eccentric RV hypertrophy, dilatation, and systolic impairment.
Functionally, diabetic cardiomyopathy is associated with abnormalities of LV diastolic performance, progressing from mild changes (delayed myocardial relaxation) to increased LV filling pressure frequently associated with left atrial enlargement and atrial fibrillation. This diastolic dysfunction often co-exists with systolic dysfunction ranging from highly prevalent reductions in LV longitudinal deformation with preserved ejection fraction (EF) which independently predict incident new-onset HF, to frank reductions in LV EF.