Heart failure with preserved ejection fraction (HFpEF) currently accounts for approximately half of all new heart failure cases in the community. HFpEF is closely associated with chronic lifestyle-related diseases, such as obesity and type 2 diabetes, and clinical outcomes are worse in those with than without comorbidities. HFpEF is pathophysiologically distinct from heart failure with reduced ejection fraction, which may explain, in part, the disparity of treatment options available between the two heart failure phenotypes. The mechanisms underlying HFpEF are complex, with coronary microvascular dysfunction (MVD) being proposed as a potential key driver in its pathophysiology. In this review, the authors highlight the evidence implicating MVD in HFpEF pathophysiology, the diagnostic approaches for identifying MVD (both invasive and non-invasive) and the prevalence and prognostic significance of MVD.

The global burden of heart failure (HF) is on the rise owing to an increasing incidence of lifestyle related diseases, predominantly type 2 diabetes mellitus (T2D). Diabetes is an independent risk factor for cardiovascular disease, and up to 75% of those with T2D develop HF in their lifetime. T2D leads to pathological alterations within the cardiovascular system, which can progress insidiously and asymptomatically in the absence of conventional risk factors. Reduced exercise tolerance is consistently reported, even in otherwise asymptomatic individuals with T2D, and is the first sign of a failing heart. Because aggressive modification of cardiovascular risk factors does not eliminate the risk of HF in T2D, it is likely that other factors play a role in the pathogenesis of HF. Early identification of individuals at risk of HF is advantageous, as it allows for modification of the reversible risk factors and early initiation of treatment with the aim of improving clinical outcomes. In this review, cardiac and extra-cardiac contributors to reduced exercise tolerance in people with T2D are explored.