Ventricular-arterial coupling in heart failure with preserved ejection fraction: the devil is in the details

The syndrome of heart failure with preserved ejection fraction (HFPEF) continues to arouse controversy. Any research that can shed light on mechanisms and thereby offer specific targets for treatment should be welcomed. Patients may develop pulmonary oedema that can be triggered by acute increases in conduit arterial stiffness1 and exacerbated by simultaneous volume-loading.2 In this issue of Cardiovascular Research, Pe´rez del Villar and colleagues report an invasive clinical investigation in which they assessed how acute increases in systemic arterial pressure influence left ventricular (LV) diastolic function and pressures.3 They suggest that the main mechanism is a direct effect on end-diastolic stiffness rather than delayed relaxation. Before these results are generalized, it is important to consider some details of their study.

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