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Heart failure with preserved ejection fraction (HFpEF) is estimated to account for about 1/2 of all patients with heart failure. Yet effective medical therapy for HFpEF has been elusive with only minimal benefit from pharmacologic approaches of proven benefit for heart failure with reduced ejection fraction (HFrEF). As the word cardiovascular implies, normal circulatory function depends on normal function of both the heart and the vascular system. Systemic vascular dysfunction is recognized as a key contributor to symptoms and poor outcomes in HFrEF and is a key therapeutic target. However, the role of vascular dysfunction in HFpEF has been less well characterized.
In this issue of Heart, Lee and colleagues (see page 278) provide detailed studies of vascular function in 24 patients with HFpEF compared to 23 control subjects. The function of larger conduit arteries was measured by brachial artery flow mediated dilation whereas microvascular function was assessed by reactive hyperemia after a period of cuff occlusion. They found that flow mediated dilation was no different in patients with HFpEF compared to controls, when normalized for shear stress stimulus. In contrast, microvascular function was abnormal with an approximately 30% reduction in reactive hyperemia in HRpEF patients (figure 1). The authors suggest that the differing types of vascular dysfunction in heart failure – abnormal conduit function in HFrEF versus abnormal microvascular function in HFpEF—might be account for some of the differences in therapeutic responses in these two types of heart failure.
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