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Evidence of microvascular dysfunction in heart failure with preserved ejection fraction
  1. Joshua F Lee1,2,
  2. Zachary Barrett-O'Keefe2,3,
  3. Ryan S Garten1,2,
  4. Ashley D Nelson1,
  5. John J Ryan4,
  6. Jose N Nativi4,
  7. Russell S Richardson1,2,3,
  8. D Walter Wray1,2,3
  1. 1Department of Internal Medicine, University of Utah, Salt Lake City, Utah, USA
  2. 2Geriatric Research, Education, and Clinical Center, VA Medical Center, Salt Lake City, Utah, USA
  3. 3Department of Exercise & Sport Science, University of Utah, Salt Lake City, Utah, USA
  4. 4Division of Cardiovascular Medicine, Department of Medicine, University of Utah, Salt Lake City, Utah, USA
  1. Correspondence to Dr D Walter Wray, Department of Internal Medicine, Division of Geriatrics, University of Utah, VAMC SLC, GRECC 182, Bldg. 2 Rm 1D22, 500 Foothill Drive, Salt Lake City, UT 84148, USA; walter.wray{at}


Objective While vascular dysfunction is well defined in patients with heart failure (HF) with reduced ejection fraction (HFrEF), disease-related alterations in the peripheral vasculature of patients with HF with preserved ejection fraction (HFpEF) are not well characterised. Thus, we sought to test the hypothesis that patients with HFpEF would demonstrate reduced vascular function, at the conduit artery and microvascular levels, compared with controls.

Methods We examined conduit artery function via brachial artery flow-mediated dilation (FMD) and microvascular function via reactive hyperaemia (RH) following 5 min of ischaemia in 24 patients with Class II–IV HFpEF and 24 healthy controls matched for age, sex and brachial artery diameter.

Results FMD was reduced in patients with HFpEF compared with controls (HFpEF: 3.1±0.7%; Controls: 5.1±0.5%, p=0.03). However, shear rate at time of peak brachial artery dilation was lower in patients with HFpEF compared with controls (HFpEF: 42 070±4018/s; Controls: 69 018±9509/s, p=0.01), and when brachial artery FMD was normalised for the shear stimulus, cumulative area-under-the-curve (AUC) at peak dilation, the between-group differences were eliminated (HFpEF: 0.11±0.03%/AUC; Controls: 0.09±0.01%/AUC, p=0.58). RH, assessed as AUC, was lower in patients with HFpEF (HFpEF: 454±35 mL; Controls: 660±63 mL, p<0.01).

Conclusions Collectively, these data suggest that maladaptations at the microvascular level contribute to the pathophysiology of HFpEF, while conduit artery vascular function is not diminished beyond that which occurs with healthy aging.

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