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Study identifies relationship between HFpEF, microvascular dysfunction
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Maladaptations at the microvascular level may be involved in the pathophysiology of HF with preserved ejection fraction, according to study findings.
However, researchers did not find any connection between conduit artery vascular function and HF with preserved ejection (HFpEF) beyond what is seen with healthy aging.
According to the study background, it was not well known whether changes caused by disease in the peripheral vasculature contributed to HFpEF.
Joshua F. Lee, PhD, from the department of internal medicine, University of Utah, and the Geriatric Research, Education and Clinical Center, VA Medical Center, Salt Lake City, and colleagues hypothesized that patients with HFpEF would have impaired vascular function in the microvasculature and the conduit artery.
They compared conduit artery function by measuring brachial artery flow-mediated dilation and microvascular function by measuring reactive hyperemia after 5 minutes of ischemia in 24 patients with NYHA class II, III or IV HFpEF and 24 healthy individuals matched by age, sex and brachial artery diameter.
Compared with controls, those with HFpEF had reduced flow-mediated dilation (HFpEF group, 3.1%; controls, 5.1%; P = .03), but shear rate during peak brachial artery dilation was lower in those with HFpEF than in controls (42,070/s vs. 69,018/s; P = .01). After normalizing flow-mediated dilation for shear stimulus, there were no differences between the groups in cumulative area under the curve (AUC) at peak flow-mediated dilation (HFpEF group, 0.11% AUC; controls, 0.09% AUC; P = .58), according to the researchers.
Reactive hyperemia when measured as AUC was lower in those with HFpEF (HFpEF group, 454 mL; controls, 660 mL; P < .01), they wrote.
“In combination, these findings provide new evidence in support of the concept that vascular dysfunction in the conduit vessels is not a requisite feature in the pathophysiology of HFpEF, implicating instead a reduction in peripheral microvascular function that may contribute significantly to clinical status and disease progression on this patient group,” Lee and colleagues wrote. – by Erik Swain
Disclosure: The researchers report no relevant financial disclosures.
Perspective
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C. Noel Bairey Merz, MD, FACC, FAHA
It is uncertain what the findings mean for microvascular dysfunction because there is no reference, validation or discussion of this passage in the introduction: “Determination of reactive hyperemia (RH) subsequent to a period of cuff occlusion fills this void, providing an index of microvascular function that is complimentary to conduit vascular function assessed via FMD (flow-mediated dilation).” Specifically, both the FMD and the RH Index (RHI) involve post-cuff occlusion shear stress, so adjusting the FMD but not the RHI for this is not convincing. If the RHI is adjusted by the contralateral arm, this needs to be provided in detail and defended as a rationale for the findings. Validation of RHI as a test of microvascular function does not exist, that I am aware of. More research on this needs to be conducted.
What the findings tell us about HFpEF is that peripheral conduit artery function is not compromised. The area is ripe for investigation and the need is great, as currently there is no effective treatment for HFpEF.
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