Heart failure with preserved ejection fraction (HFpEF) is frequently accompanied by
co-morbidities and a systemic proinflammatory state, resulting in coronary microvascular
dysfunction (CMD), as well as myocardial fibrosis. The purpose of this study is to
examine the relation between myocardial perfusion reserve (MPR) and diffuse myocardial
fibrosis in patients with HFpEF using cardiovascular magnetic resonance. A single
center study was performed in 19 patients with clinical HFpEF and 15 healthy control
subjects who underwent quantitative first-pass perfusion imaging to calculate global
MPR. T1 mapping was used to assess fibrosis and to calculate extracellular volume.
Spiral cine displacement encoded stimulated echo was used to calculate myocardial
strain. Comprehensive 2D echocardiograms with speckle tracking, cardiopulmonary exercise
testing, and brain natriuretic peptide levels were also obtained. In patients with
HFpEF, mean left ventricular EF was 61% ± 9% and left ventricular mass index 45 ±
12 g/m2. Compared with controls, HFpEF patients had reduced global MPR (2.29 ± 0.64 vs 3.38
± 0.76, p = 0.002) and VO2 max (16.5 ± 6.8 vs 30.9 ± 7.7 ml/kg min, p <0.001) whereas extracellular volume (0.29
± 0.04 vs 0.25 ± 0.04, p = 0.02), pulmonary artery systolic pressure (35.4 ± 13.7
vs 22.3 ± 5.4 mm Hg, p = 0.004), and average E/e’ (15.0 ± 7.6 vs 8.6 ± 2.0, p = 0.005)
were increased. Displacement encoded stimulated echo peak systolic circumferential
strain (p = 0.60) as well as echocardiographic derived global longitudinal strain
(p = 0.07) were similar between both groups. The prevalence of CMD, defined as global
MPR <2.5, in the HFpEF group was 69%. In conclusion, HFpEF patients have a high prevalence
of CMD and diffuse fibrosis. These parameters may be useful clinical end points for
future therapeutic trials.
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Article Info
Publication History
Published online: August 22, 2019
Received in revised form:
August 5,
2019
Received:
May 30,
2019
Footnotes
Funding: Drs. Löffler, Balfour, and Shaw were supported by NIH 5T32EB003841 . Dr. Salerno was funded by NIH R01 HL131919 . This work was funded by the UVA- AstraZeneca Alliance.
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