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Evaluation of computed tomography myocardial perfusion in women with angina and no obstructive coronary artery disease

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Abstract

Women with angina and no obstructive coronary artery disease (CAD) have worse cardiovascular prognosis than asymptomatic women. Limitation in myocardial perfusion caused by coronary microvascular dysfunction (CMD) is one of the proposed mechanisms contributing to the adverse prognosis. The aim of this study was to assess myocardial perfusion in symptomatic women with no obstructive CAD suspected for CMD compared with asymptomatic sex-matched controls using static CT perfusion (CTP). We performed a semi-quantitative assessment of the left ventricular myocardial perfusion and myocardial perfusion reserve (MPR), using static CTP with adenosine provocation, in 105 female patients with angina and no obstructive CAD (< 50% stenosis) and 33 sex-matched controls without a history of angina or ischemic heart disease.  Patients were on average 4 years older (p = 0.04) and had a higher burden of cardiovascular risk factors. While global perfusion during rest was comparable between the groups (age-adjusted p = 0.12), global perfusion during hyperemia was significantly reduced in patients compared with controls (163 ± 23 HU vs. 171 ± 25 HU; age-adjusted p = 0.023). The ability to increase myocardial perfusion during adenosine-induced vasodilation was significantly diminished in patients (MPR 148% vs. 158%; age-adjusted p < 0.001). This remained unchanged after adjustment for cardiovascular risk factors (p = 0.008). Women with angina and no obstructive CAD have reduced hyperemic myocardial perfusion and MPR compared with sex-matched controls. Impaired myocardial perfusion may be related to the presence of CMD in some of these women.

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Abbreviations

AD:

Attenuation density

BMI:

Body mass index

CAC:

Coronary artery calcium

CAD:

Coronary artery disease

CCTA:

Coronary computed tomography angiography

CHD:

Coronary heart disease

CMD:

Coronary microvascular dysfunction

CT:

Computed tomography

CTP:

CT perfusion

DFB:

Daria Frestad Bechsgaard

HU:

Hounsfield units

IHD:

Ischemic heart disease

JJL:

Jesper James Linde

MPR:

Myocardial perfusion reserve

LAD:

Left anterior descending coronary artery

LV:

Left ventricle

LCX:

Left circumflex coronary artery

PET:

Positron emission tomography

RCA:

Right coronary artery

TPR:

Transmural perfusion ratio

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Acknowledgements

This work was supported by the Danish Heart, Arvid Nilssons Foundation and Hvidovre Hospital Research Council. The Authors would like to thank the Copenhagen City Heart study, Departments of Cardiology and Radiology, Hvidovre University Hospital, and Department of Cardiology, Bispebjerg University Hospital, for their collaboration on this project. We thank chief radiologist Dennis Møller and radiologists Tina Berland Larsen, Anja Nielsen, Linn Haraldseid, and the nursing head of the outpatient department of Cardiology Sussie Foghmar for their assistance in data acquisition. Lastly, we want to express our deepest gratitude to the women participating in the iPOWER study for their time and willingness to contribute to the research.

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Correspondence to Daria Frestad Bechsgaard.

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Appendix

Appendix

See Figs. 3, 4, 5 and Table 4.

Fig. 3
figure 3figure 3

a, b Correlation plots with fitted values and Bland–Altman plots assessing the intra-observer agreement for a global attenuation density and b global transmural perfusion ratio at rest and hyperemia

Fig. 4
figure 4figure 4

a, b Correlation plots with fitted values and Bland–Altman plots assessing the inter-observer agreement for a global attenuation density and b global transmural perfusion ratio at rest and hyperemia

Fig. 5
figure 5

Flow-chart. Overview of participants enrolled in the study

Table 4 Cardiac-CT characteristics

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Bechsgaard, D.F., Gustafsson, I., Michelsen, M.M. et al. Evaluation of computed tomography myocardial perfusion in women with angina and no obstructive coronary artery disease. Int J Cardiovasc Imaging 36, 367–382 (2020). https://doi.org/10.1007/s10554-019-01723-5

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