PET-based assessment of coronary microvascular dysfunction and its relation to plaque burden and vascular remodeling: integration with microvascular resistance reserve.
Authors
Affiliations (11)
Affiliations (11)
- Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands. [email protected].
- School of Medicine, Nankai University, Tianjin, China. [email protected].
- Department of Cardiology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
- Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
- Faculty of Medicine, Universitas Brawijaya, Malang, Indonesia.
- Department of Vascular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands.
- Department of Radiology and Nuclear Medicine, Amsterdam UMC, Vrije Universiteit, Amsterdam, the Netherlands.
- Division of Cardiology, The George Washington University School of Medicine, Washington, DC, USA.
- Turku University Hospital and University of Turku, Turku, Finland.
- School of Medicine, Nankai University, Tianjin, China.
- University Medical Center Utrecht, Utrecht, The Netherlands.
Abstract
Coronary microvascular dysfunction (CMD) contributes to myocardial ischemia in patients with angina and non-obstructive coronary artery disease. Quantitative positron emission tomography (PET) allows noninvasive assessment of myocardial blood flow and identification of CMD. To investigate the association between PET-assessed coronary microvascular dysfunction (CMD), coronary plaque burden, and vascular remodeling, integrating microvascular resistance reserve (MRR). This post hoc analysis of the PACIFIC-1 trial included coronary arteries from symptomatic patients with suspected stable CAD who underwent [<sup>15</sup>O]water PET, coronary CT angiography (CTA), and invasive fractional flow reserve (FFR). Coronary arteries were categorized into three groups: non-ischemic vessels (normal FFR and hyperemic myocardial blood flow [hMBF], n = 352), CMD vessels (normal FFR but impaired hMBF, n = 88), and epicardial flow-limiting vessels (abnormal FFR, n = 159). MRR was calculated by integrating PET-derived coronary flow reserve with invasive FFR. AI-based CTA quantified plaque burden and remodeling. Diameter stenosis and plaque burden increased progressively from non-ischemic to CMD to epicardial flow-limiting vessels (all P < 0.05). CMD vessels demonstrated the largest lumen volume (583.75 mm<sup>3</sup> [IQR 337.02-754.30]) and lumen area (4.63 mm<sup>2</sup> [IQR 3.77-6.67]) among the three groups (both P < 0.05). In non-ischemic vessels, noncalcified plaque burden was associated with worse microvascular function detected by MRR (B = -0.12, 95%CI [-0.21, -0.04], P = 0.006). In CMD vessels, remodeling index was independently associated with higher MRR after adjustment (B = 0.10, 95%CI [0.05, 0.15], P < 0.001). CMD is associated with an intermediate atherosclerotic burden and paradoxical lumen enlargement, representing a distinct functional-structural phenotype defined by PET-derived microvascular dysfunction and CT-based plaque characteristics. URL: https://www. gov ; Unique identifier: NCT01521468.