Microvascular resistance reserve in relation to total and vessel-specific atherosclerotic burden

Abstract

<div><p><strong>Aims</strong><br></p><p> The relationship between coronary artery atherosclerosis and microvascular resistance remains unclear. This study aims to clarify the relationship between total atherosclerotic and vessel-specific atherosclerotic burden and microvascular resistance reserve (MRR). <br></p><p><strong>Methods and results</strong><br></p></div><div><p> In this <em>post hoc</em> analysis of the PACIFIC 1 trial, symptomatic patients without prior coronary artery disease (CAD) underwent [¹⁵O]H₂O positron emission tomography, coronary computed tomography angiography (CCTA), and invasive fractional flow reserve (FFR). MRR was assessed across all three coronary branches, utilizing PET-derived coronary flow reserve and invasive FFR measurements. CCTA was used to assess patient and vessel-specific plaque volumes. Percentage atheroma volume (PAV) was defined as total plaque volume divided by vessel volume. The study included 142 patients (55% male, 57.5 ± 8.6 years) with 426 vessels with a mean MRR of 3.77 ± 1.64. While a significantly higher PAV was observed in the left anterior descending artery territory, MRR was similar across the three coronary branches. Generalized estimating equations without correction for cardiovascular risk factors identified that patient-specific PAV tertiles but not vessel-specific PAV tertiles were related to vessel-specific MRR. After correction for cardiovascular risk factors, compared with the first tertile of patient-specific PAV, the second tertile showed a vessel-specific MRR decrease of <em>β</em> = −0.362, <em>P</em> = 0.018, and the third tertile showed a decrease of <em>β</em> = −0.347, <em>P</em> = 0.024. <br></p></div><div><p> <strong>Conclusion </strong><br></p><p> In patients without prior CAD, patient-specific plaque burden was negatively associated to vessel-specific MRR; however, vessel-specific plaque burden was not related to vessel-specific MRR. Our findings suggest that the relation between atherosclerotic burden and an impaired microcirculatory function is of systemic origin. <br></p></div>