Differential Interaction of High Microvascular Resistance With Coronary Flow Reserve Across Coronary Microvascular Dysfunction Endotypes

Tas A., Alan Y., Damman P., van de Hoef T. P., Kara Tas I., Türkmenoğlu E. G., ...Daha Fazla

JACC: Advances, cilt.4, sa.12P2, 2025 (ESCI, Scopus) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 4 Sayı: 12P2
  • Basım Tarihi: 2025
  • Doi Numarası: 10.1016/j.jacadv.2025.102353
  • Dergi Adı: JACC: Advances
  • Derginin Tarandığı İndeksler: Emerging Sources Citation Index (ESCI), Scopus
  • Anahtar Kelimeler: ANOCA, arterial reservoir pressure analysis, coronary microvascular dysfunction, Windkessel
  • İstanbul Üniversitesi Adresli: Evet

Özet

Background: In contrast to reduced coronary flow reserve (CFR), increased minimal hyperemic microvascular resistance (hMR) lacks prognostic relevance in stable chronic coronary syndromes. Objectives: The aim of the study is to investigate the local and systemic hemodynamics, including diastolic rate constant (s−1) and arterial reservoir function (reservoir-excess pressure [Pr-Pxs] parameters), as they relate to coronary microvascular dysfunction (CMD; CFR <2.5) and hMR. Methods: Functional CMD (CFR <2.5; hMR <2.5, nvessel = 82, npatient = 77), structural CMD (CFR <2.5; hMR ≥2.5, nvessel = 160, npatient = 149), no CMD-low hMR (CFR ≥2.5; hMR <2.5, nvessel = 44, npatient = 42), and no CMD-high hMR(CFR ≥2.5; hMR ≥2.5, nvessel = 26, npatient = 26) endotypes were compared using generalized linear mixed models adjusting for the multiple coronary arteries within same patients. Results: CMD endotypes were associated with a higher diastolic rate constant (s−1; functional-CMD: 2.0 [1.7-2.2], structural-CMD: 1.9 [1.7-2.1], no CMD-low hMR: 1.5 [1.3-1.7]; no CMD-high hMR 1.5 [1.4-1.6]; P = 0.006) and lower Pr/Pxs (functional CMD: 18.8 [17.6-20.1]; structural CMD: 19.6 [18.5-20.8]; no CMD-low hMR: 21.9 [20.1-23.8]; no CMD-high hMR: 23.8 [22.4-25.2], P < 0.001), suggesting a systemic relative hyperemic state, with lower vasotonus and arterial compliance irrespective of high hMR. Despite similar hMR, No CMD-high hMR endotype distinctively had the lowest Pxs (mm Hg) (4.0 [3.4-4.6]), whereas structural CMD (5.1 [4.8-5.4]) had the highest Pxs (P < 0.001). In no CMD, a milder increase in hMR accompanied higher basal microvascular resistance than CMD (β = 0.128 [0.106-0.149], P < 0.001; β = 0.167 [0.155-0.180], P < 0.001; P = 0.002). Higher hMR was associated with lower CFR in the CMD cases (β = −0.057 [−0.082 to −0.033], P < 0.001), but not in the no CMD group (β = 0.066 [0.013-0.118] P = 0.014). Conclusions: In this hypothesis-generating study, patients with high hMR-normal CFR exhibit favorable characteristics of coronary and aortic hemodynamics and reservoir function.