Coronary Microvascular Dysfunction Alters the Pulsatile Behavior of the Resting Coronary Blood Flow

Tas A., Alan Y., Tas I. K., Aydin O. E., Atay Z., Yilmaz S., ...Daha Fazla

Microcirculation, cilt.32, sa.6, 2025 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 32 Sayı: 6
  • Basım Tarihi: 2025
  • Doi Numarası: 10.1111/micc.70021
  • Dergi Adı: Microcirculation
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, MEDLINE
  • Anahtar Kelimeler: coronary flow acceleration, coronary flow reserve, coronary microvascular dysfunction, microvascular resistance reserve, resting coronary flow
  • İstanbul Üniversitesi Adresli: Evet

Özet

Background: Variations in resting pulsatile coronary flow velocity acceleration/deceleration characteristics (dU/dt) with respect to epicardial lesions and coronary microvascular dysfunction (CMD) remain incompletely understood. Method: The coronary dU/dt pattern was extracted from the first derivative of the intracoronary Doppler velocity signal. Univariable and multivariable models evaluated the relationships between the dU/dt amplitudes, epicardial disease as well as CMD, defined by a blunted coronary flow reserve (CFR) adjusted for the concomitant epicardial disease severity (fractional flow reserve, FFR) yielding the microvascular resistance reserve (MRR). Functional CMD was defined by a blunted MRR (≤ 3.0) but normal hyperemic microvascular resistance (hMR < 2.5) whereas structural CMD was defined by a blunted MRR (≤ 3.0) combined with increased hMR (≥ 2.5). Six major acceleration or deceleration peaks were identified in each cardiac cycle; these were a (amplitude of peak diastolic acceleration), b (amplitude of early diastolic deceleration nadir), c (amplitude of peak diastolic re-acceleration), j (amplitude of end-diastolic deceleration nadir), x (amplitude of peak systolic acceleration), and z (amplitude of end-systolic deceleration nadir) waves. Results: Functional CMD was associated with amplification of a (β = 55.944, 95% CI [21.112, 90.777], p = 0.002) and × (β = 44.069, 95% CI [20.182, 67.955], p < 0.001), b (β = −34.019, 95% CI [−50.865, −17.173], p < 0.001), j (β = −48.723, 95% CI [−71.272, −26.174], p < 0.001), and z (β = −31.047, 95% CI [−53.596, −8.498], p = 0.007) waves. Structural CMD was associated with blunted a (β = −76.938, 95% CI [−113.125, −40.751], p < 0.001) and j (β = 24.787, 95% CI [1.361, 48.213], p = 0.039). Conclusion: Epicardial disease severity is minimally associated with alterations in the resting dU/dt pattern, whereas CMD endotypes are associated with distinctively altered intrabeat pulsatility characteristics. Stronger acceleration magnitudes at rest do not indicate a healthier microcirculation or absence of CMD. Trial Registration: ClinicalTrials.gov (NCT02328820).