Tas Ahmet, Alan Yaren, Tas Ilke Kara, Aydin Omer E, Atay Zeynep, Yilmaz Sule, Ozcan Alp, van de Hoef Tim P, Umman Sabahattin, Piek Md Jan J, Sezer Murat
Department of Cardiology, Amsterdam UMC, Heart Centre, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands.
Emergency Department, Gomec State Hospital, Balikesir, Turkey.
Microcirculation. 2025 Aug;32(6):e70021. doi: 10.1111/micc.70021.
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.
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.
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).
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.
ClinicalTrials.gov (NCT02328820).
关于心外膜病变和冠状动脉微血管功能障碍（CMD），静息搏动性冠状动脉血流速度加速/减速特征（dU/dt）的变化仍未完全明确。
冠状动脉dU/dt模式从冠状动脉内多普勒速度信号的一阶导数中提取。单变量和多变量模型评估了dU/dt幅度、心外膜疾病以及CMD之间的关系，CMD由根据伴随的心外膜疾病严重程度（血流储备分数，FFR）调整后的冠状动脉血流储备（CFR）降低来定义，从而得出微血管阻力储备（MRR）。功能性CMD定义为MRR降低（≤3.0）但充血性微血管阻力正常（hMR < 2.5），而结构性CMD定义为MRR降低（≤3.0）且hMR增加（≥2.5）。在每个心动周期中识别出六个主要的加速或减速峰值；这些分别是a（舒张期加速峰值幅度）、b（舒张早期减速最低点幅度）、c（舒张期再次加速峰值幅度）、j（舒张期末减速最低点幅度）、x（收缩期加速峰值幅度）和z（收缩期末减速最低点幅度）波。
功能性CMD与a波（β = 55.944，95%可信区间[21.112, 90.777]，p = 0.002）、x波（β = 44.069，95%可信区间[20.182, 67.955]，p < 0.001）、b波（β = -34.019，95%可信区间[-50.865, -17.173]，p < 0.001）、j波（β = -48.723，95%可信区间[-71.272, -26.174]，p < 0.001）和z波（β = -31.047，95%可信区间[-53.596, -8.498]，p = 0.007）的放大相关。结构性CMD与a波（β = -76.938，95%可信区间[-113.125, -40.751]，p < 0.001）和j波（β = 24.787，95%可信区间[1.361, 48.213]，p = 0.039）减弱相关。
心外膜疾病严重程度与静息dU/dt模式的改变关联极小，而CMD的不同类型与心动周期内明显改变的搏动性特征相关。静息时更强的加速幅度并不表明微循环更健康或不存在CMD。
ClinicalTrials.gov（NCT02328820）。
