From the Departments of Biomedical Engineering and Physics (M.C.R., L.C., J.A.E.S., M.S.) and Cardiology (E.M.A.W., Z.-Y.Y., K.T.K., M.V., J.J.P., J.B.), Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Circ Cardiovasc Interv. 2016 Apr;9(4):e002356. doi: 10.1161/CIRCINTERVENTIONS.114.002356.
Aortic valve stenosis (AS) can cause angina despite unobstructed coronary arteries, which may be related to increased compression of the intramural microcirculation, especially at the subendocardium. We assessed coronary wave intensity and phasic flow velocity patterns to unravel changes in cardiac-coronary interaction because of transcatheter aortic valve implantation (TAVI).
Intracoronary pressure and flow velocity were measured at rest and maximal hyperemia in undiseased vessels in 15 patients with AS before and after TAVI and in 12 control patients. Coronary flow reserve, systolic and diastolic velocity time integrals, and the energies of forward (aorta-originating) and backward (microcirculatory-originating) coronary waves were determined. Coronary flow reserve was 2.8±0.2 (mean±SEM) in control and 1.8±0.1 in AS (P<0.005) and was not restored by TAVI. Compared with control, the resting backward expansion wave was 45% higher in AS. The peak of the systolic forward compression wave was delayed in AS, consistent with a delayed peak aortic pressure, which was partially restored after TAVI. The energy of forward waves doubled after TAVI, whereas the backward expansion wave increased by >30%. The increase in forward compression wave with TAVI was related to an increase in systolic velocity time integral. AS or TAVI did not alter diastolic velocity time integral.
Reduced coronary forward wave energy and systolic velocity time integral imply a compromised systolic flow velocity with AS that is restored after TAVI, suggesting an acute relief of excess compression in systole that likely benefits subendocardial perfusion. Vasodilation is observed to be a major determinant of backward waves.
尽管冠状动脉无阻塞，主动脉瓣狭窄（AS）仍可引起心绞痛，这可能与心外膜下的壁内微循环受压增加有关。我们评估了冠状动脉波强度和相位血流速度模式，以揭示经导管主动脉瓣植入术（TAVI）引起的心脏-冠状动脉相互作用的变化。
在 TAVI 前后，我们在 15 例 AS 患者和 12 例对照患者的无病变血管中测量了静息和最大充血时的冠状动脉内压力和血流速度。确定了冠状动脉储备、收缩期和舒张期速度时间积分以及前向（起源于主动脉）和后向（起源于微循环）冠状动脉波的能量。对照组的冠状动脉储备为 2.8±0.2（平均值±SEM），AS 组为 1.8±0.1（P<0.005），TAVI 并未恢复。与对照组相比，AS 患者的静息后扩张波高 45%。AS 患者的收缩期前向压缩波峰值延迟，与主动脉压峰值延迟一致，TAVI 后部分恢复。TAVI 后前向波能量增加一倍，而后向扩张波增加>30%。TAVI 后前向压缩波增加与收缩期速度时间积分增加有关。AS 或 TAVI 均未改变舒张期速度时间积分。
冠状动脉前向波能量和收缩期速度时间积分降低表明 AS 存在收缩期流速受损，TAVI 后可恢复，提示收缩期过度压迫得到急性缓解，可能有益于心内膜下灌注。舒张期主要取决于后向波。
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