W ith progressive outflow obstruction in aortic valve stenosis (AS), myocardial adaptations ensue to maintain adequate left ventricular (LV) output. These compensatory mechanisms lead to hypertrophy with increased LV mass and inotropic state. 1,2 Thirty to forty percent of patients with AS have angina despite unobstructed coronary arteries, but the definitive cause of angina in AS remains uncertain. 3-5 Ischemia in AS is frequently associated with reduced coronary flow reserve (CFR), especially

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... in the subendocardium. 6-8 An impaired CFR in AS-related hypertrophy may result both from augmented basal flow caused by a higher myocardial oxygen demand and compromised hyperemic flow caused by capillary rarefaction, increased oxygen diffusion distance, intensified compression of intramural vessels, and possible reduced diastolic time fraction (DTF). 9,10 After surgical valve replacement, the long-term regression of hypertrophied LV mass was associated with a decrease in resting myocardial flow and restoration of CFR. 11,12 Transcatheter aortic valve implantation (TAVI) offers the opportunity to dissociate acute effects of AS removal on coronary blood flow from those of subsequent hypertrophy regression. The coronary flow waveform is largely determined by the intramyocardial pump mechanism 13 which is modulated by aortic pressure (P a ), LV pressure, and inotropic state. 9,14 Cardiac contraction increases intramural tissue and Background-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). Methods and Results-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 (microcirculatoryoriginating) 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. Conclusions-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. (Circ Cardiovasc Interv. 2016;9:e002356.