Background-Aortic stenosis causes angina despite unobstructed arteries. Measurement of conventional coronary hemodynamic parameters in patients undergoing valvular surgery has failed to explain these symptoms. With the advent of percutaneous aortic valve replacement (PAVR) and developments in coronary pulse wave analysis, it is now possible to instantaneously abolish the valvular stenosis and to measure the resulting changes in waves that direct coronary flow. Methods and Results-Intracoronary pressure and flow velocity were measured immediately before and after PAVR in 11 patients with unobstructed coronary arteries. Using coronary pulse wave analysis, we calculated the intracoronary diastolic suction wave (the principal accelerator of coronary blood flow). To test physiological reserve to increased myocardial demand, we measured at resting heart rate and during pacing at 90 and 120 bpm. Before PAVR, the basal myocardial suction wave intensity was 1.9Ϯ0.3ϫ10 Ϫ5 W ⅐ m Ϫ2 ⅐ s Ϫ2 , and this increased in magnitude with increasing severity of aortic stenosis (rϭ0. 59, Pϭ0.05). This wave decreased markedly with increasing heart rate ( coefficientϭϪ0. ; Pϭ0.014). Conclusions-In aortic stenosis, the coronary physiological reserve is impaired. Instead of increasing when heart rate rises, the coronary diastolic suction wave decreases. Immediately after PAVR, physiological reserve returns to a normal positive pattern. This may explain how aortic stenosis can induce anginal symptoms and their prompt relief after PAVR. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT01118442. Key Words: aortic stenosis Ⅲ aortic valve Ⅲ coronary arteries Ⅲ coronary flow Ⅲ heart valve prosthesis implantation Ⅲ microvessels Ⅲ wavelet analysis U ncorrected severe aortic stenosis has an extremely poor prognosis, carrying a 3-year mortality of Ͼ50%, 1 which rises to Ͼ80% in subjects with significant cardiac comorbidity. 2 As the severity of aortic stenosis increases, physiological and pathological adaptations occur in the left ventricle (LV). 3 These include increases in the inotropic state and the development of LV hypertrophy. 4
Editorial see p 1505 Clinical Perspective on p 1572Although LV hypertrophy can be viewed as a physiological adaptation to the increase in afterload, it encompasses a pathological hypertrophic response with increased extracellular matrix deposition and perivascular fibrosis. 5 These pathological changes slow myocardial relaxation, which in turn diminishes normal ventricular filling and reduces coronary blood flow. 6,7 This is compounded by the increase in work and myocardial mass, which results in elevated myocardial oxygen demand and a decrease in microvascular density, 8 leading to reduced coronary vascular reserve. 9 As the severity of the aortic stenosis increases, this process is exacerbated by ever-increasing afterload and decreasing coronary perfusion pressures, leading to the development of ischemia, which has been reported with the use of several different techniques. 10...