CHANGES IN PHASIC CORONARY BLOOD PLOW VELOCITY PROFILE IN RELATION TBCHANGES IN HEMODYNAMIC PARAMETERS DURING STRESS IN PATIENTS WITH AORTIC-VALVE STENOSIS

Background Alterations in phasic coronary flow profile have been demon strated at rest in patients with aortic valve stenosis (AVS) but have never been studied under conditions of hemodynamic stress. Methods and Results Thirty-four patients with significant pure AVS (21 with exert ional symptoms [group 1], 13 asymptomatic [group 2]) and 9 control sub jects (group 3), all with normal coronary arteries, were studied succe ssively at rest, during rapid atrial pacing, and after dobutamine infu sion (5 to 30 mu g . kg(-1) . min(-1) IV) by proximal left anterior de scending (LAD) intracoronary Doppler flow velocimetry concomitant with hemodynamic measurements. Systolic retrograde coronary flow velocity (CFV) was recorded only in patients with AVS, and its resting peak val ue was positively correlated with peak aortic pressure gradient (APG) (r=.63, P<.001). In group 1, there was lower aortic valve area (0.58+/ -0.10 versus 0.75+/-0.08 cm(2), P<.001) and higher resting APG and pea k systolic retrograde CFV than in group 2, and also higher resting pea k diastolic and mean CFV than in groups 2 and 3. In the two AVS groups , there were no changes from rest in APG and retrograde CFV at peak pa cing rate; however, these parameters increased concomitantly and signi ficantly at peak debotamine stress. The ratio of the resting systolic to diastolic CFV curve area was inversely correlated with mean APG (r = -.54, P<.001); it was significantly lower in group 1 than in groups 2 and 3 (0.19+/-0.07 versus 0.29+/-0.10 and 0.30+/-0.04, respectively, both P<.005) and increased at peak pacing (group 1, to 0.29+/-0.14; g roup 2, to 0.39+/-0.12; group 3, to 0.38+/-0.07; all P<.001). At peak dobutamine stress, it decreased in patients with AVS (group 1, to 0.05 +/-0.05; group 2, to 0.08+/-0.03; both P<.001) but did not change in g roup 3 (0.25+/-0.05). From rest to peak dobutamine stress, in both AVS groups there was increased retrograde systolic (group 1, 441+/-483%; group 2, 681+/-356%; both P<.001), decreased total systolic (group 1, -66+/-25%, P<.001; group 2, -19+/-24%; P=NS), and increased diastolic (group 1, 33.4+/-31.7%; group 2, 197.7+/- 105.1%; both P<.001; group 1 versus group 2, P<.001) CFV curve area. In contrast, group 3 showed c omparable increases in both systolic (143.5+/-44.4%) and diastolic (19 7.1+/-75.2%) CFV area (both P<.001). The stress-induced increases in t he mean CFV and blood flow exceeded or were comparable with the concom itant increases in the estimated myocardial metabolic demand in groups 2 and 3 but were significantly lower in group 1. Conclusions Stress-i nduced changes in LAD phasic CFV profile differ significantly between patients with and without AVS. In AVS, these changes are closely relat ed to the concomitant stress-induced changes in hemodynamic parameters .