Changes in phasic coronary blood flow velocity profile in relation to changes in hemodynamic parameters during stress in patients with aortic valve stenosis.
BACKGROUND
Alterations in phasic coronary flow profile have been demonstrated at rest in patients with aortic valve stenosis (AVS) but have never been studied under conditions of hemodynamic stress.


RESULTS
Thirty-four patients with significant pure AVS (21 with exertional symptoms [group 1], 13 asymptomatic [group 2]) and 9 control subjects (group 3), all with normal coronary arteries, were studied successively at rest, during rapid atrial pacing, and after dobutamine infusion (5 to 30 micrograms.kg-1.min-1 i.v.) by proximal left anterior descending (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 value 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 cm2, P < .001) and higher resting APG and peak systolic retrograde CFV than in group 2, and also higher resting peak 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 pacing rate; however, these parameters increased concomitantly and significantly at peak dobutamine 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; group 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 group 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 comparable increases in both systolic (143.5 +/- 44.4%) and diastolic (197.1 +/- 75.2%) CFV area (both P < .001). The stress-induced increases in the mean CFV and blood flow exceeded or were comparable with the concomitant increases in the estimated myocardial metabolic demand in groups 2 and 3 but were significantly lower in group 1.


CONCLUSIONS
Stress-induced changes in LAD phasic CFV profile differ significantly between patients with and without AVS. In AVS, these changes are closely related to the concomitant stress-induced changes in hemodynamic parameters.
Petropoulakis
P N
PN
Department of Cardiology, Hippokration Hospital, University of Athens, Greece.
Kyriakidis
M K
MK
Tentolouris
C A
CA
Kourouclis
C V
CV
Toutouzas
P K
PK
D000368:Aged; D001024:Aortic Valve Stenosis / Q000503:physiopathology*; D001783:Blood Flow Velocity; D002304:Cardiac Pacing, Artificial; D003326:Coronary Circulation; D003971:Diastole; D004280:Dobutamine / Q000494:pharmacology*; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism; D013599:Systole
D004280:Dobutamine