This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Petropoulakis, P. N. Articles by Toutouzas, P. K. Search for Related Content PubMed PubMed Citation Articles by Petropoulakis, P. N. Articles by Toutouzas, P. K. Pubmed/NCBI databases Compound via MeSH Substance via MeSH

(Circulation. 1995;92:1437-1447.)
© 1995 American Heart Association, Inc.

Articles

Changes in Phasic Coronary Blood Flow Velocity Profile in Relation to Changes in Hemodynamic Parameters During Stress in Patients With Aortic Valve Stenosis

Panaghiotis N. Petropoulakis, MD; Michael K. Kyriakidis, MD; Costas A. Tentolouris, MD; Costas V. Kourouclis, MD; Pavlos K. Toutouzas, MD

From the Department of Cardiology, Hippokration Hospital, University of Athens, Greece.

Correspondence to Panaghiotis N. Petropoulakis, MD, Giannari 6 Koridallos, Piraeus Attica 181 20, Greece.

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.

Methods and 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 µg · kg^-1 · min^-1 IV) 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.

Key Words: aorta • catheterization • inotropic agents • valves

This article has been cited by other articles:

				D. Garcia, P. G. Camici, L.-G. Durand, K. Rajappan, E. Gaillard, O. E. Rimoldi, and P. Pibarot Impairment of coronary flow reserve in aortic stenosis J Appl Physiol, January 1, 2009; 106(1): 113 - 121. [Abstract] [Full Text] [PDF]

				N. Westerhof, C. Boer, R. R. Lamberts, and P. Sipkema Cross-talk between cardiac muscle and coronary vasculature. Physiol Rev, October 1, 2006; 86(4): 1263 - 1308. [Abstract] [Full Text] [PDF]

				H. Wieneke, K. Sattler, C. von Birgelen, D. Bose, M. Haude, W. Rechenberg, S. Sack, N. Dagres, and R. Erbel Impact of intraventricular conduction delay on coronary haemodynamics: a study with intracoronary Doppler in patients with bundle branch blocks and normal coronary arteries. Europace, March 1, 2006; 8(3): 151 - 156. [Abstract] [Full Text] [PDF]

				P. Lancellotti, F. Lebois, M. Simon, C. Tombeux, C. Chauvel, and L. A. Pierard Prognostic Importance of Quantitative Exercise Doppler Echocardiography in Asymptomatic Valvular Aortic Stenosis Circulation, August 30, 2005; 112(9_suppl): I-377 - I-382. [Abstract] [Full Text] [PDF]

				H. Wieneke, C. von Birgelen, M. Haude, H. Eggebrecht, S. Mohlenkamp, A. Schmermund, D. Bose, C. Altmann, T. Bartel, and R. Erbel Determinants of coronary blood flow in humans: quantification by intracoronary Doppler and ultrasound J Appl Physiol, March 1, 2005; 98(3): 1076 - 1082. [Abstract] [Full Text] [PDF]

				C. M. Otto, B. K. Lind, D. W. Kitzman, B. J. Gersh, D. S. Siscovick, and The Cardiovascular Health Study Association of Aortic-Valve Sclerosis with Cardiovascular Mortality and Morbidity in the Elderly N. Engl. J. Med., July 15, 1999; 341(3): 142 - 147. [Abstract] [Full Text] [PDF]