(Circulation. 1999;100:243-249.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Effects of Dobutamine on Coronary Stenosis Physiology and Morphology
Comparison With Intracoronary Adenosine
From the Cardiovascular Center, Aalst, Belgium.
Correspondence to Bernard de Bruyne, MD, PhD, Cardiovascular Center, OLV Ziekenhuis, Moorselbaan 164, B-9300 Aalst, Belgium. E-mail bernard.de.bruyne{at}olvz-aalst.be
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Abstract |
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Background—The mechanisms leading to dobutamine-induced ischemia are not fully understood. In the present study, we investigated the effects of high-dose intravenous dobutamine on morphological and physiological indexes of coronary stenoses.
Methods and Results—Twenty-two patients with normal left ventricular function and isolated coronary stenoses were studied. At catheterization, mean aortic pressure (Pa), mean distal coronary pressure (Pd), and Pd/Pa as an index of myocardial resistance were recorded at rest, after intracoronary adenosine, and during intravenous infusion of dobutamine (10 to 40 µg · kg-1 · min-1). Reference vessel diameter and minimal luminal diameter, as assessed by coronary angiography, did not change during dobutamine infusion compared with baseline (2.84±0.49 versus 2.77±0.41 mm and 1.35±0.38 versus 1.27±0.31 mm, respectively; both P=NS). During peak dobutamine infusion, Pd and Pd/Pa reached similar levels as during adenosine infusion (60±18 versus 59±18 mm Hg and 0.68±0.18 versus 0.68±0.17, respectively; all P=NS). In 9 patients, an additional bolus of intracoronary adenosine given at the peak dose of dobutamine failed to further decrease Pd/Pa. Furthermore, in patients with dobutamine-induced wall motion abnormalities, the maximal decrease in Pd/Pa was similar during dobutamine and adenosine infusions.
Conclusions—High-dose intravenous infusion of dobutamine does not modify the dimensions of the epicardial coronary stenosis. However, much like the direct coronary vasodilator adenosine, dobutamine fully exhausts myocardial resistance regardless of the presence of mechanical dysfunction.
Key Words: dobutamine • hemodynamics • ischemia • coronary disease • stress
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Introduction |
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Dobutamine has a predominant positive inotropic effect associated with an increase in coronary blood flow and a mild positive chronotropic effect.1 Because of these characteristics, dobutamine leads to an increase in contractility without major changes in perfusion of the acutely ischemic myocardium.2 3 In current practice, high-dose dobutamine is increasingly used to detect and evaluate coronary artery disease. However, only a few experimental2 3 4 and clinical studies5 have investigated the effects of dobutamine on regional myocardial perfusion. Results of these studies suggested that mechanical dysfunction during dobutamine is usually associated with a blunted increase (or paradoxical decrease) in regional blood flow. However, these studies used models of acute or chronic myocardial ischemia2 3 4 or included many patients after myocardial infarction.5 In addition, it is not clear whether changes in myocardial perfusion during dobutamine infusion are related solely to changes in microvascular resistance or whether they are associated with changes in the morphology of an epicardial coronary stenosis. Therefore, in the present study, we tested the hypothesis that hemodynamic response of physiological indexes of stenosis severity during intravenous dobutamine is similar to the response induced by intracoronary adenosine. We also investigated whether dobutamine-induced changes in stenosis physiology are associated with changes in epicardial stenosis morphology.
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Methods |
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Patients
The study population consisted of 22 patients (3 women; mean age, 58±8 years) with normal left ventricular function and isolated coronary stenoses referred for coronary angioplasty. In all patients, cardiac medications were stopped
36 hours before protocol and replaced by aspirin 100 mg/d and
molsidomine 4 mg TID. Molsidomine was routinely administered to prevent
any vasomotion during wire manipulation. Stenoses were located
in the left anterior descending artery in 9 patients, in the right
coronary artery in 12 patients, and in the left circumflex
coronary artery in 1 patient.
Dobutamine Echocardiography
Echocardiography was performed on the same
day as the catheterization as previously described in
detail elsewhere.6
Catheterization Protocol
A 7.5F or 8F introduction sheath was introduced into the femoral
artery, and a 7F guiding catheter without side holes was engaged in the
coronary ostium. Distal coronary pressure was measured
with a fluid-filled (n=10, Schneider Europe) or high-fidelity (n=12,
Radi Medical) pressure-monitoring guidewire as previously described in
detail.7 8 After baseline recordings,
intracoronary adenosine (18 µg into the left
coronary artery and 12 µg into the right coronary
artery) was given to induce maximal coronary
hyperemia.9 After hemodynamic
parameters returned to baseline, dobutamine was
infused at 10, 20, 30, and 40 µg ·
kg-1 · min-1 for 3
minutes at each stage. The end points for infusion were maximal dose,
target heart rate, unbearable chest pain, ST-segment depression >0.3
mV, or severe side effects. In 9 patients, an additional bolus of
intracoronary adenosine was injected during the last 30
seconds of dobutamine infusion. Figure 1
shows an example of pressure
recordings performed at rest, during maximal hyperemia,
and during dobutamine infusion.
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Quantitative Coronary Angiography
Quantitative assessment of the stenosis geometry was
performed with the ACA system as previously described.10
The interpolated reference diameter, minimal luminal diameter, percent
diameter stenosis, and area stenosis were
calculated.
Data Acquisition
Mean aortic pressure (Pa), mean distal
coronary pressure (Pd), mean
translesional pressure gradient (
P), and the ratio of mean distal
coronary pressure to mean aortic pressure
(Pd/Pa) were monitored
under baseline conditions, during intravenous infusion of
dobutamine, and before and during adenosine
infusion. Angiographic measurements of the segment under study were
performed at baseline and at the end of dobutamine
infusion.
Statistical Analysis
Data are expressed as mean±SD. Statistical comparison was made
by ANOVA, followed by the Newman-Keuls test. Changes in vessel
diameters during infusion of dobutamine were
analyzed by Student's paired t test. A value of
P0.05 was considered statistically nonsignificant.
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Results |
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Effects of Intravenous Dobutamine on Stenosis Dimensions
At baseline, reference vessel diameter ranged from 2.10 to 3.82 mm (mean, 2.77±0.41 mm); minimal luminal diameter ranged from 0.64 to 1.89 mm (mean, 1.27±0.31 mm); percent diameter stenosis ranged from 36% to 79% (mean 53±11%); and area stenosis ranged from 60% to 90% (mean 76±9%) (Table 1
). Dobutamine had no
significant effect on these indexes of stenosis morphology
(Figure 2).
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Comparative Effects of Intravenous
Dobutamine and Intracoronary Adenosine on
Systemic and Coronary Hemodynamics.
Major individual and mean data in response to
dobutamine and adenosine are given in Tables 2 and 3 and
Figure 3. Adenosine had no effect
on heart rate, systolic blood pressure, or rate-pressure
product. Intravenous dobutamine
significantly increased heart rate and rate-pressure product. Heart
rate and rate-pressure product continued to increase significantly
when dobutamine was increased from 20 to 40 µg ·
kg-1 · min-1
(Figure 3).
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P<0.05 vs BL1.
Mean aortic pressure did not change during dobutamine or
intracoronary adenosine infusion. Translesional
pressure gradient increased, and distal coronary pressure and
the Pd/Pa ratio decreased
to a similar level during both dobutamine and
adenosine infusion. Figure 3
shows dose-dependent
changes in Pd/Pa during
intracoronary adenosine and dobutamine.
Pd/Pa decreased
significantly at 20 µg · kg-1 ·
min-1. There was a mild but statistically
nonsignificant decrease in
Pd/Pa when
dobutamine was increased from 20 to 30 µg ·
kg-1 · min-1.
Increasing dobutamine from 30 to 40 µg ·
kg-1 · min-1 did
not produce any additional decrease in
Pd/Pa. In contrast, heart
rate and rate-pressure product did increase further at
dobutamine >20 µg ·
kg-1 · min-1.
Figure 4 shows the near identity of the
values of Pd/Pa after
intracoronary adenosine and during peak
dobutamine.
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In 9 patients, an additional bolus of intracoronary adenosine given during peak dobutamine infusion induced a significant decrease in blood pressure (89±15 mm Hg before versus 82±15 mm Hg 15 seconds after an additional bolus of adenosine, P<0.05) and a proportional decrease in distal coronary pressure (60±18 versus 53±14 mm Hg, P<0.05) but no change in heart rate (139±17 versus 144±19 bpm, P=NS), pressure gradient (29±18 versus 29±18 mm Hg, P=NS), and Pd/Pa (0.68±0.19 versus 0.66±0.18, P=NS).
Coronary Hemodynamics According to the
Presence or Absence of Dobutamine-Induced Ischemia
In 10 patients, dobutamine
echocardiography was negative, whereas in 12
patients, dobutamine-induced wall motion abnormalities
could be detected by echocardiography (Tables 4 and 5 and Figure 5). There were no differences between the
anterior and inferior walls in response to
dobutamine. As expected, patients with abnormal
dobutamine echocardiograms had significantly higher
transstenotic pressure gradients and lower distal
coronary pressures and
Pd/Pa ratios during both
adenosine and dobutamine infusion. However, the
dose-dependent response of systemic hemodynamics and
stenosis physiology to dobutamine was similar in
both groups. Both distal coronary pressure and
Pd/Pa decreased to a
similar level during dobutamine and adenosine
infusion regardless of ischemia. Likewise, an increase in
translesional pressure gradient during dobutamine was
similar in both groups compared with adenosine, suggesting that
the changes in myocardial resistance induced by either
intracoronary adenosine or intravenous
dobutamine were similar in both groups.
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Discussion |
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The present study investigates in humans the effects of intravenous dobutamine at dosages used for pharmacological stress testing on coronary atherosclerotic stenoses and resistive vessel function. The results can be summarized as follows. First, in patients taking oral molsidomine, intravenous dobutamine did not modify the severity of the epicardial coronary stenosis. Second, despite a less-than-maximal increase in rate-pressure product, dobutamine induced a decrease in distal coronary perfusion pressure similar to that with adenosine. Because vasodilation was not associated with changes in stenosis morphology, the present data suggest that intravenous infusion of dobutamine decreased myocardial resistance to a minimum much like adenosine. Third, in most patients, myocardial resistances did not further decrease at dobutamine doses >20 µg · kg-1 · min-1.
Dobutamine and Epicardial Vasomotion
Stimulation of ß1-adrenergic receptors by
isoproterenol has been shown to induce an
endothelium-independent vasodilation of large
coronary arteries in dog experiments.11 In the
same species, however, the endothelium is essential for
mediation of exercise-induced epicardial coronary
vasodilation.12 Likewise, in humans, the response of
epicardial coronary arteries to sympathetic stimulation by the
cold pressor test depends on the functional integrity of the
endothelium.13 14 In contrast, in the
present study conducted in patients with angiographically
documented atherosclerosis, no changes in minimal
luminal diameter or reference diameter were observed during high-dose
dobutamine. Yet the effect of dobutamine is
difficult to appreciate because all patients received oral molsidomine.
The latter, an endothelium-independent vasodilator,
might have precluded any dobutamine-induced vasomotion.
Nevertheless, preliminary results suggest that in patients with diffuse
coronary atherosclerosis not pretreated with
molsidomine, dobutamine induces a mild increase in
coronary dimensions.15 Thus, in contrast to
sympathetic stimulation by the cold pressor test or
exercise,13 14 our data suggest that high-dose
dobutamine infusion causes either no change or vasodilation
rather than paradoxical vasoconstriction even in atherosclerotic
conduit vessels.
Distal Coronary Pressure as an Index of Myocardial
Resistance
In the presence of an epicardial stenosis,
adenosine infusion induces vasodilation, which in turn induces
a decrease in coronary pressure distal to the stenosis.
This increases pressure gradient and augments transstenotic
flow. At constant aortic pressure, changes in distal coronary
pressure may be due to changes in the severity of the epicardial
stenosis (ie, changes in the epicardial resistance), changes in
myocardial resistance, or a combination. In the case of a fixed
stenosis, changes in Pd are related
exclusively to changes in myocardial resistance and flow. In the
present study, no changes were observed in stenosis
dimensions. Therefore, changes in Pd (corrected
for eventual changes in aortic pressure) can be considered an index of
changes in myocardial resistance.
Dobutamine and Arteriolar Vasodilation
Several studies have shown that adenosine induces maximal
vasodilation.9 In addition, the magnitude of
adenosine-induced hyperemia appears to be similar to
that induced by exercise-induced ischemia16 and
postocclusional hyperemia.17 18 Our data suggest
that in humans intravenous dobutamine at doses
used for stress testing also induces maximal vasodilation regardless of
whether ischemia is present. Furthermore, an additional
intracoronary bolus of adenosine given during peak
dobutamine did not further decrease myocardial resistances.
These findings are in contrast to earlier experimental
reports.2 3 4 However, they corroborate previous studies
demonstrating an 
3-fold increase in myocardial flow during
dobutamine infusion19 and an 4-fold
increase during intravenous infusion of 300 µg ·
kg-1 · min-1
adenosine.20 In addition, our data are
consistent with those from a study of Skopicki et
al,21 who reported a similar increase in myocardial
blood flow as assessed by [13N]ammonia in
stenotic regions during adenosine and
dobutamine infusion.
Furthermore, in the present study, a vasodilation close to that obtained by adenosine was reached already at 20 and 30 µg · kg-1 · min-1 dobutamine. Indeed, the Pd/Pa ratio did not significantly decrease further when dobutamine was increased from 30 to 40 µg · kg-1 · min-1. Because during maximal vasodilation a linear relationship exists between coronary driving pressure and myocardial flow, these data suggest that myocardial flow did not significantly increase when dobutamine was increased to >20 µg · kg-1 · min-1. Of note, corroborating our data, Petroukilas et al22 observed a maximal increase in coronary flow velocity reserve in stenotic coronary arteries already at intermediate doses of dobutamine.
Mechanisms of Dobutamine-Induced Vasodilatation
In the presence of a fixed coronary stenosis, flow
maldistribution and myocardial ischemia are ascribed to an
increase in cardiac work and oxygen consumption. Yet in this study, as
in other studies,22 23 24 25 26 27 28 29 30 the rate-pressure product
reached during dobutamine infusion is far from that usually
reported during exercise despite a maximal decrease in myocardial
resistance. Despite this modest increase in rate-pressure product,
the ability of dobutamine
echocardiography and scintigraphy to
detect coronary artery disease is similar to that of exercise
echocardiography.27 29 31 32
Several factors may explain this apparent paradox.
First, dobutamine may increase contractility more than physical exercise. Previous animal experiments have shown a larger dP/dt during dobutamine infusion than during exercise.33 In humans, Dagianti et al34 also showed that at the ischemic threshold, the ratio of systolic blood pressure to end-systolic volume index, a variable related to myocardial contractility, was significantly higher during dobutamine infusion than during exercise.
Second, experimental studies suggested a direct coronary vasodilating effect of dobutamine mediated by ß2-adrenergic receptors contributing to a decrease in myocardial resistance and an increase in myocardial flow in a feed-forward manner.1 35 In chronically instrumented pigs, Duncker et al36 also noticed that ß-adrenoreceptor activity contributed in a feed-forward manner to coronary vasodilation during exercise. In patients with congestive heart failure, dobutamine induced an increase in coronary blood flow associated with an increase in coronary oxygen content but without changes in myocardial oxygen consumption,37 which is also consistent with a direct coronary vasodilatory effect of dobutamine. In the present study, a decrease in myocardial resistance reached a plateau at 20 µg · kg-1 · min-1 of dobutamine, whereas heart rate and rate-pressure product continued to increase. Using PET, Severi et al38 also found no significant increase in myocardial blood flow at dobutamine >20 µg · kg-1 · min-1 despite a progressive increase in heart rate at higher doses. This blunted increase in myocardial flow is in contrast with a progressive and continued increase in systolic wall thickening at higher doses of dobutamine.39 Taken together, these data suggest a dissociation between an increase in myocardial flow and an increase in myocardial mechanical work. Furthermore, they are consistent with a direct effect of dobutamine on myocardial resistive vessels that most likely override the metabolic regulation of myocardial flow.
Third, myocardial ischemia itself causes vasodilation and might explain a decrease in distal coronary perfusion pressure. However, in the present study, a similar decrease in the Pd/Pa ratio was observed in patients with and without ischemia-induced wall motion abnormalities. This suggests that myocardial ischemia is not a direct cause of the maximal vasodilation observed in our study. In sharp contrast to our finding that myocardial resistance uniformly decreases during dobutamine-induced ischemia, Sambuceti et al,40 using coronary Doppler flow velocity measurements, recently reported an inappropriate, severe microvascular vasoconstriction during pacing-induced ischemia that could be totally abolished by intracoronary adenosine.
Finally, an alternative mechanism that can contribute to dobutamine-induced ischemia is the so-called oxygen-wasting effects of catecholamines, ie, an increase in energy utilization at a comparable workload. This phenomenon has recently been demonstrated to occur in humans during intravenous administration of dobutamine even at doses as low as 10 µg · kg-1 · min-1.41
Study Limitations
This study has several limitations. First, patients with
coronary atherosclerosis often show an impaired
vasodilator response of the microvasculature. Unfortunately, pressure
measurements without simultaneous coronary flow
velocity measurements cannot assess the presence of microvascular
disease. Nevertheless, in the present study, this does not confound
the comparison between intracoronary adenosine and
intravenous dobutamine because each patient
served as his or her own control. Second, our study included only
patients with single-vessel disease and normal left
ventricular function. Thus, our data must be interpreted
with caution in cases of extensive coronary artery disease or
left ventricular dysfunction. Furthermore, responses in the
stenotic coronary arteries were not compared with
contralateral "normal" vessels. Recent studies suggested that in
normal segments, the dobutamine-induced increase in
coronary22 or myocardial blood flow21
is lower than during intracoronary or intravenous
adenosine. Nevertheless, our data suggest that in patients with
a mild stenosis, the magnitude of the response of
stenosis physiology to dobutamine is similar to
that of adenosine. In addition, it seems unlikely that
alternative routes of adenosine administration would have
different hyperemic effects.9 42 43 Fourth, all
patients were off ß-blockers. Considering the effect of ß-blockade
on systemic hemodynamics, it remains unclear whether
treatment with ß-blockers alters the effects of
dobutamine on stenosis physiology.
Conclusions
Although high-dose intravenous dobutamine
infusion did not affect the geometry of an epicardial coronary
stenosis, in patients pretreated with molsidomine, it fully
exhausted myocardial resistances at doses that do not cause a maximal
increase in cardiac work.
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Acknowledgments |
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The secretarial help of Josefa Cano is sincerely acknowledged.
Received January 13, 1999; revision received March 30, 1999; accepted April 27, 1999.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Vatner SF, McRitchie RJ, Braunwald E. Effects of dobutamine on left ventricular performance, coronary dynamics and distribution of cardiac output in conscious dogs. J Clin Invest. 1974;53:1265–1273.
2.
Tuttle RR, Pollock GD, Todd G, MacDonald B, Tust R,
Dusenberry W. The effect of dobutamine on cardiac oxygen
balance, regional blood flow, and infarction severity after
coronary artery narrowing in dogs. Circ Res. 1977;41:357–364.
3.
Willerson JT, Hutton I, Watson JT, Platt MR, Templeton
GH. Influence of dobutamine on regional myocardial blood
flow and ventricular performance during acute and
chronic myocardial ischemia in dogs. Circulation. 1976;53:828–833.
4.
Vatner SF, Baig H. Importance of heart rate in
determining the effects of sympathomimetic amines on regional
myocardial function and blood flow in conscious dogs with acute
myocardial ischemia. Circ Res. 1979;45:793–803.
5. Severi S, Underwood R, Mohiaddin RH, Boyd H, Paterni M, Camici PG. Dobutamine stress: effects on regional myocardial blood flow and wall motion. J Am Coll Cardiol. 1995;26:1187–1195.[Abstract]
6. Bartunek J, Marwick TH, Vincent M, Rodrigues CT, Van Schuerbeeck E, Sys SU, De Bruyne B. Dobutamine-induced wall motion abnormalities: correlations with myocardial fractional flow reserve and quantitative coronary angiography. J Am Coll Cardiol. 1996;27:1489–1496.
7. De Bruyne B, Pijls NHJ, Paulus WJ, Vantrimpont PJ, Sys SU, Heyndrickx GR. Transstenotic coronary pressure gradient measurement in man: in vitro and in vivo evaluation of a new pressure monitoring PTCA guide wire. J Am Coll Cardiol. 1993;22:119–126.[Abstract]
8. Emanuelsson H, Dohnal M, Lamm C, Tenerz L. Initial experiences with a miniaturized pressure transducer during coronary angioplasty. Cathet Cardiovasc Diagn. 1991;24:137–143.[Medline] [Order article via Infotrieve]
9.
Wilson RF, Wyche K, Christensen BV, Zimmer S, Laxson
DD. Effects of adenosine on human coronary
arterial circulation. Circulation. 1990;82:1595–1606.
10. Haase J, Di Mario C, Slager CJ, Keane D, Foley DP, den Boer A, Doriot PA, Serruys PW. In vivo validation of on-line and off-line geometric coronary measurements using insertion of stenosis phantom in porcine coronary arteries. Cathet Cardiovasc Diagn. 1992;27:16–27.[Medline] [Order article via Infotrieve]
11.
Ghaleh B, Béa ML, Dubois-Randé JL,
Giudicelli JF, Hittinger L, Berdeaux A. Endothelial
modulation of ß-adrenergic dilation of large coronary
arteries in conscious dogs. Circulation. 1995;92:2627–2635.
12.
Berdeaux A, Ghaleh B, Dubois-Randé JL,
Vigué B, Drieu La Rochelle C, Hittinger L, Giudicelli JF. Role of
vascular endothelium in exercise-induced dilation of
large epicardial coronary arteries in conscious dogs.
Circulation. 1994;89:2799–2808.
13.
Nabel EG, Ganz P, Gorden JB, Alexander WR, Selwyn AP.
Dilation of normal and constriction of atherosclerotic coronary
arteries caused by the cold pressor test. Circulation. 1988;77:43–52.
14. Zeiher AM, Drexler H, Wollschlaeger H, Saurbier B, Just H. Coronary vasomotion in response to sympathetic stimulation in humans: importance of the functional integrity of the endothelium. J Am Coll Cardiol. 1989;14:1181–1190.[Abstract]
15. Wyffels E, Wijns W, Heyndrickx GR, De Bruyne B. Does high-dose dobutamine induce a "paradoxical" coronary vasoconstriction of atherosclerotic coronary arteries? Eur Heart J. 1998;18(suppl):334. Abstract.
16. Vatner SF, McRitchie RJ, Maroko PH, Patrick TA, Braunwald E. Effects of catecholamines, exercise, and nitroglycerin on the normal and ischemia myocardium in conscious dogs. J Clin Invest. 1974;54:563–575.
17. Serruys PW, Di Mario C, Meneveau N, de Jaegere P, Strikwerda S, de Feyter PJ, Emanuelsson H. Intracoronary pressure and flow velocity from sensor tip guide wires: a new methodological comprehensive approach for the assessment of coronary hemodynamics before and after interventions. Am J Cardiol. 1993;71:41D–53D.[Medline] [Order article via Infotrieve]
18. Pijls NHJ, De Bruyne B. Coronary Pressure. Norwell, Mass: Kluwer Academic Publishers; 1997:16–18.
19.
Calnon DA, Glover DK, Beller GA, Vanzetto G, Smith WH,
Watson DD, Ruiz M. Effects of dobutamine stress on
myocardial blood flow, 99mTc sestamibi uptake,
and systolic wall thickening in the presence of
coronary artery stenoses. Circulation. 1997;96:2353–2360.
20.
Glover DK, Ruiz M, Edwards NC, Cunningham M, Simanis
JP, Smith WH, Watson DD, Beller GA. Comparison between
201TL and 99mTc sestamibi
uptake during adenosine-induced vasodilation as a function of
coronary stenosis severity. Circulation. 1995;91:813–820.
21.
Skopicki HA, Abraham SA, Picard MH, Alpert NM, Fischman
AJ, Gewirtz H. Effects of dobutamine at maximally tolerated
dose on myocardial blood flow in humans with ischemic heart
disease. Circulation. 1997;96:3346–3352.
22. Petroukilas P, Pavlides G, Athanassopoulos G, Vassilikos V, Cokkinos DV. Coronary flow velocity changes in adjacent stenotic and normal coronary arteries during incremental intravenous dobutamine stress in patients with coronary artery disease: comparison and combination with intracoronary adenosine. Eur Heart J 1998;18(suppl):334. Abstract.
23. Martin TW, Seaworth JF, Johns JP. Comparison of exercise electrocardiography and dobutamine echocardiography. Clin Cardiol. 1992;15:641–646.[Medline] [Order article via Infotrieve]
24. Previtali M, Lanzarini L, Fetiveau R, Poli A, Ferrario M, Falcone C, Mussini A. Comparison of dobutamine stress echocardiography, dipyridamole stress echocardiography and exercise stress testing for diagnosis of coronary artery disease. Am J Cardiol. 1993;72:865–870.[Medline] [Order article via Infotrieve]
25. Mazeika PK, Nadazdin A, Oakley CM. Dobutamine stress echocardiography for detection and assessment of coronary artery disease. J Am Coll Cardiol. 1992;19:1203–1211.[Abstract]
26. Berthe C, Pierard LA, Hiernaux M, Trotteur G, Lempereur P, Carlier J, Kulbertus HE. Predicting the extent and location of coronary artery disease in acute myocardial infarction by echocardiography during dobutamine infusion. Am J Cardiol. 1986;58:1167–1172.[Medline] [Order article via Infotrieve]
27. Cohen JL, Ottenweller JE, George AK, Duvvuri S. Comparison of dobutamine and exercise echocardiography for detecting coronary artery disease. Am J Cardiol. 1993;72:1226–1231.[Medline] [Order article via Infotrieve]
28.
Beleslin BD, Ostojic M, Stepanovic J, Djordjevic-Dikic
A, Stojkovic S, Nedeljkovic M, Stankovic G, Petrasinovic Z, Gojkovic L,
Vasiljevic-Pokrajcic Z, Nedeljkovic S. Stress
echocardiography in the detection of myocardial
ischemia. Circulation. 1994;90:1168–1176.
29. Marwick T, D'Hondt AM, Baudhuin T, Willemart B, Wijns W, Detry JM, Melin J. Optimal use of dobutamine stress for the detection and evaluation of coronary artery disease: combination with echocardiography or scintigraphy, or both? J Am Coll Cardiol. 1993;22:159–167.[Abstract]
30.
Marwick TH, D'Hondt AM, Mairesse GH, Baudhuin T, Wijns
W, Detry JM, Melin JA. Comparative ability of dobutamine
and exercise stress in inducing myocardial ischemia in active
patients. Br Heart J. 1994;72:31–38.
31. Bartunek J, Van Schuerbeeck E, De Bruyne B. Comparison of exercise electrocardiography and dobutamine echocardiography with invasively assessed myocardial fractional flow reserve in evaluation of severity of coronary arterial narrowing. Am J Cardiol. 1997;79:478–481.[Medline] [Order article via Infotrieve]
32. Hoffmann R, Lethen H, Kleinhans E, Weiss M, Flachskampf FA, Hanrath P. Comparative evaluation of bicycle and dobutamine stress echocardiography with perfusion scintigraphy and bicycle electrocardiogram for identification of coronary artery disease. Am J Cardiol. 1993;72:555–559.[Medline] [Order article via Infotrieve]
33. Vatner SF, McRitchie RJ, Maroko PR, Patrick TA, Braunwald E. Effects of catecholamines, exercise, and nitroglycerin on the normal and ischemic myocardium in conscious dogs. J Clin Invest. 1974;54:563–575.
34. Dagianti A, Penco M, Agati L, Sciomer S, Dagianti A, Rosanio S, Fedele F. Stress echocardiography: comparison of exercise, dipyridamole and dobutamine in detecting and predicting the extent of coronary artery disease. J Am Coll Cardiol. 1995;26:18–25.[Abstract]
35.
Miyashiro JK, Feigl EO. Feedforward control of
coronary blood flow via coronary ß-receptor
stimulation. Circ Res. 1993;73:252–263.
36.
Duncker DJ, Stubenitsky R, Verdouw PD. Autonomic
control of vasomotion in the porcine coronary circulation
during treadmill exercise. Circ Res. 1998;82:1312–1322.
37. Dubois-Randé JL, Merlet P, Duval-Moulin AM, Adnot S, Saal JP, Chabrier E, Castaigne A, Geschwind H. Coronary vasodilating action of dobutamine in patients with idiopathic dilated cardiomyopathy. Am Heart J. 1993;125:1329–1336.[Medline] [Order article via Infotrieve]
38. Severi S, Underwood R, Mohiaddin R, Boyd H, Paterni M, Camici PG. Dobutamine stress: effects on regional myocardial blood flow and wall motion. J Am Coll Cardiol. 1995;26:1187–1195.
39. Panza JA, Laurienzo JM, Curiel RV, Unger EF, Quyyumi AA, Dilsizian V, Cannon RO III. Investigation of the mechanism of chest pain in patients with angiographically normal coronary arteries using transesophageal dobutamine stress echocardiography. J Am Coll Cardiol. 1997;29:293–301.[Abstract]
40.
Sambuceti G, Marzilli M, Marraccini P, Schneider-Eicke
J, Gliozheni E, Parodi O, L'Abbate A. Coronary
vasoconstriction during myocardial ischemia induced by rises in
metabolic demand in patients with coronary artery
disease. Circulation. 1997;95:2652–2659.
41.
Vanoverschelde JL, Wijns W, Essamri B, Bol A, Robert A,
Labar D, Cogneau M, Michel C, Melin JA. Hemodynamic and
mechanical determinants of myocardial O2
consumption in normal human heart: effects of dobutamine.
Am J Physiol. 1993;265:H1884–H1892.
42. Kern MJ, Deligonul U, Tatinemi S, Serota H, Aguirre F, Hilton TC. Intravenous adenosine, continuous infusion and low dose bolus administration for determination of coronary vasodilator reserve in patients with and without coronary artery disease. J Am Coll Cardiol. 1991;18:718–729.[Abstract]
43. van der Voort P, van Hegen E, Hendrix G, Van Gelder B, Bech GJW, Pijls NHJ. Comparison of intravenous adenosine to intracoronary papaverine for calculation of pressure-derived fractional flow reserve. Cathet Cardiovasc Diagn. 1996;39:120–125.[Medline] [Order article via Infotrieve]
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