| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Hypertension. 1997;29:1232-1239.)
© 1997 American Heart Association, Inc.
Articles |
Safety and Feasibility of Dobutamine-Atropine Stress Testing in Hypertensive Patients
From the Thoraxcenter, University Hospital Rotterdam-Dijkzigt, Erasmus University, Rotterdam, Netherlands.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Abstract Dobutamine stress testing is increasingly used for the diagnosis and functional evaluation of coronary artery disease. The aim of this study was to assess the hemodynamic profile, safety, and feasibility of dobutamine stress testing in hypertensive patients. Dobutamine (up to 40 µg/kg per min-ute)–atropine (up to 1 mg) stress echocardiography was performed for the detection of myocardial ischemia in 1164 patients with limited exercise capacity (age, 60±12 years; 761 men); 446 patients were known to have hypertension. The test was considered feasible when 85% of the maximal heart rate and/or an ischemic end point (new or worsened wall motion abnormalities, ST segment depression, or angina) was achieved. No myocardial infarction or death occurred during the test. Dobutamine induced a significant increase of heart rate in patients with and without hypertension (59±25 and 63±23 beats per minute, respectively). Peak rate pressure product was similar in patients with and without hypertension (18 566±4584 and 18 230±4508). Hypotension (systolic pressure drop >40 mm Hg) during the test was more frequent in hypertensive patients (7% versus 4% in normotensive, P<.05). Independent predictors of hypotension were baseline systolic pressure greater than 140 mm Hg (odds ratio, 6.9; 95% confidence interval, 3.4 to 14), older age (odds ratio, 1.04; 95% confidence interval, 1.01 to 1.07), and medication with calcium channel blockers (odds ratio, 1.8; 95% confidence interval, 1.1 to 3.5). The prevalence of ventricular tachycardia was similar (4.1%) in both groups. Episodes of 10 beats or more (0.06% of patients) were terminated promptly by intravenous metoprolol administration. Dobutamine stress testing was considered feasible in 91% of patients with and 92% of patients without hypertension. Dobutamine-atropine stress echocardiography is a safe and feasible method for the assessment of hypertensive patients referred for evaluation of myocardial ischemia. Despite the higher prevalence of dobutamine-induced hypotension in these patients, the feasibility of the test is comparable to that in individuals without hypertension.
Key Words: dobutamine • echocardiography • safety • coronary artery disease
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Exercise electrocardiography has been shown to have a limited accuracy in the diagnosis of coronary artery disease in hypertensive individuals.1 2 3 Several studies have also indicated that exercise perfusion scintigraphy and radionuclide angiography may yield positive results in the absence of significant epicardial coronary artery disease in these patients.4 5 6 7 Dobutamine-atropine stress echocardiography (DSE) is increasingly used for the diagnosis and functional evaluation of coronary artery disease, particularly in individuals with limited exercise capacity.8 9 10 11 12 13 Dobutamine is a ß1- and ß2-agonist that results in a positive inotropic and chronotropic effect and a reduction of systemic vascular resistance.14 15 16 Intravenous atropine is frequently used in conjunction with high doses of dobutamine in patients with an inadequate chronotropic response.17 The final effect of dobutamine infusion on systolic pressure is determined by the interaction of different mechanisms, including the extent of reduction in systemic vascular resistance, the magnitude of increase in cardiac output, and the possible occurrence of intracavitary obstruction or stimulation of vagal reflexes.18 19 20 21 22 The diagnosis of coronary artery disease using high doses of dobutamine infusion is based on the induction of myocardial ischemia by increasing myocardial oxygen demand through positive inotropic and chronotropic effects.14 15 16 A recent study has demonstrated a higher accuracy of DSE than exercise electrocardiography for the diagnosis of coronary artery disease in hypertensive patients.23 A few studies have evaluated the safety and feasibility of dobutamine stress testing,24 25 26 27 but the hemodynamic profile, safety, and feasibility of dobutamine stress testing in hypertensive patients have not been studied. Such a study would be particularly important because dobutamine may induce a marked increase or decrease of systolic pressure, and it is not known to what extent hypertensive patients can tolerate such changes. The autonomic nervous system dysregulation in hypertensive patients28 may be assumed to influence the feasibility of dobutamine stress testing. Several studies have suggested that postsynaptic ß-adrenoceptor function may be attenuated with a concomitant facilitation of postsynaptic
-adrenergic function in human
hypertension.28 29 30 31 Other studies have reported a reduced
vagal tone in hypertensive patients,32 which may be
assumed to reduce the chronotropic response to atropine. Additionally,
it is not known whether hypertensive patients have a particular
vulnerability to the arrhythmogenic effect of dobutamine
infusion.33 The aim of this study was to assess the safety and feasibility of DSE in hypertensive patients referred for the diagnosis of myocardial ischemia who were not able to perform exercise stress testing and to compare the safety and hemodynamic profiles with those of normotensive individuals.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Patient Population
The study population comprised 1164 consecutive patients with limited exercise capacity referred to our imaging laboratory for evaluation of myocardial ischemia by DSE between January 1991 and April 1996. Hypertension, as diagnosed by the referring physician, was present in 446 patients (group 1); group 2 comprised 718 patients without the diagnosis of hypertension. Along with the information in our database, patient clinical reports were revised to confirm the presence or absence of a clinical diagnosis of hypertension by the treating physician. DSE was not performed in cases of severe heart failure, significant valvular heart disease, severe hypertension (blood pressure
180/110 mm Hg), hypotension (blood
pressure <90/60 mm Hg), or unstable chest pain. Mean age was
60±12 years (761 men). The Hospital Ethics Committee approved the use
of DSE for evaluation of patients with known or suspected
coronary artery disease. Patient characteristics, medications,
and indications of stress testing in both groups are presented
in Table 1
.
|
Dobutamine Stress Test
Dobutamine was infused through an antecubital vein
starting at a dose of 5 µg/kg per minute followed by 10 µg/kg per
minute (3-minute stages), increasing by 10 µg/kg per minute every 3
minutes to a maximum of 40 µg/kg per minute. Atropine (up to 1 mg)
was given in patients not achieving 85% of age-predicted maximal heart
rate, and dobutamine infusion was continued.17
The electrocardiogram was monitored throughout
dobutamine infusion and recorded each minute. Cuff
blood pressure was measured at rest, every 3 minutes during stress, and
at maximal stress. The test was interrupted if any of the following
appeared during the test: severe chest pain, ST segment depression
greater than 2 mm, significant ventricular or
supraventricular arrhythmia, hypertension (blood
pressure 240/120 mm Hg), systolic pressure fall greater
than 40 mm Hg, or any intolerable side effect regarded as being
caused by dobutamine. Metoprolol (1 to 5 mg) was available
and used intravenously to reverse the effects of
dobutamine if they did not revert spontaneously and
quickly. Ischemia at the electrocardiogram was
defined as greater than or equal to 0.1 mV horizontal or downsloping ST
segment depression 80 milliseconds from the J-point
compared with baseline level or greater than or equal to 0.1 mV ST
segment elevation in electrocardiographic leads corresponding to
segments without resting wall motion abnormalities.34 The
test was considered feasible if the patient could achieve 85% of the
maximal heart rate predicted for age and/or when an ischemic
end point (angina, ST segment depression, new or worsened wall motion
abnormalities) was reached. All patients gave verbal informed consent
to undergo the study.
Stress Echocardiography
Echocardiographic images were acquired when
patients were at rest and during stress and recovery. The
echocardiograms were recorded on videotapes and were also digitized
on optical disk and displayed side by side in quad-screen format
(Vingmed-CFM 800, Vingmed Sound A/S) to facilitate the comparison of
rest and stress images. The left ventricular wall was
divided into 16 segments and scored with a four-point scale (1=normal,
2=hypokinesis, 3=akinesis, 4=dyskinesis). Wall motion score index was
derived by dividing the summation of the individual scores of the 16
segments by 16. Images were interpreted by two experienced observers
without the knowledge of the patients' clinical data. In case of
disagreement, a majority decision was achieved by a third observer. In
our laboratory, the interobserver and intraobserver agreements for DSE
assessment were 92% and 94%, respectively.35
Ischemia was defined as new or worsening wall motion
abnormalities. As we have previously concluded,36 37
ischemia was not considered when akinetic segments at rest
became dyskinetic during stress without improvement at a low dose of
dobutamine (5 to 10 µg/kg per minute).
Coronary Angiography
Coronary angiography was performed within 3 months from
DSE in 283 patients. Lesions were quantified as previously
described.38 In short, the 35-mm films were
analyzed with the Cardiovascular Angiography
Analysis System II (CAAS II, Pie Medical). For edge detection,
a region of interest of 512x512 pixels was selected and digitized with
a high-fidelity charge-coupled device video camera. The vessel diameter
was determined by computing the shortest distance between the right and
left contours. A computer-derived estimation of the original
arterial dimension was used to calculate the interpolated
reference diameter. Significant coronary artery disease was
defined as a stenosis diameter greater than or equal to 50% in
one or more major epicardial artery. Coronary arteries were
assigned to myocardial segments as previously described.13
Peri-infarction zone was defined as myocardial segments in the
distribution of infarct-related artery.
Statistical Analysis
Unless specified, data are presented as mean±SD. The
2 test was used to compare differences between
proportions. Student's t test was used for analysis
of continuous data. Stepwise logistic regression models were fitted to
identify independent predictors of hypotension. The difference in risk
was expressed as odds ratio (OR) with the corresponding 95% confidence
interval (CI). Differences were considered significant if the null
hypothesis could be rejected at the .05 probability level. To compare
and visualize the predictive value of continuous variables for the
occurrence of hypotension, we used a receiver operator characteristics
curve. Sensitivity, specificity, and accuracy of DSE for the diagnosis
of significant coronary artery disease were derived according
to standard definitions and were presented with the
corresponding 95% CI.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Symptoms and Hemodynamic Response
No death or myocardial infarction occurred during or shortly after the test. Systolic pressure and heart rate increased significantly from rest to peak stress (133±22 [range, 90 to 178] versus 137±30 [range, 60 to 280] mm Hg, P<.00005; 72±14 [range, 41 to 110] versus 134±16 [range, 65 to 210] beats per minute, P<.00001), whereas diastolic pressure decreased significantly (76±13 [range, 60 to 109] versus 72±16 [range, 38 to 138] mm Hg, P<.00005). Atropine was administered in 515 patients (44%); the mean dose was similar in both groups (0.61±0.30 and 0.60±0.28 mg). Atropine induced a significant comparable increase in heart rate and no significant change in systolic or diastolic pressures in both groups. Table 2
demonstrates the
hemodynamic responses in both groups. Patients of group
1 had higher systolic and diastolic pressures at
rest and peak stress. Systolic pressure increased significantly
in group 2 but not group 1. Rate pressure product was higher in
group 1 at rest and similar for both groups at peak stress.
Systolic pressure exceeded 240 mm Hg during stress in
only 1 patient (group 1), who developed atypical chest pain; the test
was terminated. No patient reached a diastolic pressure of
120 mm Hg or higher during stress. Angina occurred in 305
patients (26%). Other symptoms during the test included nausea in 52
patients (4%), flushing in 10 (1%), dizziness in 35 (3%), anxiety in
25 (2%), chills in 49 (4%), and headache in 51 (4%). The prevalence
of symptoms was similar in both groups, except for a higher prevalence
of angina in group 1 (Table 3).
|
|
The target heart rate (85% of the maximal heart rate predicted for
age) was reached in 935 patients (80%). Reasons for termination of the
test are shown in Table 4. There was no significant
difference between the groups with regard to the percentage of patients
reaching the target heart rate. In patients who were not receiving
ß-blockers, the target heart rate was reached in 234 of 279 patients
in group 1 (84%) and 411 of 484 patients in group 2 (85%). Among the
229 patients who failed to achieve the target heart rate, an
ischemic end point was reached in 132 patients. Thus, the test
was considered feasible (reaching the target heart rate and/or an
ischemic end point) in 1067 patients (92%). This comprised 404
patients in group 1 (91%) and 663 patients in group 2 (92%).
|
Predictors of Hypotension
A systolic pressure drop of greater than 40 mm Hg
occurred in 56 patients (5%) during stress. These patients were older
(64±11 versus 60±12 years, P<.01) and had a higher
baseline systolic pressure (153±21 versus 132±22 mm Hg,
P<.00001), a higher prevalence of history of hypertension
(54% versus 38%, P<.05) and medications with calcium
channel blockers (48% versus 35%, P<.05), a relatively
lower prevalence of ß-blockers medication (23% versus 35%,
P=.07), and a similar prevalence of ischemia at
echocardiography (32% versus 33%).
Multivariate analysis identified as independent
predictors of hypotension baseline systolic pressure greater
than 140 mm Hg (OR, 6.9; 95% CI, 3.4 to 14), older age (OR,
1.04; 95% CI, 1.01 to 1.07), and medication with calcium channel
blockers (OR, 1.8; 95% CI, 1.1 to 3.5). When the combinations of
vasoactive medications (calcium antagonists,
angiotensin-converting enzyme inhibitors,
nitrates, and diuretics) were added to the
multivariate analysis for prediction of
hypotension, calcium antagonists alone remained the only
significant medication predicting hypotension; none of the combinations
of these medications was independently predictive of hypotension. Blood
pressure failed to increase from rest to peak stress in patients
receiving dihydropyridines, who constituted 51% of
patients receiving calcium antagonists (139±21 at rest
versus 139±30 mm Hg at peak stress), and in patients receiving
nondihydropyridine derivatives, who constituted
51% of patients receiving calcium antagonists (141±22 at
rest versus 141±27 mm Hg at peak stress). Intake of either type
of calcium antagonist was associated with the same
prevalence of hypotension (6% in both).
Hypotension was the reason for test termination in only 18 of the 56 patients who developed hypotension. The test was considered feasible in 5 of these 18 patients because they had ischemia at DSE. Reasons for termination of the test in other patients included angina (5 patients), target heart rate (29 patients), maximal dose (1 patient), ST depression (1 patient), and arrhythmias (2 patients). Hypotension was associated with symptoms (dizziness, nausea, headache, chills, anxiety) in 5 patients in group 1 and 8 patients in group 2.
Prevalence of Arrhythmias
Table 5 shows the prevalence of arrhythmias
during DSE. In the overall population, premature atrial contractions
occurred in 78 patients (7%), premature ventricular
contractions in 368 (32%), supraventricular
tachycardia in 44 (4%), atrial fibrillation in 14 (1%),
and ventricular tachycardia (three or more
consecutive premature ventricular contractions) in 57 (5%)
(10 beats in 7 patients). Metoprolol was used if
tachyarrhythmias persisted after discontinuation of
dobutamine infusion. Only 1 patient (in group 2) had
persistent atrial fibrillation and was successfully treated with
medical cardioversion. There was no significant difference between the
groups with regard to the prevalence of various types of
arrhythmias.
|
Patients Without Previous Myocardial Infarction
In patients without previous myocardial infarction (219 patients
in group 1 and 322 patients in group 2), both hypertensive and
normotensive patients had a comparable prevalence of
supraventricular tachycardia (2% versus 3%),
atrial fibrillation (2% versus 2%), ventricular
tachycardia less than 10 beats (3% versus 4%), and
ventricular tachycardia greater than 10 beats
(0.9% versus 0.6%). Hypotension occurred more frequently in group 1
(7% versus 3%, P<.05).
Stress Echocardiography
Wall motion abnormalities were present at rest in 256 patients
in group 1 (57%) and 425 in group 2 (59%). Ischemia (new or
worsened wall motion abnormalities) was detected in 150 patients in
group 1 (34%) and 231 in group 2 (32%), whereas 145 patients in group
1 (33%) and 245 in group 2 (34%) had normal wall motion at both rest
and peak stress. Wall motion score index increased significantly from
rest to peak stress in group 1 (1.36±0.49 versus 1.41±0.5,
P<.00001) and group 2 (1.42±0.49 versus 1.45±0.56,
P<.0001). The two groups did not differ significantly with
regard to rest and peak wall motion score index or the prevalence of
baseline or stress-induced wall motion abnormalities.
Accuracy of DSE for Diagnosis of Coronary Artery
Disease
Coronary angiography was performed in 283 patients within
3 months of DSE (109 in group 1 and 174 in group 2). Significant
coronary artery disease was detected in 220 patients (87 in
group 1 and 133 in group 2), whereas 63 patients (22 in group 1 and 41
in group 2) had a normal coronary angiogram or insignificant
lesions. Tables 6 and 7 demonstrate the
accuracy of DSE in both groups for the diagnosis of significant
coronary artery disease on the basis of ischemia in
patients without and with previous myocardial infarction. Sensitivity,
specificity, and accuracy were comparable in the groups for the overall
diagnosis of coronary artery disease, single-vessel disease,
and multivessel disease; for the identification of multivessel disease
on the basis of inducible ischemia in one or more vascular
territory; and in the diagnosis of infarct-related and remote
coronary artery stenosis.
|
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Hypertension is a risk factor frequently encountered in patients referred for noninvasive diagnosis or functional evaluation of coronary artery disease.3 39 Exercise electrocardiography and myocardial perfusion scintigraphy may have limitations in the diagnosis of coronary artery disease in these patients.1 2 3 4 5 6 Alternatively, DSE is being increasingly used, particularly in patients with limited exercise capacity.8 9 10 11 12 13 This is the first study that evaluates the hemodynamic profile, safety, and feasibility of DSE in hypertensive patients.
Our study demonstrates that DSE is a feasible and safe method for evaluation of coronary artery disease in hypertensive patients with suspected myocardial ischemia and limited exercise capacity. No myocardial infarction or death occurred during the test. The feasibility of the test was similar in patients with and without hypertension (91% and 92%, respectively). Despite the higher prevalence of dobutamine-induced hypotension in hypertensive patients, the prevalence of hypotension necessitating termination of the test was rare (1.5%) and comparable with that in patients without hypertension. The test was terminated because of a marked systolic pressure increase in only one patient. The prevalence of arrhythmias was similar in patients with and without hypertension. Ventricular tachycardia was terminated in all cases spontaneously by stopping dobutamine infusion or with metoprolol administration. Minor side effects, including chills, dizziness, headache, nausea, and anxiety, were common and occurred in 11% of the whole population. However, these symptoms were usually well tolerated and led to termination of the test in only a minority of patients (1%). The prevalence of these side effects was similar in patients with and without hypertension.
Hemodynamic Response of Hypertensive Patients
to Dobutamine
Systolic pressure failed to increase from rest to peak
stress in patients with as opposed to without hypertension, in whom a
significant increase of systolic pressure occurred.
Additionally, peak heart rate was slightly lower in hypertensive
patients. Despite these findings, rate pressure product at peak
stress was similar in the two groups because of the initially higher
systolic pressure at rest in hypertensive patients. This would
ensure a similar hemodynamic stress for the provocation
of myocardial ischemia in patients with and without
hypertension.40 The relatively lower peak heart rate in
hypertensive patients can be explained by the older age and higher
prevalence of females in the hypertensive group, with a lower predicted
maximal heart rate. The proportion of patients reaching the target
heart rate and the chronotropic response to atropine administration
were similar in patients with and without hypertension. This was also
observed in patients who were not taking ß-blockers. This suggests
that the reductions of ß-receptor function and parasympathetic tone
reported in hypertensive patients29 30 31 32 do not reduce the
chronotropic response to dobutamine or atropine in
hypertensive patients with suspected myocardial ischemia under
usual clinical circumstances.
The failure of systolic pressure to increase in hypertensive
patients may be due to many factors, including the older age, the
higher frequency of medication with calcium channel blockers, or a
diminished ß1-mediated inotropic response with an
inappropriate increase of cardiac output. However, if sympathetic
dysfunction was influencing blood pressure response in these patients,
a diminished response to ß2-mediated
peripheral vasodilatation and an increased response to
reflex -mediated vasoconstriction are expected to protect against
dobutamine-induced hypotension. This theory is also not
supported by the finding of an adequate chronotropic response in
hypertensive patients comparable to that in normotensive patients.
Patients with essential hypertension were reported to have a contracted
intravascular volume,41 42 which may contribute to their
tendency for developing a hypotensive response during
dobutamine infusion.
In the multivariate analysis, a history of hypertension was not an independent predictor of dobutamine-induced hypotension, whereas baseline systolic pressure greater than 140 mm Hg was the most powerful independent predictor of hypotension. One could speculate that proper control of hypertension before the test would decrease the prevalence of hypotensive episodes during the test. It is noteworthy that a higher baseline systolic pressure before DSE is started does not invariably imply a clinical diagnosis of hypertension. These patients may represent a hyperkinetic hemodynamic state or the so-called fight-or-flight reaction described with anxiety (which is expected in anticipation of stress testing, particularly with this unpopular technique) and in patients with borderline hypertension.28 43 Dobutamine-induced hypotension in these patients may represent increased sympathetic responsiveness, with profound ß2-mediated reduction of systemic vascular resistance.
The higher prevalence of hypotension among patients receiving calcium channel blockers may be explained by the potent peripheral vasodilator action of these medications, leading to a reduction of systemic vascular resistance and a possible negative inotropic effect, which results in an inappropriate increase of cardiac output in the face of a further decrease of systemic vascular resistance during dobutamine infusion. Another possibly contributing mechanism is the inhibition of sympathetic-mediated vasoconstriction in response to the reduction of systolic pressure mediated by the peripheral vasodilator action of dobutamine. It has been demonstrated that dihydropyridine blunts the forearm arteriolar response to norepinephrine without interfering with ß-adrenergic receptor–mediated vasorelaxation.44 In this study, both dihydropyridine and nondihydropyridine derivatives were associated with an impaired systolic pressure response to dobutamine and a similar prevalence of hypotension. The association between hypotension and older age has been previously reported.21 This may be explained by a reduced inotropic response or diminished vascular adaptive mechanisms to systolic pressure changes induced by dobutamine infusion.16
Diastolic pressure decreased significantly at peak stress, as reported previously.45 However, hypertensive patients had a more significant reduction. The reduction of diastolic pressure may provide an additional mechanism of provoking myocardial ischemia during dobutamine infusion by reducing coronary artery perfusion pressure.46
Comparison With Previous Studies
Senior et al23 studied 43 hypertensive patients with
DSE and exercise treadmill electrocardiography.
DSE had a higher sensitivity (93% versus 72%) and higher specificity
(100% versus 29%) than exercise
electrocardiography for the detection of
coronary artery disease. The prevalence of hypotension (defined
as a systolic pressure drop >30 mm Hg) was 28%.
The prevalence of different types of arrhythmias during dobutamine stress testing was similar in patients with and without hypertension. The overall prevalences of supraventricular tachycardia (including atrial fibrillation) (4.8%) and ventricular tachycardia (4.8%) in our study are consistent with those reported by Meters et al24 (4.1% and 4.2%, respectively). Arrhythmias were the reason for termination of the test in 1.7% of patients in our study, comparable to the findings of Meters et al (2.1%) and lower than that reported by Picano et al27 (5.7% comprising 50% of submaximal tests). This may be explained by the use of frequent polymorphic premature ventricular contractions as the criteria for test termination in the latter study. There was no difference between patients with and without hypertension regarding the feasibility of dobutamine stress testing. Overall feasibility (92%) was comparable to that reported by Poldermans et al26 (98%), Cornel et al25 (97%), and Picano et al27 (88%).
Accuracy of DSE in Patients With and Without Hypertension
To our knowledge, this is the first study that compares the
diagnostic accuracy of DSE in patients with and without
hypertension. Sensitivity, specificity, and accuracy were fairly
comparable in both groups for the overall diagnosis of coronary
artery disease, single-vessel disease, and multivessel disease; for the
identification of multivessel disease on the basis of inducible
ischemia in one or more vascular territory; and in the
diagnosis of infarct-related and remote coronary artery
stenosis. This indicates that hypertension does not limit the
diagnostic accuracy of DSE despite the more frequent
occurrence of hypotension during the test. The moderate sensitivity and
high specificity of DSE in our study are aligned with the results of
previous studies.8 9 10 11 12 13
Study Limitations
The majority of patients in the present study were receiving
cardiac medications that may modify the cardiovascular
response to dobutamine infusion. We did not study the
changes of systemic vascular resistance and cardiac output in response
to dobutamine-atropine stress testing; therefore, we could
not identify the definitive mechanisms underlying blood pressure
changes. However, this does not limit our conclusion regarding the
safety and feasibility of dobutamine stress testing in
hypertensive patients under usual clinical circumstances.
The definition of hypertension relied on the diagnosis of the referring physician rather than repeated blood pressure measurements. Since hypertension is well known to be a major risk factor for coronary artery disease, it would be appropriate to emphasize that physicians are aware of the importance of the diagnosis of this modifiable risk factor in their clinical evaluation of patients with known or suspected coronary artery disease. Patients diagnosed as having hypertension receive therapy to reduce their elevated blood pressure. Consequently, blood pressure measurements on the day of the test are not reliable for the diagnosis of hypertension. Despite the fact that most of the hypertensive patients were receiving medication, their mean resting systolic pressure (although obtained by a single measurement before stress) fell in the hypertensive range (141±23 mm Hg). Both systolic and diastolic pressures were significantly higher in patients with than without hypertension, denoting that most of patients were accurately classified with regard to the presence or absence of hypertension.
Clinical Implications and Conclusions
We conclude that DSE is a safe and feasible method for evaluation
of coronary artery disease in hypertensive patients, with a
diagnostic accuracy comparable to that in patients without
hypertension. Dobutamine and atropine induce a similar
chronotropic response in patients with and without hypertension. A
baseline systolic pressure greater than 140 mm Hg, older
age, and medication with calcium channel blockers are independent
predictors of the occurrence of hypotension during
dobutamine stress testing. Despite the higher prevalence of
dobutamine-induced hypotension in hypertensive patients,
the feasibility of the test is high and comparable to that in patients
without hypertension. Since elevated systolic pressure rather
than a history of hypertension was an independent predictor of the
occurrence of hypotension during the test, it is assumed that proper
control of elevated blood pressure before dobutamine stress
testing would reduce the incidence of hypotension during the test.
|
Footnotes |
|---|
Reprint requests to Abdou Elhendy, MD, PhD, Thoraxcenter, Ba 300, Dr Molewaterplein 40, 3015 GD Rotterdam, Netherlands.
Received July 31, 1996; first decision August 21, 1996; accepted December 3, 1996.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Gianrossi R, Detrano R, Mulvihill D, Lehmann K, Dubach P, Colombo A, McArthur D, Froelicher V. Exercise-induced ST depression in the diagnosis of coronary artery disease: a meta analysis. Circulation. 1989;80:87-98.
2.
Harris CN, Aronow WS, Parker DP, Kaplan MA.
Treadmill stress test in left ventricular
hypertrophy. Chest. 1973;63:353-357.
3. Frohlich ED, Apstein C, Chobanian AV, Devereux RB, Dustan HP, Dzau V, Fauad-Tarazi F, Horan MJ, Marcus M, Massie B, Pfeffer MA, Re RN, Roccella EJ, Savage D, Shub C. The heart in hypertension. N Engl J Med. 1992;327:998-1008.[Medline] [Order article via Infotrieve]
4.
Schulman DS, Francis CK, Black HR, Wackers FJ.
Thallium 201 stress imaging in hypertensive patients.
Hypertension. 1987;10:16-21.
5. Houghton JL, Frank MJ, Carr AA, von Dohlen TW, Prisant LM. Relations among impaired coronary flow reserve, left ventricular hypertrophy and thallium perfusion defects in hypertensive patients without obstructive coronary artery disease. J Am Coll Cardiol. 1990;15:43-51.[Abstract]
6. DePuey EG, Guertler-Krawczynska E, Perkins JV, Robbins WL, Whelchel JD, Clemens SD. Alteration in myocardial thallium-201 distribution in patients with chronic systemic hypertension undergoing single-photon emission computed tomography. Am J Cardiol. 1988;62:234-238.[Medline] [Order article via Infotrieve]
7. Wasserman AG, Katz RJ, Varghese PJ, Leiboff RH, Bren GG, Schlesselman S, Varma VM, Reba RC, Ross AM. Exercise radionuclide ventriculographic responses in hypertensive patients with chest pain. N Engl J Med. 1984;311:1276-1280.[Abstract]
8.
Sawada SG, Segar DS, Ryan T, Brown SE, Dohan AM,
Williams R, Fineberg NS, Armstrong WF, Feigenbaum H.
Echocardiographic detection of coronary artery
disease during dobutamine infusion.
Circulation. 1991;83:1605-1614.
9.
Salustri A, Fioretti PM, Pozzoli MMA, McNeill AJ,
Roelandt JRTC. Dobutamine stress
echocardiography: its role in the diagnosis of
coronary artery disease. Eur Heart J. 1992;13:70-77.
10. Elhendy A, Geleijnse ML, Roelandt JRTC, Cornel JH, van Domburg RT, El-Refaee M, Ibrahim MM, El-Said GM, Fioretti PM. Assessment of patients after coronary artery bypass grafting by dobutamine stress echocardiography. Am J Cardiol. 1996;77:1234-1236.[Medline] [Order article via Infotrieve]
11. Elhendy A, Geleijnse ML, Roelandt JRTC, van Domburg RT, TenCate FJ, Nierop PR, Bax JJ, El-Refaee M, Ibrahim MM, El-Said GM, Fioretti PM. Comparison of dobutamine stress echocardiography and 99M-technetium sestamibi SPECT myocardial perfusion scintigraphy in predicting the extent of coronary artery disease in patients with healed myocardial infarction. Am J Cardiol. 1997;79:7-12.[Medline] [Order article via Infotrieve]
12.
Elhendy A, van Domburg RT, Roelandt JRTC, Geleijnse ML,
Cornel JH, El-Said GM, Fioretti PM. Accuracy of
dobutamine stress echocardiography for
the diagnosis of coronary artery stenosis in patients
with myocardial infarction: the impact of extent and severity of left
ventricular dysfunction. Heart. 1996;76:123-128.
13. Marwick TH, D'Hondt AM, Baudhuin T, Willemat A, Wijns W, Detry J, Melin J. Optimal use of dobutamine stress for the detection and evaluation of coronary artery disease: combination with echocardiography, scintigraphy or both? J Am Coll Cardiol. 1993;22:159-167.[Abstract]
14. Ruffolo RR. The pharmacology of dobutamine. Am J Med Sci. 1987;294:244-248.[Medline] [Order article via Infotrieve]
15. Meyer SL, Curry GC, Donsey MS, Twieg DB, Parkey RW, Willerson JT. Influence of dobutamine on hemodynamics and coronary blood flow in patients with and without coronary artery disease. Am J Cardiol. 1976;38:103-108.[Medline] [Order article via Infotrieve]
16.
Blomstrand P, Engvall J, Swahn E, Safstrom K, Thulesius
O. Cardiovascular effects of
dobutamine stress testing in women with suspected
coronary artery disease. Heart. 1996;75:463-468.
17.
Fioretti PM, Poldermans D, Salustri A, Forster T,
Belloti E, Boersma E, McNeill AJ, El-Said EM, Roelandt JRTC.
Atropine increases the accuracy of dobutamine stress
echocardiography in patients taking
beta-blockers. Eur Heart J. 1994;15:355-360.
18. Tanimoto M, Pai RG, Jintapakorn W, Shah PM. Mechanism of hypotension during dobutamine stress echocardiography in patients with coronary artery disease. Am J Cardiol. 1995;76:26-30.[Medline] [Order article via Infotrieve]
19. Mazieka PK, Nadazdin A, Oakley CM. Clinical significance of abrupt vasodepression during dobutamine stress echocardiography. Am J Cardiol. 1992;69:1484-1487.[Medline] [Order article via Infotrieve]
20. Lieberman EB, Heinle SK, Wildermann N, Waugh RA, Kisslo JA, Bashore TM. Does hypotension during dobutamine stress echocardiography correlate with anatomic or functional cardiac impairment? Am Heart J. 1995;129:1121-1126.[Medline] [Order article via Infotrieve]
21. Marcovitz PA, Bach DS, Mathias W, Shayana V, Armstrong WF. Paradoxic hypotension during dobutamine stress echocardiography: clinical and diagnostic implications. J Am Coll Cardiol. 1993;21:1080-1086.[Abstract]
22.
Pellikka PA, Oh JK, Bailey KR, Nichols BA, Monahan
KH, Tajik J. Dynamic intraventricular
obstruction during dobutamine stress
echocardiography: a new observation.
Circulation. 1992;86:1429-1432.
23.
Senior R, Basu S, Handler C, Raftery EB, Lahiri
A. Diagnostic accuracy of dobutamine
stress echocardiography for detection of
coronary heart disease in hypertensive patients.
Eur Heart J. 1996;17:289-295.
24.
Meters H, Sawada SG, Ryan T, Segar DS, Kovacs R, Foltz
J, Feigenbaum H. Symptoms, adverse effects and complications
associated with dobutamine stress
echocardiography: experience in 1118
patients. Circulation. 1993;88:15-19.
25. Cornel JH, Balk AHMM, Arnese M, Maat PWM, Elhendy A, Salustri A, Ten Cate FJ, Fioretti PM. Safety and feasibility of dobutamine-atropine stress echocardiography in patients with ischemic left ventricular dysfunction, J Am Soc Echocardiogr. 1996;9:27-32.[Medline] [Order article via Infotrieve]
26. Poldermans D, Fioretti PM, Boersma E, Forster T, Urk H, Cornel JH, Arnese M, Roelandt JRTC. Safety of dobutamine atropine stress echocardiography in patients with suspected coronary artery disease. Am J Cardiol. 1994;73:456-459.[Medline] [Order article via Infotrieve]
27. Picano E, Mathias W Jr, Pingitore A, Bigi R, Previtali M. Safety and tolerability of dobutamine-atropine stress echocardiography: a prospective multicenter study. Lancet. 1994;344:1190-1192.[Medline] [Order article via Infotrieve]
28. Julius S. Autonomic nervous system dysregulation in human hypertension. Am J Cardiol. 1991;67:3B-7B.[Medline] [Order article via Infotrieve]
29.
Trimarco B, Volpe M, Ricciardelli B, Picotti GB, Galva
MA, Petracca R, Condorelli M. Studies of the mechanisms
underlying impairment of beta adrenoceptor-mediated effects in human
hypertension. Hypertension. 1983;5:584-590.
30. Feldman RD. Beta-adrenergic receptor alteration in hypertension: physiological and molecular correlates. Can J Physiol Pharmacol. 1987;46:1666-1672.
31. Yurenev AP, Parfyonova EV, Krasnikova TL, Aripova NA. Alteration of beta-adrenoreceptor function in hypertensive patients with different degrees of left ventricular hypertrophy. Am J Hypertens. 1992;5:164S-168S.[Medline] [Order article via Infotrieve]
32. Guzzetti S, Piccaluga E, Casati R, Cerutti S, Lombardi F, Pagani M, Malliani A. Sympathetic predominance in essential hypertension: a study employing spectral analysis of heart rate variability. J Hypertens. 1988;6:711-717.[Medline] [Order article via Infotrieve]
33. Mayet J, Shahi M, Poulter NR, Sever PS, Thom SA, Foale RA. Ventricular arrhythmias in hypertension: in which patients do they occur? J Hypertens. 1995;13:269-276.[Medline] [Order article via Infotrieve]
34. Elhendy A, Geleijnse ML, Roelandt JRTC, Domburg RT, Cornel JH, TenCate FJ, Postma-Tjoa J, Reijs AEM, El-Said GM, Fioretti PM. Evaluation by quantitative 99 m-technetium MIBI SPECT and echocardiography of myocardial perfusion and wall motion abnormalities in patients with dobutamine-induced ST-segment elevation. Am J Cardiol. 1995;76:441-448.[Medline] [Order article via Infotrieve]
35. Bellotti P, Fioretti PM, Forster T, McNeill AJ, El-Said EM, Salustri A, Roelandt JRTC. Reproducibility of the dobutamine-atropine echocardiography stress test. Echocardiography. 1993;10:93-97.
36. Elhendy A, Cornel JH, Roelandt JRTC, van Domburg RT, Nierop PR, El-Said GM, Fioretti PM. Relation between contractile response of akinetic segments during dobutamine stress echocardiography and ischemia assessed by simultaneous 201 thallium SPECT. Am J Cardiol. 1996;77:955-959.[Medline] [Order article via Infotrieve]
37.
Elhendy A, Cornel JH, Roelandt JRTC, van Domburg RT,
Fioretti PM. Akinesis becoming dyskinesis during
dobutamine stress echocardiography: a
predictor of poor functional recovery after surgical
revascularization. Chest. 1996;110:155-158.
38. Baptista J, Arnese M, Roelandt JRTC, Fioretti P, Keane D, Escaned J, Boersma E, Di Mario C, Serruys PW. Quantitative coronary angiography in the estimation of the functional significance of coronary stenosis: correlation with dobutamine-atropine stress test. J Am Coll Cardiol. 1994;23:1434-1439.[Abstract]
39. Weber MA. Coronary heart disease and hypertension. Am J Hypertens. 1994;7:146S-153S.[Medline] [Order article via Infotrieve]
40. Elhendy A, Geleijnse ML, Roelandt JRTC, van Domburg RT, TenCate FJ, Cornel JH, Reijs AEM, El-Said GM, Fioretti PM. Dobutamine-induced hypoperfusion without transient wall motion abnormalities: less severe ischemia or less severe stress? J Am Coll Cardiol. 1996;27:323-329.[Abstract]
41.
Frohlich ED, Tarazi RC, Dustan HP.
Clinical-physiological correlations in the
development of hypertensive heart disease.
Circulation. 1971;44:446-455.
42. Frohlich ED. Pathophysiology of systemic arterial hypertension. In: Schlant RC, Alexander RW, O'Rourke RA, eds. The Heart. 8th ed. New York, NY: McGraw-Hill; 1994:1391-1401.
43.
Anderson EA, Sinkey CA, Lawton WJ, Mark AL.
Elevated sympathetic nerve activity in borderline hypertension in
humans: evidence from direct intraneural recordings.
Hypertension. 1989;14:177-183.
44. Pedrinelli R, Panarace G, Salvetti A. Calcium entry blockade and adrenergic vascular reactivity in hypertensives: differences between nicardipine and diltiazem. Clin Pharmacol Ther. 1991;49:86-93.[Medline] [Order article via Infotrieve]
45.
Coma-Canella I, Ortuno F. Comparison of
diastolic blood pressure changes with
dobutamine and exercise test. Eur Heart
J. 1992;13:1245-1250.
46.
Alderman MH, Ooi WL, Madhaven S, Cohen H.
Treatment-induced blood pressure reduction and the risk of myocardial
infarction. JAMA. 1989;262:920-924.
This article has been cited by other articles:
 |
|
 |
|
  A. Elhendy, J. J. Bax, and D. Poldermans Dobutamine Stress Myocardial Perfusion Imaging in Coronary Artery Disease J. Nucl. Med., December 1, 2002; 43(12): 1634 - 1646. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Elhendy, R. T. van Domburg, J. J. Bax, R. Valkema, A. E. M. Reijs, E. P. Krenning, and J. R. T. C. Roelandt Safety, Hemodynamic Profile, and Feasibility of Dobutamine Stress Technetium Myocardial Perfusion Single-Photon Emission CT Imaging for Evaluation of Coronary Artery Disease in the Elderly Chest, March 1, 2000; 117(3): 649 - 656. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A Elhendy, R T van Domburg, J J Bax, D Poldermans, P R Nierop, M L Geleijnse, and J R T C Roelandt The grade of worsening of regional function during dobutamine stress echocardiography predicts the extent of myocardial perfusion abnormalities Heart, January 1, 2000; 83(1): 35 - 39. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A Elhendy, R T van Domburg, J J Bax, P R Nierop, M L Geleijnse, M M Ibrahim, and J R T C Roelandt The functional significance of chronotropic incompetence during dobutamine stress test Heart, April 1, 1999; 81(4): 398 - 403. [Abstract] [Full Text]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||