REVIEW ARTICLE
Dobutamine stress myocardial perfusion imaging
Marcel L. Geleijnse, MD, PhDa,
Abdou Elhendy, MD, PhDa,
Paolo M. Fioretti, MD, PhD, FACCa and
Jos R. T. C. Roelandt, MD, PhD, FACCa
a Thoraxcenter Rotterdam, University Hospital Rotterdam-Dijkzigt, Rotterdam, The Netherlands
Manuscript received January 13, 2000;
revised manuscript received June 27, 2000,
accepted August 16, 2000.
Reprint requests and correspondence: Marcel L. Geleijnse, MD, Thoraxcenter, Ba 302, Dr Molewaterplein 40, 3015 GD Rotterdam, The Netherlands
ml.geleijnse{at}worldonline.nl
 |
Abstract
|
|---|
In patients with limited exercise capacity and (relative) contraindications to direct vasodilators such as dipyridamole or adenosine, dobutamine stress nuclear myocardial perfusion imaging (DSMPI) represents an alternative, exercise-independent stress modality for the detection of coronary artery disease (CAD). Nondiagnostic test results (absence of reversible perfusion defects with submaximal stress) do occur in approximately 10% of patients. Serious side effects during DSMPI are rare, with no death, myocardial infarction or ventricular fibrillation reported in three DSMPI safety reports for a total of 2,574 patients. On the basis of a total number of 1,014 patients reported in 20 studies, the sensitivity, specificity and accuracy of the test for the detection of CAD were 88%, 74% and 84%, respectively. Mean sensitivities for one-, two- and three-vessel disease were 84%, 95% and 100%, respectively. The sensitivity for detection of left circumflex CAD (50%) was lower, compared with that for left anterior descending CAD (68%) and right CAD (88%). The sensitivity of predicting multivessel disease by multiregion perfusion abnormalities varied widely, from 44% to 89%, although specificity was excellent in all studies (89% to 94%). In direct diagnostic comparisons, DSMPI was more sensitive, but less specific, than dobutamine stress echocardiography and comparable with direct vasodilator myocardial perfusion imaging. In the largest prognostic study, patients with a normal DSMPI study had an annual hard event rate less than 1%. An ischemic scan pattern provided independent prognostic value, with a direct relationship between the extent and severity of the perfusion defects and prognosis. In conclusion, DSMPI seems a safe and useful nonexercise-dependent stress modality to detect CAD and assess prognosis.
|
Abbreviations and Acronyms
| | CAD | = coronary artery disease | | CI | = confidence interval | | DSE | = dobutamine stress echocardiography | | DSMPI | = dobutamine stress myocardial perfusion imaging | | ECG | = electrocardiogram or electrocardiographic | | LBBB | = left bundle branch block | | LVH | = left ventricular hypertrophy | | MI | = myocardial infarction | | MPI | = myocardial perfusion imaging |
|
Confirming or excluding coronary artery disease (CAD) in patients with chest pain remains a challenge because this disease is still the leading cause of death in the western world (1). Traditionally, exercise stress testing is performed as a first-line noninvasive diagnostic stress test (2). However, large numbers of patients referred for evaluation of chest pain are unable to perform adequate exercise testing, mainly because of deconditioning or neurologic, respiratory, peripheral vascular or orthopedic limitations (3). In these patients, pharmacological stress nuclear myocardial perfusion imaging (MPI) represents an alternative, exercise-independent stress modality. Usually, dipyridamole or adenosine is used as a stressor because of their superiority in creating blood flow heterogeneity (4) and the extensive experience with these stress modalities. For patients with (relative) contraindications to these direct vasodilators, such as severe obstructive airway disease (particularly patients with active wheezing or recent hospitalization for an exacerbation), high-grade atrioventricular block, arterial hypotension, ingestion of caffeine-containing beverages <12 h before testing or the use of dipyridamole or theophylline-containing compounds or medications <24 h before testing, dobutamine stress myocardial perfusion imaging (DSMPI) represents an alternative stress modality. Since its clinical introduction in 1984, DSMPI is increasingly used for detecting CAD and assessing prognosis (5–32). This review article deals with the: 1) methodology, 2) feasibility and safety, 3) diagnostic value for the detection of CAD and 4) prognostic value of DSMPI.
|
Methods and statistical analysis
|
|---|
A Medline search on DSMPI (search terms dobutamine and thallium or technetium) studies published in the major English language journals until the end of 1998 was performed. Studies were only included for diagnostic analysis if these studies included patients with and without angiographically defined CAD and if it was stated how many patients with and without CAD had negative and positive DSMPI results. Reports indicating that the patients included were subsets of larger published studies were excluded. Also excluded from the primary diagnostic analysis were studies describing special issues, such as the value of DSMPI in patients with left bundle branch block (LBBB) or left ventricular hypertrophy (LVH) and studies involving only patients with prior myocardial infarction (MI). These subgroups were discussed separately. When DSMPI was compared with other stress modalities, only those studies making direct comparisons in the same patients were included.
Sensitivity was defined as the number of true positive tests divided by the total number of patients with angiographically significant CAD. Specificity was defined as the number of true negative tests divided by the total number of patients without angiographically significant CAD. Accuracy was defined by the total number of true positive and true negative tests divided by the total number of patients. Mean values for sensitivity, specificity and accuracy were calculated by combining the results of individual patient data from multiple studies. Comparisons of sensitivity, specificity and accuracy were performed using the standardized normal distribution test. Statistical significance was defined at p < 0.05.
|
Test methodology
|
|---|
Dobutamine: pharmacology and mechanism of action.
Dobutamine is a synthetic catecholamine with a relatively short plasma half-life of approximately 2 min due to rapid metabolization in the liver to inactive metabolites (33,34). It has strong ß1-receptor and mild  1- and ß2-receptor agonist activity. When used at low dose (up to 10 µg/kg body weight per min), marked inotropic effects (mediated by both 1- and ß1-receptor stimulation) are encountered. These effects are extensively used for treatment of heart failure and the identification of dysfunctional, but viable, cardiac muscle. When used at high-dose (up to 40 µg/kg/min), heart rate is progressively increased (mediated by ß1-receptor stimulation). Despite a clear increase in cardiac output, systemic blood pressure increases only minimally due to a decrease in systemic vascular resistance because of peripheral vasoconstrictive effects (mediated by 1-receptor stimulation) overwhelmed by vasodilative effects (mediated by ß2-receptor stimulation). In patients without a sufficient increase in heart rate, the addition of atropine has been proposed to further increase heart rate by its vagolytic effects (25,35). As a result of the hemodynamic changes, there is an increase in oxygen demand resulting in a secondary dilation of the coronary arteries and, thus, an increase in blood flow. Additionally, dobutamine may also have a (minor) direct vasodilatative effect on coronary vessels. For high-dose dobutamine infusion, this increase in blood flow in normal coronary arteries has been reported as three times baseline (36). However, in myocardial regions supplied by a coronary artery with a critical stenosis, the increase in oxygen demand cannot be met by an adequate increase in blood flow (37). For successful MPI, dobutamine should not only create an adequate flow disparity between myocardial regions supplied by normal and stenotic arteries, but the radionuclide tracer (thallium-201 or technetium-99m) must be distributed in the myocardium in proportion to blood flow over the range of flows induced by dobutamine also. Several studies (4,38) have shown that dobutamine-induced cardiac thallium-201 uptake expressed as a percentage of whole body uptake is intermediate between exercise and direct vasodilator stress and that heart-to-background ratios of thallium-201 uptake are similar to direct vasodilator stress (but less than exercise stress). Recently published studies on dogs, however, reported that myocardial technetium-99m uptake underestimated the relative blood flow deficit induced by dobutamine, and it was suggested that dobutamine adversely affects myocardial technetium-99m binding (39,40).
Protocol.
Protocols for DSMPI vary from institution to institution, particularly with regard to dobutamine dose (range 20 to 50 µg/kg/min), atropine addition (range 0 to 2 mg) and stage duration (range 3 to 5 min) (Table 1). Usually, centers that use lower peak doses of dobutamine (used mainly in the early reports) use longer infusion stage durations and stop beta-adrenergic blocking agent treatment more often before the test (Table 1). To date, the most widely used protocol uses dobutamine up to 40 µg/kg/min, with the addition of atropine up to 1 mg.
According to this protocol, a rest electrocardiogram (ECG) is acquired; intravenous access is secured, and dobutamine is then administered intravenously by an infusion pump, starting at 10 µg/kg/min for 3 min, increasing by 10 µg/kg/min every 3 min up to a maximum of 40 µg/kg/min. For patients not achieving 85% of their theoretical maximal heart rate (220 – age) and without symptoms or signs of myocardial ischemia, atropine is administered on top of the maximal dose of dobutamine starting with 0.25 mg intravenously and repeated up to a maximum of 1.0 mg within 4 min, with continuation of dobutamine infusion. The radionuclide tracer should be injected at peak heart rate, and dobutamine infusion should be continued for at least 1 min. Throughout dobutamine infusion, the ECG (3 leads) is continuously monitored and recorded (12 leads) at 1-min intervals. Blood pressure is measured and recorded by sphygmomanometry or automatic device every 3 min. Reasons for interruption of the test are: horizontal or downsloping ST segment depression >0.2 mV at an interval of 80 ms after the J point compared with baseline, ST segment elevation >0.1 mV in patients without a previous MI, severe angina, a symptomatic reduction in systolic blood pressure  40 mm Hg from baseline, hypertension (blood pressure 240/120 mm Hg); significant tachyarrhythmias and any serious side effect was regarded as due to dobutamine. A beta-adrenergic blocking agent that can be injected intravenously must be available to reverse the effects of dobutamine if they do not revert spontaneously and quickly. For patients with obstructive airway disease (and in particular those with active wheezing), nitrates should be preferred because the safety of even short-acting selective beta-blockers was never demonstrated in these patients. Contraindications to (high-dose) DSMPI include: critical aortic stenosis, hypertrophic cardiomyopathy, uncontrolled hypertension, uncontrolled atrial fibrillation, known severe ventricular arrhythmias and disorders in potassium homeostasis (41,42). The addition of atropine is contraindicated for patients with narrow-angle glaucoma, myasthenia gravis, obstructive uropathy or obstructive gastrointestinal disorders.
Scintigraphic interpretation.
Stress scintigraphic imaging should take place immediately after the stress test with thallium-201 and approximately 1 h after the stress test with technetium-99m to optimize the scintigraphic images and to prevent redistribution in the case of imaging with thallium-201. To facilitate the interpretation and comparison of cardiac tomographic images, a standardized nomenclature and display of the images is recommended by the Society of Nuclear Medicine (43). A positive test is denoted by a completely or partially reversible perfusion defect, but, sometimes, fixed perfusion defects are also used as a criterion for CAD.
Other possible dobutamine stress-induced markers of myocardial ischemia.
ECG changes
Whereas ST segment changes are the hallmark of ischemia in exercise tests (2), they seem to have less value during dobutamine stress. In an early study of patients with severe coronary lesions, dobutamine stress-induced ST segment depression was described as a highly sensitive and specific diagnostic test (44). However, subsequent reports of patients with less severe coronary lesions (8,11,18,22,45) could never confirm the sensitivity of dobutamine stress-induced ST segment depression for the detection of CAD. Whether this is due to less stress (lower rate-pressure product compared with exercise tests) or other factors, such as inclusion of patients with abnormal baseline ECGs still needs to be established. The specificity (and, thus, positive predictive value) of dobutamine stress-induced ST segment depression, however, seems excellent, ranging from 88% to 93% (8,22,45). Also, as in exercise testing (46), dobutamine stress-induced ST segment elevation in patients without a previous MI was consistently reported to be associated with (severe) CAD (44,45,47).
Sinus node deceleration
Dobutamine stress-induced sinus node deceleration, defined as an initial increase and subsequent decrease in heart rate with progressive dobutamine infusion, occurs more often during dobutamine infusion than during exercise (48–51). In a small DSMPI study (49), it was reported to be a specific marker of reversible inferior wall perfusion defects. Larger, dobutamine stress echocardiography (DSE) studies (50,51), however, found no clear relationship between dobutamine stress-induced sinus node deceleration and inferior wall motion abnormalities or right CAD. It was postulated that cardiac slowing, in particular in combination with hypotension (see later), may also result from a neurally mediated cardiovascular vasodepressor reflex (52,53). After exclusion of ischemia (angina or ECG changes), it is our policy to administer atropine to reverse sinus node deceleration.
Hypotension
Generally, dobutamine stress causes an increase in cardiac output and a reduction in systemic vascular resistance (54,55) with a small increase in systolic blood pressure as a net result (5–32). Although the pathophysiology of dobutamine stress-induced hypotension has not been completely defined, theoretically, it may result from: 1) an inadequate increase in cardiac output to compensate for an expected decrease in systemic vascular resistance or 2) a disproportionate decrease in systemic vascular resistance in the presence of a normal increase in cardiac output. An inadequate increase in cardiac output may be due to inadequate contractile reserve, severe ischemic left ventricular dysfunction or left-sided obstructive heart disease. Dynamic left ventricular cavity obliteration due to strong inotropic stimulation was proposed as an important cause for reduced cardiac output and hypotension (56), especially in patients with dehydration. Later studies could not confirm this mechanism (57), and the proposed bolus of saline before dobutamine infusion (56,58) did not prevent cavity obliteration in a canine model (59). The second mechanism, a disproportionate decrease in systemic vascular resistance, may be due to excessive sensitivity of the peripheral circulation to ß2-receptor stimulation, increased ß2-receptor density (deconditioned patients) or a neurally mediated mechanism in which vigorous myocardial contraction stimulates the intramyocardial mechanoreceptors, resulting in sympathetic withdrawal and enhanced parasympathetic activity, the Bezold-Jarisch reflex (53). In contrast with exercise stress-induced hypotension (60), all presently available data indicate that there is no relation between dobutamine stress-induced hypotension and reversible perfusion defects (61), ischemic left ventricular systolic dysfunction (55,57,62,63) or angiographically detected CAD (61,62). After discontinuation of dobutamine infusion and putting the patient in a Trendelenburg position, active treatment (apart as described earlier) with infusion of fluids is rarely required.
|
Feasibility and safety
|
|---|
Approximately 10% of DSMPI tests are nondiagnostic (defined as absence of reversible perfusion defects in submaximal tests) because of an insufficient hemodynamic response to dobutamine-atropine or limiting side effects (7,29). Noncardiac side effects (nausea, headache, chills, urgency and anxiety) are not uncommon but are usually well tolerated, without the need for test termination. The most common cardiovascular side effects are angina, hypotension and cardiac arrhythmias. Although angina occurs in approximately 25% of patients (7), severe angina as a test end point without accompanying reversible perfusion defects is rare. Dobutamine stress-induced hypotension (defined as a 20 mm Hg decrease in systolic blood pressure) occurs in approximately 15% of patients (5,7,61). Severe, symptomatic hypotension necessitating test termination, however, occurs only rarely. Minor cardiac arrhythmias, such as premature atrial or ventricular contractions, often occur, and supraventricular and ventricular tachycardias occur each in approximately 4% of patients (5–7) (Table 2). Supraventricular tachycardias may be controlled with the injection of a beta-blocker or (in patients with obstructive airway disease) verapamil. Of note, digoxin (although often used) is, in our opinion, not indicated for the acute management of atrial fibrillation because of a delayed onset of action. Ventricular tachycardias are usually nonsustained and have been attributed to ß1-receptor stimulation and dobutamine-induced reduction in plasma potassium concentrations (42). These arrhythmias are more frequently seen in patients with a history of previous ventricular arrhythmias (6,64) or markers for left ventricular dysfunction such as (extensive) fixed perfusion defects (7) or baseline wall motion abnormalities (64). No study has reported an association between ventricular tachycardias and the addition of atropine (64) or reversible perfusion defects (7). Sustained ventricular tachycardias may be managed with an injection of a beta-blocker or lidocaine. In the case of hemodynamic instability, electrical cardioversion is indicated. In three major DSMPI safety reports (5–7) for a total of 2,574 patients, no patient suffered death, MI or ventricular fibrillation, although, in a DSE review on safety, sporadic cases of MI or ventricular fibrillation were described (65). It should be recognized that these severe complications can occur up to 20 min after dobutamine withdrawal (66), and it has been suggested that, in these patients, 1-mediated coronary and systemic vasoconstriction might be paradoxically exacerbated, not reversed, by beta-blocker administration. Atropine intoxication (a central anticholinergic syndrome causing confusion or sedation, treated by physostigmine 0.5 to 2.0 mg intravenously), although generally requiring a dose of atropine of at least 5 mg (67), has been reported during DSE in a few patients receiving  1 mg of atropine (66).
|
Diagnostic value
|
|---|
Detection of CAD.
As with other tests for detection of CAD, the diagnostic accuracy of DSMPI is expressed by its sensitivity and specificity. These indexes depend on the presence of referral bias (coronary arteriography may be guided by stress test results) and several technical factors such as the stress protocol, the radiotracer (thallium-201 or technetium-99m), the imaging technique (planar or single-photon emission computed tomography), the definition of a positive test and the threshold for defining significant CAD. In addition, several characteristics of the patients studied may affect these indexes, such as the presence or absence of MI, the use of beta-blockers, the number of male patients, the presence of collaterals, the type of lesion and the severity (percentage stenosis) and extent (number of diseased vessels) of CAD.
The reported sensitivity, specificity and accuracy for each of the 20 diagnostic studies identified by Medline search (8–27) are shown in Table 1. The overall (weighted mean) sensitivity, specificity and accuracy of DSMPI for a total of 1,014 patients was 88% (95% confidence interval [CI] 86 to 90), 74% (95% CI 71 to 77) and 84% (95% CI 81 to 86), respectively (Fig. 1).
View larger version (10K):
[in this window]
[in a new window]
|
Figure 1 Sensitivity, specificity and accuracy of dobutamine stress myocardial perfusion imaging for the detection of CAD.
|
|
Different reports from center to center are most likely due to the aforementioned factors, in particular the stress protocol and the use of beta-blockers. In the eight studies (12,19,21,22,24–27) that used 40 µg dobutamine with atropine, sensitivity for the detection of CAD was higher compared with the six studies (13–15,17,20,23) that used 40 µg dobutamine without atropine (90% vs. 82%, p < 0.02), without a loss in specificity. This finding was also confirmed in the only study directly comparing the diagnostic accuracy of DSMPI with, versus without, atropine in the same patients (25). The use of atropine is especially recommended for patients using beta-blockers. These latter medications lower the chronotropic and inotropic response (and, thus, peak cardiac workload) during dobutamine stress (18,68,69) and, thus, have the potential to lower the sensitivity of the test (70,71).
The effect of the number of diseased coronary arteries was assessed in nine studies (9,11,15–17,20,22,24,25) for a total of 311 patients. Mean sensitivity increased significantly from 84% for single-vessel disease to 95% for double-vessel disease and to 100% for triple-vessel disease (Fig. 2).
View larger version (11K):
[in this window]
[in a new window]
|
Figure 2 Sensitivity of dobutamine stress myocardial perfusion imaging for detection of CAD by number of diseased vessels.
|
|
Bayesian analysis.
Although values for sensitivity and specificity have a useful role, the use of DSMPI in diagnostic practice is to assist in the clinical recognition of CAD. In this sense, tests are used to reclassify the initial clinical impression of the probability of CAD into high-, low- and intermediate-risk subgroups. According to the Bayes theorem, the likelihood of a positive test result is determined by the probability of CAD in the patient studied, as well as the accuracy of the test (72). In one report (73) that included 223 patients without a previous MI, the study cohort was grouped into those with a high- (>80%), intermediate- (10% to 80%) and low-probability (<10%) of CAD before and after DSMPI, and the ability of DSMPI to restratify patients was analyzed. According to the pretest likelihood of CAD, 68 patients (30%) were regarded as having a "diagnostic" low- or high-probability of CAD. By application of the Bayes theorem, DSMPI defined 97 patients (43%) as being in the high or low posttest probability groups. Importantly, the accuracy of predicting CAD in the high-probability group and the absence of CAD in the low-probability group after DSMPI was excellent (91%).
Detection of disease in individual coronary arteries.
The coronary arteries and their branches supply different regions of the left ventricular myocardium. Based on the known anatomic relationship between coronary arteries and various myocardial regions, general guidelines have been developed for the assignment of these myocardial regions to specific coronary arteries. It is, therefore, possible to infer disease of a given coronary artery by noting the location of the perfusion abnormalities. Figure 3 summarizes the sensitivity and specificity for the identification of disease in the left anterior descending, left circumflex and right coronary arteries. The mean reported sensitivities, as assessed in seven studies (11,15–17,19,24,25) for a total of 333 patients, were 68%, 50% and 88%, respectively, and the mean specificities were 90%, 94% and 81%, respectively. Specificity for detection of right CAD was lower than that for left anterior descending CAD (p < 0.02) and left circumflex CAD (p < 0.0001). Sensitivity for detection of left circumflex CAD was lower than that for left anterior descending CAD (p < 0.005) and right CAD (p < 0.0001). The lower sensitivity for detection of disease in the left circumflex artery may be related to variation in coronary anatomy with a small circumflex territory in some patients.
View larger version (16K):
[in this window]
[in a new window]
|
Figure 3 Sensitivity (open bars) and specificity (solid bars) of dobutamine stress myocardial perfusion imaging for detection of CAD in individual coronary arteries. Numbers within bars indicate number of vessels. Included in the analysis were patients with single-vessel and multivessel CAD disease. CAD = coronary artery disease; LAD = left anterior descending coronary artery; LCx = left circumflex coronary artery; RCA = right coronary artery. Only the p values for sensitivity are displayed.
|
|
Identification of extensive CAD.
An important goal of noninvasive stress testing is the identification of patients with left-main or three-vessel CAD. Such patients could benefit from revascularization from a prognostic point of view (74). Patients with multivessel CAD can be differentiated from patients with single-vessel CAD by detection of perfusion abnormalities in two or more coronary territories. Investigators who examined the prediction of multivessel CAD by this method (11,17,25,26) consistently reported a high specificity (range 89% to 94%). However, the sensitivity of DSMPI for the prediction of multivessel CAD varied markedly from 44% to 89%. Several factors may contribute to the underestimation of multivessel CAD: inadequate stress protocols, the premature cessation of stress because of the development of limiting angina, imperfect assignment of myocardial perfusion regions to coronary arteries, collateral circulations and anatomically significant, but functionally nonsignificant, lesions.
Comparison with other stress modalities in patients with limited exercise capacity.
DSE
In myocardial regions supplied by a coronary artery with a significant stenosis, dobutamine stress-induced increase in oxygen demand may result in regional ischemia resulting in wall motion abnormalities that can be detected by two-dimensional echocardiography (65). In eight studies (11–13,17,21,22,24,26) comparing DSMPI with DSE in the same 593 patients, sensitivity was 86% versus 80% (p < 0.05); specificity was 73% versus 86% (p < 0.005), and accuracy was 82% versus 82% (Fig. 4). The finding that DSMPI is more sensitive (especially in patients with single-vessel CAD) is in line with the "ischemic cascade" theory (75), which states that perfusion abnormalities due to limited coronary flow reserve precede wall motion abnormalities.
View larger version (18K):
[in this window]
[in a new window]
|
Figure 4 Sensitivity, specificity and accuracy of dobutamine stress myocardial perfusion imaging (open bars) versus DSE (solid bars) for detection of CAD.
|
|
Vasodilator perfusion scintigraphy
Direct vasodilators (adenosine or dipyridamole) are considered to be the most effective drugs to create coronary blood flow heterogeneity (4,37,38). Indeed, one study (76) reported that dipyridamole MPI correlated better than DSMPI with a "coronary extent score." However, these results were based on a small group of patients, and the dobutamine dose used was extremely low. Only two studies (26,77) reported the diagnostic accuracy of DSMPI versus direct vasodilator MPI for the detection of CAD in the same patients. In these two studies in 157 patients, sensitivity was 84% versus 90%; specificity was 77% versus 78%, and accuracy was 81% versus 85%. Although there is no clear evidence for a superiority of direct vasodilator MPI over DSMPI, the use of the former as the drug of choice for MPI in patients with limited exercise capacity seems reasonable on the basis of theoretical grounds, diagnostic accuracy and extensive experience. However, it should be recognized that in the U.S. (unlike Europe) direct vasodilators (and in particular adenosine) are very expensive in comparison with dobutamine. Whether DSMPI is a more cost-effective test is yet unproven. This requires further, stronger exploration of the relative diagnostic accuracies of both tests, and it should be realized that, despite marked differences in stressor costs, these costs constitute only a small portion of total perfusion scintigraphy costs.
Special subgroups.
Patients with LBBB
The ability of noninvasive tests to diagnose or localize CAD in patients with LBBB has been disappointing. Exercise-induced changes in the ECG are nondiagnostic in the presence of LBBB (78). Moreover, several scintigraphic studies (especially when exercise stress is used) have reported false-positive results for detecting CAD in the left anterior descending coronary artery in the presence of LBBB (79). Reports on the use of DSMPI for patients with LBBB are scarce. Two small studies in respectively 24 and 27 patients (80,81) reported excellent specificities of 80% and 92% for detection of disease in the left anterior descending coronary artery. In another very small study in 19 patients (82), specificity was dramatically low. It should be noted that in this latter study, for unclear reasons, exceptionally high heart rates were achieved, one of the conditions believed to be related with false positive perfusion defects (79).
Patients with LVH
The specificity of exercise electrocardiography and scintigraphy to diagnose CAD in patients with LVH has also been disappointing, even in the absence of baseline ECG abnormalities (83,84). In one study (13) specificity for the detection of CAD by DSMPI was indeed disappointing (59%). In another study (85), however, specificity was good (85%) and comparable to DSE. Clearly, further, larger studies are necessary to establish the role of DSMPI for patients with LBBB and/or LVH.
Patients after MI
The major goals of DSMPI in patients with a previous MI are (apart from viability issues) to assess infarct-related coronary artery patency and to identify patients with multivessel CAD. Only a few studies have been specifically addressed to these topics. Infarct-related coronary artery patency was assessed in two studies (86,87). In one thallium-201 study (86), sensitivity was 71%, and specificity was 83%; in a technetium-99m study (87), sensitivity was 44%, and specificity was 82%. The presence of multivessel CAD for patients with a previous MI should ideally be based on reversible perfusion defects in two coronary vascular territories. In three studies (86–88) sensitivity ranged from 14% to 64%, and specificity ranged from 80% to 100%. An approach in which remote (outside the infarct-related coronary artery territory) perfusion defects are considered diagnostic for multivessel CAD was assessed in one study (88); sensitivity was 18% and specificity was 100%.
|
Prognostic value
|
|---|
The prognostic value of DSMPI was assessed in three studies (from the same institution) in patients with stable chest pain (28–30), in one study in patients with known coronary anatomy (31) and in two studies in patients undergoing vascular surgery (10,32). The largest published study of patients with stable chest pain involved 392 patients (mean age 60 ± 12 years, 220 men, 190 with a previous MI) who underwent high-dose dobutamine-atropine technetium-99m sestamibi single-photon emission computed tomography imaging (29). During a mean follow-up period of 22 ± 13 months, 44 patients (11%) suffered a hard cardiac event (cardiac death or nonfatal MI), and 78 patients (20%) suffered any event (hard event or a late revascularization procedure). Normal scan results were associated with a favorable prognosis over the follow-up period with an annual event rate of 0.8% for hard events and 2.5% for all events. In contrast, patients with fixed perfusion defects alone, reversible perfusion defects alone and fixed plus reversible perfusion defects had a significantly increased cardiac event rate of 6.8%, 8.1% and 11.6%, respectively, for hard events and 11.4%, 14.5% and 19.9%, respectively for all events (Fig. 5). In a multivariate analysis only age, history of heart failure or typical angina and abnormal scan patterns were independent predictors of cardiac events. Moreover, the (for stress level corrected) extent and severity of reversible perfusion defects was an important predictor of events (Fig. 6). In a study involving 220 of the above described patients (30), all patients underwent both DSMPI and DSE. No differences in prognostic value could be detected between the two imaging modalities. In another very small study (31) of patients with known coronary anatomy, an annual event rate of 3% for patients with a normal scan and 44% for patients with reversible perfusion defects was found. At multivariate analysis the only predictors of events were a history of previous MI and the extent of reversible perfusion defects. Unfortunately, the authors did not analyze whether the extent of reversible perfusion defects had a better predictive value than coronary anatomy. Two studies (10,32) described the value of DSMPI for assessing cardiac risk associated with vascular surgery. Both studies, in respectively 126 and 142 patients, found a significantly increased risk for perioperative major cardiac events in patients with reversible perfusion defects (50% versus 5% and 19% versus 3%, respectively).
View larger version (11K):
[in this window]
[in a new window]
|
Figure 5 Histogram showing the annual event rate for hard events (open bars) and all events (solid bars) according to the MIBI imaging pattern. The number of patients in each category was 130, 102, 60 and 100, respectively. Reproduced with permission (29).
|
|
View larger version (11K):
[in this window]
[in a new window]
|
Figure 6 Histogram showing the annual event rate for hard events (open bars) and all events (solid bars) according to the (for stress level corrected) extent and severity score of reversible MIBI perfusion defects. The number of patients in each category was 100, 100, 109, 62 and 21, respectively. Reproduced with permission (29).
|
|
|
Conclusions
|
|---|
Despite some theoretical limitations, DSMPI is a safe and useful nonexercise-dependent stress modality to assess the presence, localization and extent of CAD and to assess prognosis. In particular, this stress modality may be of great value for patients with limited exercise capacity and (relative) contraindications to dipyridamole or adenosine stress.
|
References
|
|---|
1. National Heart, Lung and Blood Institute. Morbidity from Coronary Heart Disease in the United States. National Heart, Lung and Blood Institute Data Fact Sheet. Bethesda (MD): 1990.
2. Chaitman BR. The changing role of the exercise electrocardiogram as a diagnostic and prognostic test for chronic ischemic heart disease. J Am Coll Cardiol. 1986;8:1195–1210[Abstract]
3. Marwick T. Current status of noninvasive techniques for the diagnosis of myocardial ischemia. Acta Clin Belg. 1992;47:1–5[Medline]
4. Pennel DJ, Ell PJ. Whole-body imaging of thallium-201 after six different stress regimens. J Nucl Med. 1994;35:425–428[Abstract/Free Full Text]
5. Dakik HA, Vempathy H, Verani MS. Tolerance, hemodynamic changes and safety of dobutamine stress perfusion imaging. J Nucl Cardiol. 1996;3:410–414[CrossRef][Medline]
6. Hanson MW, Morris EI, Borges-Neto S, DeLong DM. Analysis of cardiac arrhythmias during dobutamine pharmacologic stress testing in nuclear cardiology as related to the presence or absence of baseline arrhythmias. J Nucl Cardiol. 1997;4:372–378[CrossRef][Medline]
7. Elhendy A, Valkema R, Van Domburg RT, et al. Safety of dobutamine-atropine stress myocardial perfusion scintigraphy. J Nucl Med. 1998;39:1662–1666[Abstract/Free Full Text]
8. Mason JR, Palac RT, Freeman ML, et al. Thallium scintigraphy during dobutamine infusion: nonexercise-dependent screening test for coronary disease. Am Heart J. 1984;107:481–485[CrossRef][Medline]
9. Pennel DJ, Underwood RS, Swanton RH, Walker JM, Ell PJ. Dobutamine thallium myocardial perfusion tomography. J Am Coll Cardiol. 1991;18:1471–1479[Abstract]
10. Elliott BM, Robison JG, Zellner JL, Hendrix GH. Dobutamine-201Tl imaging: assessing cardiac risk associated with vascular surgery. Circulation. 1991;84(Suppl III):III54–III60
11. Günalp B, Dokumaci B, Uyan C, et al. Value of dobutamine technetium-99m-sestamibi single-photon emission computed tomography and echocardiography in the detection of coronary artery disease compared with coronary angiography. J Nucl Med. 1993;34:889–894[Abstract/Free Full Text]
12. Forster T, McNeill AJ, Salustri A, et al. Simultaneous dobutamine stress echocardiography and 99m-technetium isonitrile single-photon emission computed tomography in patients with suspected coronary artery disease. J Am Coll Cardiol. 1993;21:1591–1596[Abstract]
13. Marwick T, D’Hondt A, Baudhuin T, et al. 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]
14. Pennel DJ, Underwood RS, Ell PJ. Safety of dobutamine stress for thallium-201 myocardial perfusion tomography in patients with asthma. Am J Cardiol. 1993;71:1346–1350[CrossRef][Medline]
15. Hays JT, Mahmarian JJ, Cochran AJ, Verani MS. Dobutamine thallium-201 tomography for evaluating patients with suspected coronary artery disease unable to undergo exercise or vasodilator pharmacologic stress testing. J Am Coll Cardiol. 1993;21:1583–1590[Abstract]
16. Warner MF, Pippin JJ, DiSciascio G, et al. Assessment of thallium scintigraphy and echocardiography during dobutamine infusion for the detection of coronary artery disease. Cathet Cardiovasc Diagn. 1993;29:122–127[Medline]
17. Senior R, Sridhara BS, Anagnostou E, Handler C, Raftery EB, Lahiri A. Synergistic value of simultaneous stress dobutamine sestamibi single-photon emission computerized tomography and echocardiography in the detection of coronary artery disease. Am Heart J. 1994;128:713–718[CrossRef][Medline]
18. Herman SD, Labresh KA, Santos-Ocampo CD, et al. Comparison of dobutamine and exercise using technetium-99m sestamibi imaging for the evaluation of coronary artery disease. Am J Cardiol. 1994;73:164–169[CrossRef][Medline]
19. Thorley PJ, Ball J, Sheard KL, Sivananthan UM. Evaluation of 99Tcm-tetrofosmin as a myocardial perfusion agent in routine clinical use. J Nucl Med Comm. 1995;16:733–740
20. Henzlova MJ, Padilla ML, Freilich A, et al. Dobutamine thallium 201 perfusion imaging in candidates for lung transplantation. J Heart Lung Transplant. 1995;14:251–256[Medline]
21. Di Bello V, Bellina CR, Gori E, et al. Incremental diagnostic value of dobutamine stress echocardiography and dobutamine scintigraphy (technetium 99m-labeled sestamibi single-photon emission computed tomography) for assessment of presence and extent of coronary artery disease. J Nucl Cardiol. 1996;3:212–220[CrossRef][Medline]
22. Kisacik HL, Özdemir K, Altinyay E, et al. Comparison of exercise stress testing with simultaneous dobutamine stress echocardiography and technetium-99m isonitrile single-photon emission computerized tomography for the diagnosis of coronary artery disease. Eur Heart J. 1996;17:113–119[Abstract/Free Full Text]
23. Iftikhar I, Koutelou JJ, Mahmarian JJ, Verani MS. Simultaneous perfusion tomography and radionuclide angiography during dobutamine stress. J Nucl Med. 1996;37:1306–1310[Abstract/Free Full Text]
24. Huang PJ, Ho YL, Wu CC, et al. Simultaneous dobutamine stress echocardiography and thallium perfusion imaging for the detection of coronary artery disease. Cardiology. 1997;88:556–562[Medline]
25. Caner B, Karanfil A, Uysal U, et al. Effect of an additional atropine injection during dobutamine infusion for myocardial SPECT. J Nucl Med Comm. 1997;18:567–573
26. Santoro GM, Sciagrá R, Buonamici P, et al. Head-to-head comparison of exercise stress testing, pharmacologic stress echocardiography and perfusion tomography as first-line examination for chest pain in patients without a history of coronary artery disease. J Nucl Cardiol. 1998;5:19–27[CrossRef][Medline]
27. San Román JA, Vilacosta I, Castillo JA, et al. Selection of the optimal stress test for the diagnosis of coronary artery disease. Heart. 1998;80:370–376[Abstract/Free Full Text]
28. Geleijnse ML, Elhendy A, Van Domburg RT, Cornel JH, Reijs AEM, Fioretti PM. Prognostic significance of normal dobutamine-atropine stress sestamibi scintigraphy in women with chest pain. Am J Cardiol. 1996;77:1057–1061[CrossRef][Medline]
29. Geleijnse ML, Elhendy A, Van Domburg RT, et al. Prognostic value of dobutamine-atropine stress technetium-99m sestamibi perfusion scintigraphy in patients with chest pain. J Am Coll Cardiol. 1996;28:447–454[Abstract]
30. Geleijnse ML, Elhendy A, Cornel JH, et al. Cardiac imaging for risk stratification with dobutamine-atropine stress testing in patients with chest pain. Echocardiography, perfusion scintigraphy or both? Circulation. 1997;96:137–147[Abstract/Free Full Text]
31. Senior R, Raval U, Lahiri A. Prognostic value of stress dobutamine technetium-99m sestamibi single-photon emission computed tomography (SPECT) in patients with suspected coronary artery disease. Am J Cardiol. 1996;78:1092–1096[Medline]
32. Van Damme H, Piérard L, Gillain D, Benoit TH, Rigo P, Limet R. Cardiac risk assessment before vascular surgery: a prospective study comparing clinical evaluation, dobutamine stress echocardiography and dobutamine Tc-99m sestamibi tomoscintigraphy. Cardiovasc Surg. 1997;5:54–64[CrossRef][Medline]
33. Ruffolo RR. The pharmacology of dobutamine. Am J Med. 1987;294:244–248
34. 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[CrossRef][Medline]
35. McNeill AJ, Fioretti PM, El-Said EM, Salustri A, Forster T, Roelandt JRTC. Enhanced sensitivity for detection of coronary artery disease by addition of atropine to dobutamine stress echocardiography. Am J Cardiol. 1992;70:41–46[CrossRef][Medline]
36. Krivokapich J, Huang SC, Schelbert HR. Assessment of the effects of dobutamine on myocardial blood flow and oxidative metabolism in normal human subjects using nitrogen-13 ammonia and carbon-11 acetate. Am J Cardiol. 1993;71:1351–1356[CrossRef][Medline]
37. Fung AY, Gallagher KP, Buda AJ. The physiologic basis of dobutamine as compared with dipyridamole stress interventions in the assessment of critical coronary stenosis. Circulation. 1987;76:943–951[Abstract/Free Full Text]
38. Lee J, Chae SC, Lee K, Heo J, Iskandrian AS. Biokinetics of thallium-201 in normal subjects: comparison between adenosine, dipyridamole, dobutamine and exercise. J Nucl Med. 1994;35:535–541[Abstract/Free Full Text]
39. Wu JC, Yun JJ, Heller EN, et al. Limitations of dobutamine for enhancing flow heterogeneity in the presence of single coronary stenosis: implications for technetium-99m-sestamibi imaging. J Nucl Med. 1998;39:417–425[Abstract/Free Full Text]
40. Calnon DA, Glover DK, Beller GA, et al. Effects of dobutamine stress on myocardial blood flow, 99m Tc sestamibi uptake and systolic wall thickening in the presence of coronary artery stenosis: implications for dobutamine stress testing. Circulation. 1997;96:2353–2360[Abstract/Free Full Text]
41. Williams ME, Gervino EV, Rosa RM, et al. Catecholamine modulation of rapid potassium shifts during exercise. N Engl J Med. 1985;312:823–827[Abstract]
42. Coma-Canella I. Changes in plasma potassium during the dobutamine stress test. Int J Cardiol. 1991;33:55–60[CrossRef][Medline]
43. Society of Nuclear Medicine. Standardization of cardiac tomographic imaging. J Am Coll Cardiol. 1992;20:255–256[Medline]
44. Coma-Canella I. Dobutamine stress test to diagnose the presence and severity of coronary artery lesions in angina. Eur Heart J. 1991;12:1198–1204[Abstract/Free Full Text]
45. Mairesse GH, Marwick TH, Vanoverschelde JLJ, et al. How accurate is dobutamine stress electrocardiography for detection of coronary artery disease? J Am Coll Cardiol. 1994;24:920–927[Abstract]
46. Gallik DM, Mahmarian JJ, Verani MS. Therapeutic significance of exercise-induced ST-segment elevation in patients without previous myocardial infarction. Am J Cardiol. 1993;72:1–7[CrossRef][Medline]
47. Elhendy A, Geleijnse ML, Roelandt JRTC, et al. Evaluation by quantitative 99m-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[CrossRef][Medline]
48. Miller TD, Gibbons RJ, Squires RW, Allison TG, Gau GT. Sinus node deceleration during exercise as a marker of significant narrowing of the right coronary artery. Am J Cardiol. 1993;71:371–372[CrossRef][Medline]
49. Hopfenspirger MR, Miller TD, Christian TF, Gibbons RJ. Sinus node deceleration during dobutamine perfusion scintigraphy as a marker of inferior ischemia. Am J Cardiol. 1994;74:817–819[CrossRef][Medline]
50. Attenhofer CH, Pellikka PA, McCully RB, Roger VL, Seward JB. Paradoxical sinus deceleration during dobutamine stress echocardiography: description and angiographic correlation. J Am Coll Cardiol. 1997;29:994–999[Abstract]
51. Takeuchi M, Hanada H, Numata T. Is dobutamine-induced sinus node deceleration a marker of significant stenosis of the right coronary artery? Chest. 1998;113:306–311[Abstract/Free Full Text]
52. Mazeika PK, Nadazdin A, Oakley CM. Clinical significance of abrupt vasodepression during dobutamine stress echocardiography. Am J Cardiol. 1992;69:1484–1486[CrossRef][Medline]
53. Mark AL. The Bezold-Jarisch reflex revisited: clinical implications of inhibitory reflexes originating in the heart. J Am Coll Cardiol. 1983;11:90–102
54. Tanimoto M, Pai RG, Jintapakorn W. Normal changes in left ventricular filling and hemodynamics during dobutamine stress echocardiography. J Am Soc Echocardiogr. 1995;8:488–493[CrossRef][Medline]
55. 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[CrossRef][Medline]
56. Pellikka PA, Oh JK, Bailey KR, Nichols BA, Monahan KH, Tajik JA. Dynamic intraventricular obstruction during dobutamine stress echocardiography: a new observation. Circulation. 1992;86:1429–1432[Abstract/Free Full Text]
57. Heinle SK, Tice FD, Kisslo J. Hypotension during stress echocardiography: is it related to dynamic intraventricular obstruction? Am Heart J. 1995;130:314–317[CrossRef][Medline]
58. Rosamond TL, Vacek JL, Hurwitz A, Rowland AJ, Beauchamp GD, Crouse LJ. Hypotension during dobutamine stress echocardiography: initial description and clinical relevance. Am Heart J. 1992;123:403–407[CrossRef][Medline]
59. Weissman NJ, Nidorf SM, Weyman AE, Picard MH. Effect of hydration on cavity obliteration during dobutamine stress echocardiography. Clin Cardiol. 1995;18:17–20[Medline]
60. Dubach P, Froelicher VF, Klein J, Oakes D, Grover-Mckay M, Friis R. Exercise-induced hypotension in a male population: criteria, causes and prognosis. Circulation. 1988;78:1380–1387[Abstract/Free Full Text]
61. Geleijnse ML, Elhendy A, Van Domburg RT, et al. Prognostic significance of systolic blood pressure changes during dobutamine-atropine stress technetium-99m sestamibi perfusion scintigraphy in patients with chest pain and known or suspected coronary artery disease. Am J Cardiol. 1997;79:1031–1035[CrossRef][Medline]
62. 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]
63. 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[CrossRef][Medline]
64. Cornel JH, Balk AHMM, Boersma E, et al. Safety and feasibility of dobutamine-atropine stress echocardiography in patients with ischemic left ventricular dysfunction. J Am Soc Echocardiogr. 1996;9:27–32[CrossRef][Medline]
65. Geleijnse ML, Fioretti PM, Roelandt JRTC. Methodology, feasibility, safety and diagnostic accuracy of dobutamine stress echocardiography. J Am Coll Cardiol. 1997;30:595–606[Abstract]
66. Picano E, Mathias W Jr, Pingitore R, Bigi R, Previtali M. Safety and tolerability of dobutamine-atropine stress echocardiography: a prospective, multicenter study. Lancet. 1994;344:1190–1192[CrossRef][Medline]
67. Brown JH. Atropine, scopolamine and related antimuscarinic drugs. In: Goodman, Gildman, editors. Goodman and Gilman’s: Cardiovascular Pharmacology. Oxford: Pergamon Press, 1992.
68. Weissman NJ, Levangie MW, Newell JB, Guerrero LJ, Weyman AE, Picard MH. Effect of B-adrenergic receptor blockade on the physiologic response to dobutamine stress echocardiography. Am Heart J. 1995;130:248–253[CrossRef][Medline]
69. Shehata AR, Gillam LD, Mascitelli VA, et al. Impact of acute propranolol administration on dobutamine-induced myocardial ischemia as evaluated by myocardial perfusion imaging and echocardiography. Am J Cardiol. 1997;80:268–272[CrossRef][Medline]
70. Huang PJ, Yen RF, Chieng PU, Chen ML, Su CT. Do beta-blockers affect the diagnostic sensitivity of dobutamine stress thallium-201 single photon emission computed tomographic imaging. J Nucl Cardiol. 1998;5:34–39[CrossRef][Medline]
71. Fioretti PM, Poldermans D, Salustri A, et al. Atropine increases the accuracy of dobutamine stress echocardiography in patients taking beta-blockers. Eur Heart J. 1994;15:355–360[Abstract/Free Full Text]
72. Diamond GA, Forrester JS. Analysis of probability as an aid in the clinical diagnosis of coronary artery disease. N Engl J Med. 1979;300:1350–1358[Abstract]
73. Geleijnse ML, Marwick TH, Boersma E, Deckers JW, Melin JA, Fioretti PM. Optimal pharmacological stress testing for the diagnosis of coronary artery disease: a probabilistic approach. Eur Heart J. 1995;16(Suppl M):3–10[Abstract/Free Full Text]
74. Califf RM, Harrell FE Jr, Lee KL, et al. The evolution of medical and surgical therapy for coronary artery disease: a 15-year perspective. J Am Med Assoc. 1989;67:302–309
75. Nesto RW, Kowalchuck GJ. The ischemic cascade: temporal sequence of hemodynamic, electrocardiographic and symptomatic expressions of ischemia. Am J Cardiol. 1987;57:23C–27C
76. Kumar EB, Steel SA, Howey S, Caplin JL, Aber CP. Dipyridamole is superior to dobutamine for thallium stress imaging: a randomized crossover study. Br Heart J. 1994;71:129–134[Abstract/Free Full Text]
77. Marwick T, Willemart B, D’Hondt AM, et al. Selection of the optimal nonexercise stress for the evaluation of ischemic regional myocardial dysfunction and malperfusion. Circulation. 1993;87:345–354[Abstract/Free Full Text]
78. Orzan F, Garcia E, Mathur VS, Hall RJ. Is the treadmill exercise test useful for evaluating coronary artery disease in patients with complete left bundle branch block? Am J Cardiol. 1978;42:36–40[CrossRef][Medline]
79. Hirzel HO, Senn M, Nuesch K, et al. Thallium-201 scintigraphy in complete left bundle branch block. Am J Cardiol. 1984;53:764–769[CrossRef][Medline]
80. Mairesse GH, Marwick TH, Arnese M, et al. Improved identification of coronary artery disease in patients with left bundle branch block by use of dobutamine stress echocardiography and comparison with myocardial perfusion tomography. Am J Cardiol. 1995;76:321–325[CrossRef][Medline]
81. Vaduganathan P, Zuo-Xiang H, Raghavan C, Mahmarian JJ, Verani MS. Detection of left anterior descending coronary artery stenosis in patients with left bundle branch block: exercise, adenosine or dobutamine imaging. J Am Coll Cardiol. 1996;28:543–550[Abstract]
82. Caner B, Rezaghi C, Uysal U, et al. Dobutamine thallium-201 myocardial SPECT in patients with left bundle branch block and normal coronary arteries. J Nucl Med. 1997;38:424–427[Abstract/Free Full Text]
83. 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[Abstract/Free Full Text]
84. Schulman DS, Francis DK, Black HR, Wackers FJ. Thallium-201 stress imaging in hypertensive patients. Hypertension. 1987;10:16–21[Abstract/Free Full Text]
85. Elhendy A, Geleijnse ML, Van Domburg RT, et al. Comparison of dobutamine stress echocardiography and technetium-99m sestamibi single-photon emission tomography for the diagnosis of coronary artery disease in hypertensive patients with and without left ventricular hypertrophy. Eur J Nucl Med. 1998;25:69–78[CrossRef][Medline]
86. Elhendy A, Cornel JH, Roelandt JRTC, et al. Dobutamine 201-thallium SPECT imaging for the assessment of peri-infarction and remote myocardial ischemia in patients with prior myocardial infarction. J Nucl Med. 1996;37:1951–1956[Abstract/Free Full Text]
87. Elhendy A, Geleijnse ML, Roelandt JRTC, et al. Comparison of dobutamine stress echocardiography and 99m-technetium sestamibi SPECT myocardial perfusion scintigraphy for predicting extent of coronary artery disease in patients with healed myocardial infarction. Am J Cardiol. 1997;79:7–12[CrossRef][Medline]
88. Coma-Canella I, del Val Gómez Martínez M, Rodrigo F, Castro Beiras JM. The dobutamine stress test with thallium-201 single-photon emission computed tomography and radionuclide angiography: postinfartction study. J Am Coll Cardiol. 1993;22:399–406[Abstract]
This article has been cited by other articles:
|
|
|
|
 
C. Parsai, A. Baltabaeva, L. Anderson, M. Chaparro, B. Bijnens, and G. R. Sutherland
Low-dose dobutamine stress echo to quantify the degree of remodelling after cardiac resynchronization therapy
Eur. Heart J.,
April 2, 2009;
30(8):
950 - 958.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. J. Krenning, A. Nemes, O. I.I. Soliman, W. B. Vletter, M. M. Voormolen, J. G. Bosch, F. J. ten Cate, J. R.T.C. Roelandt, and M. L. Geleijnse
Contrast-enhanced three-dimensional dobutamine stress echocardiography: between Scylla and Charybdis?
Eur J Echocardiogr,
November 1, 2008;
9(6):
757 - 760.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S C Chua, R H Ganatra, D J Green, and A M Groves
Nuclear cardiology: myocardial perfusion imaging with SPECT and PET
Imaging,
September 1, 2006;
18(3):
166 - 177.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. A. Alsaileek, M. Osranek, K. Fatema, R. B. McCully, T. S. Tsang, and J. B. Seward
Predictive Value of Normal Left Atrial Volume in Stress Echocardiography
J. Am. Coll. Cardiol.,
March 7, 2006;
47(5):
1024 - 1028.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. M. Navare, D. Katten, L. L. Johnson, J. F. Mather, M. S. Fowler, A. W. Ahlberg, N. Miele, and G. V. Heller
Risk Stratification With Electrocardiographic-Gated Dobutamine Stress Technetium-99m Sestamibi Single-Photon Emission Tomographic Imaging: Value of Heart Rate Response and Assessment of Left Ventricular Function
J. Am. Coll. Cardiol.,
February 21, 2006;
47(4):
781 - 788.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Rizzo, M. C. R. Vono, L. Toncelli, P. Pecagna, P. Manetti, L. Stefani, and G. Galanti
The feasibility and usefulness of contrast exercise echocardiography for the assessment of left ventricular function in master athletes
Eur J Echocardiogr,
January 1, 2005;
6(1):
24 - 30.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Nasir, R. F. Redberg, M. J. Budoff, E. Hui, W. S. Post, and R. S. Blumenthal
Utility of Stress Testing and Coronary Calcification Measurement for Detection of Coronary Artery Disease in Women
Arch Intern Med,
August 9, 2004;
164(15):
1610 - 1620.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C Anagnostopoulos, M Harbinson, A Kelion, K Kundley, C Y Loong, A Notghi, E Reyes, W Tindale, and S R Underwood
Procedure guidelines for radionuclide myocardial perfusion imaging
Heart,
January 1, 2004;
90(90001):
i1 - 10.
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. F. L. Schinkel, A. Elhendy, R. T. van Domburg, J. J. Bax, R. Valkema, J. R. T. C. Roelandt, and D. Poldermans
Long-term Prognostic Value of Dobutamine Stress 99mTc-Sestamibi SPECT: Single-Center Experience with 8-year Follow-up
Radiology,
December 1, 2002;
225(3):
701 - 706.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. F.L. Schinkel, A. Elhendy, R. T. van Domburg, J. J. Bax, E. C. Vourvouri, F. B. Sozzi, R. Valkema, J. R.T.C. Roelandt, and D. Poldermans
Prognostic Value of Dobutamine-Atropine Stress Myocardial Perfusion Imaging in Patients With Diabetes
Diabetes Care,
September 1, 2002;
25(9):
1637 - 1643.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
ADDITIONAL ARTICLES ABSTRACTED IN ACP JOURNAL CLUB
Evid. Based Med.,
July 1, 2001;
6(4):
99 - 99.
[Full Text]
[PDF]
|
|
|
|
Top
Abstract
Methods and statistical analysis