Author + information
- Received March 14, 1997
- Revision received July 11, 1997
- Accepted July 21, 1997
- Published online November 1, 1997.
- Imran Afridi, MD, FACCA,1,1,
- Usman Qureshi, MD, FACCA,
- Helen A Kopelen, RDMSA,
- William L Winters Jr., MD, FACCA and
- William A Zoghbi, MD, FACCA,* ()
- ↵*Dr. William A. Zoghbi, Director, Echocardiography Research, Baylor College of Medicine, The Methodist Hospital, 6550 Fannin, SM-677, Houston, Texas 77030.
Objectives. We sought to evaluate the serial changes in the response of the hibernating myocardium to dobutamine stimulation after revascularization.
Background. An improvement in myocardial contraction during dobutamine stress echocardiography (DSE), particularly a biphasic response, predicts recovery of rest function. However, little is known about the changes in the response of the myocardium to dobutamine after revascularization.
Methods. Thirty-four patients with stable coronary artery disease and regional left ventricular dysfunction underwent DSE before, early (within 1 week) and late (>6 weeks) after coronary angioplasty. Dobutamine was given in incremental doses from 2.5 to 40 μg/kg body weight per min.
Results. Of 180 revascularized segments with severe rest dysfunction, recovery of rest function was seen in 56 segments (31%) late after angioplasty, 80% of which had early recovery. Ventricular function during DSE was similar early and late after revascularization. Patients who showed a biphasic response to DSE before revascularization (n = 12) had the most improvement in function at rest (mean [±SD] wall motion score index [WMSI] 1.98 ± 0.75 vs. 1.35 ± 0.54, p < 0.05) and during DSE (2.11 ± 0.67 vs. 1.21 ± 0.41, p < 0.05) late after revascularization. Patients with sustained improvement during DSE before revascularization had no significant change in wall motion during DSE after angioplasty. However, patients without improvement in function at low dose DSE, who demonstrated worsening of function at a high dose, had significant augmentation in wall motion during DSE after revascularization (WMSI 2.16 ± 0.50 vs. 1.60 ± 0.57, p < 0.05). Patients who had no recovery of rest function had significant improvement in wall motion response to DSE, particularly when ischemia was inducible before revascularization.
Conclusions. In myocardial hibernation, the majority of recovery of rest function occurs early after revascularization. Although patients who recover rest function show the most marked improvement in wall motion during DSE, those without recovery of rest function also have improved function during DSE, particularly when there is evidence of ischemia before revascularization.
It is now well established that left ventricular (LV) dysfunction in patients with chronic ischemic heart disease may represent viable myocardium whereby revascularization can lead to recovery of rest contractile function [1–3]. There is increasing evidence that the hibernating myocardium exhibits improved contraction in response to inotropic stimulation [4–8]. Clinical observations with dobutamine stress echocardiography (DSE) and recent experimental data, however, suggest that contractile reserve in response to inotropic stimulation is present but limited in this condition [5, 7–11]. Although the majority of patients with hibernating myocardium have a biphasic response to dobutamine (improvement in function at low doses with worsening at high doses), some patients show worsening of function without improved contraction [5, 10]. A minority of patients who ultimately recover rest function show sustained improvement or no change in wall motion during DSE before revascularization [5, 10, 11]. Whether improvement in myocardial contraction during DSE occurs after revascularization in these patients is presently unknown. Furthermore, whether an improvement in myocardial contraction occurs in response to DSE in patients who do not show recovery of rest function has not been previously elucidated.
The purpose of this study was therefore to evaluate prospectively the serial changes in ventricular function and contractile reserve in patients with chronic stable coronary artery disease and LV dysfunction undergoing revascularization. Low and high dose DSE was performed before, early and late after revascularization. Serial changes in the response of the myocardium to dobutamine were assessed. Furthermore, wall motion in response to DSE was also evaluated in patients with and without recovery of rest function.
1.1 Patient Group
The protocol was approved by the Institutional Review Boards of Baylor College of Medicine and The Methodist Hospital, Houston. Patients with coronary artery disease and rest LV dysfunction, already scheduled for percutaneous transluminal coronary angioplasty (PTCA), were screened and prospectively enrolled in the present study, which was part of a prospective, comprehensive evaluation of patients with myocardial hibernation [5, 10]. The patients evaluated herein include all patients reported on in the study by Afridi et al. and the first 14 patients in the study by Qureshi et al. . Coronary angioplasty was chosen as the mode of revascularization for its ability to assess changes in rest function and contractile reserve early (as well as late) after the procedure, because of the feasibility of DSE and fewer alterations in hemodynamic variables early after PTCA compared with coronary artery bypass graft surgery. Coronary artery disease was defined as ≥70% stenosis of at least one epicardial artery. Rest LV dysfunction was defined as the presence of a wall motion abnormality as seen on echocardiography or contrast left ventriculography. Patients were excluded if they had had a recent myocardial infarction (<6 weeks), unstable angina or any contraindication to dobutamine or if they were undergoing angioplasty of a bypass graft.
After providing written informed consent, each patient underwent rest echocardiography and DSE within 1 day before PTCA as well as early (within 1 week) and late after PTCA (>6 weeks). All echocardiograms were taken using a Hewlett Packard Sonos 1000 or 1500 equipped with a 2.5-MHz transducer. Intravenous dobutamine infusion was started at 2.5 μg/kg body weight per min and increased every 3 min to 5, 7.5, 10, 20, 30 and 40 μg/kg per min. Images from the standard parasternal and apical views were recorded on video and digitized on-line in a quad-screen format at rest and at 5- and 7.5-μg/kg per min and peak dobutamine doses and stored on disk for later interpretation (NovaMicrosonics or TomTec Imaging system). This quad-screen display format has been shown to allow optimal assessment of the biphasic response during DSE with this infusion protocol . Blood pressure and cardiac rhythm were monitored during the test. Dobutamine infusion was terminated earlier if any of the following occurred: severe angina, systolic blood pressure <80 or >220 mm Hg, >2-mm ST segment depression or significant arrhythmia, defined as >6 beats of supraventricular or >3 beats of ventricular tachycardia.
1.3 Analysis of Echocardiograms
The three DSE studies for each patient were read in random order without clinical information or knowledge of the results of serial rest echocardiograms. Each study was interpreted using cine loops from rest, 5, 7.5 and peak dobutamine doses, displayed on the quad screen. The left ventricle was divided into 16 segments, and wall motion at each stage was assessed visually using a six-grade scoring system, as previously described : hyperkinesia = 0; normal = 1; mild hypokinesia = 2; severe hypokinesia = 3; akinesia = 4; and dyskinesia = 5. The response of ventricular segments with abnormal rest function to dobutamine was classified into one of four types based on changes of one or more grades in wall motion score: 1) biphasic response: improvement in wall motion at a low dose (5 or 7.5 μg/kg per min) with worsening at a higher dose; 2) worsening: deterioration of rest wall motion during dobutamine without improvement; 3) sustained improvement: improvement in wall motion at a low dose that persisted or further improved at a high dose; and 4) no change: no change in wall motion during dobutamine. The type of DSE response in patients was classified according to the response observed in the majority of abnormal segments.
Changes in rest wall motion were interpreted separately using a simultaneous display of the three rest studies, randomized as to their sequence on the quad screen. Improvement in segmental rest function was defined as a reduction in wall motion score of ≥2 grades in segments with severe dysfunction at baseline (severe hypokinesia, akinesia or dyskinesia), based on previous analysis of reproducibility . For patients, recovery of rest function was defined as improvement in wall motion score of ≥2 grades in at least two contiguous segments.
The myocardial segments were grouped into two vascular regions: left anterior descending coronary artery (apical, septal and anterior segments, n = 7) and combined right and circumflex arteries (n = 9). Global and regional wall motion score indexes (WMSI) were derived by using the sum of segmental scores divided by the respective number of segments.
1.4 Coronary Angiography
All angiograms were analyzed by one of the investigators who had no knowledge of the echocardiographic data. The severity of coronary stenosis was determined by calipers and expressed as percent lumen diameter reduction. Significant coronary disease was defined as ≥70% stenosis of at least one epicardial artery.
1.5 Statistical Analysis
All data are expressed as mean value ± SD. Coronary artery stenoses before and after PTCA were compared using the paired ttest. Differences in frequency of recovery between revascularized and nonrevascularized segments were analyzed using the chi-square test. Analysis of variance (ANOVA) was used to compare serial changes in wall motion scores and hemodynamic variables during DSE. If the Fvalue was significant, a Student-Newman-Keuls multiple comparison test was performed. Statistical significance was set at p ≤ 0.05.
The study group consisted of 34 patients (30 men and 4 women, mean age 64 ± 13 years). Remote myocardial infarction was present in 25 patients (73%) 18 of whom had Q wave infarctions. Stable exertional angina was present in 21 patients (63%) and congestive heart failure in 8 patients (24%). Global WMSI at baseline was 2.07 ± 0.71. Twenty-two patients were taking calcium channel blockers, 14 took beta-blockers, 15 took nitrates and 9 took angiotensin-converting enzyme inhibitors. Medications were not altered throughout the duration of the study.
A total of 38 vessels were revascularized, with a reduction of stenosis from 88 ± 10% to 22 ± 10% (p = 0.0001). Thirteen were in the distribution of the left anterior descending coronary artery and 25 were in the distribution of the right and circumflex arteries. None of the patients had any cardiac events during the follow-up period. Follow-up echocardiograms were performed at a mean of 2.4 ± 2.9 days and 7 ± 2 weeks after PTCA.
2.1 Serial Changes in Rest Myocardial Function
Before revascularization, wall motion was severely abnormal in 231 LV segments: severe hypokinesia in 88 segments, akinesia in 110 segments and dyskinesia in 33 segments. One hundred eighty segments were in the distribution of the revascularized regions and 51 were in the nonrevascularized territory. Recovery of rest function occurred in 56 revascularized segments with severe dysfunction (31%) compared with only one nonrevascularized segment (2%) (p < 0.001). Recovery occurred early after revascularization in 45 segments (80%) and late in the remaining 11 segments (20%). In the revascularized territories, regional WMSI decreased significantly from 2.86 ± 0.76 at baseline to 2.34 ± 0.97 early after revascularization, with a further decrease to 2.12 ± 1.03 at late follow-up (p < 0.0001 by ANOVA), whereas no significant change occurred in the non-PTCA territories.
Patient analysis revealed that rest function recovered in 15 (44%) of 34 patients, 11 of whom (73%) had early improvement and 4 of whom (27%) had late improvement in function after PTCA. Global WMSI decreased from 2.07 ± 0.71 at baseline to 1.81 ± 0.73 early after revascularization and to 1.76 ± 0.74 at late follow-up (p < 0.0001 by ANOVA).
2.2 Serial Changes in Feasibility and Hemodynamic Data During DSE
Before revascularization, the DSE protocol was completed to a maximal dobutamine dose in 25 (74%) of 34 patients. The test was terminated early in nine patients at a mean dose of 28 ± 4.5 μg/kg per min (range 20 to 30). The reasons for termination were reaching >85% predicted maximal heart rate in four patients, angina in four patients and hypotension in one patient. At follow-up, both early and late after revascularization, a complete DSE protocol was achieved in 30 patients (88%) and terminated early in four owing to attainment of >85% predicted maximal heart rate. None of the patients had angina or hypotension during DSE after PTCA. Serial changes in the rate–pressure product (heart rate × systolic blood pressure) are shown in Fig. 1. The rate–pressure product was similar at rest and during low dose dobutamine and was higher during the maximal dose of dobutamine after revascularization.
2.3 Serial Changes in Cardiac Function During DSE After Revascularization
Results were similar for regional and global WMSI analysis, as well as between coronary artery territories. Therefore, analysis by patients is presented. Patients were grouped by the type of initial response to DSE in the majority of dysfunctional segments before revascularization (Fig. 2). There were 12 patients with a biphasic response to DSE, 8 with sustained improvement, 8 with a worsening response and 8 with no change in wall motion of abnormal segments to DSE. The number of patients taking beta-blockers in these four groups were 7, 3, 1 and 3, respectively, and this distribution was not altered during follow-up. The serial changes in cardiac function at rest and during DSE were different among the four types of responses to dobutamine and are hereby detailed.
Before revascularization, WMSI in patients with a biphasic response decreased at low dose dobutamine from 1.98 ± 0.75 to 1.55 ± 0.62 and increased at high dose dobutamine to 2.11 ± 0.67 (p < 0.0001 by ANOVA) (Fig. 2). After revascularization, rest function improved significantly in these patients, the majority early after revascularization (rest 1.98 ± 0.75; early 1.51 ± 0.61; late 1.35 ± 0.54; p < 0.0001 by ANOVA). Furthermore, significant improvement in global function was seen at low and high dose dobutamine compared with rest, early and late after PTCA (p = 0.008 and p = 0.005, respectively, by ANOVA). These changes were markedly different from those observed before revascularization (WMSI at peak dose 2.11 ± 0.67 before PTCA; 1.29 ± 0.62 early after PTCA; 1.21 ± 0.41 late after PTCA; p < 0.0001 by ANOVA). At low and peak dose dobutamine, WMSIs were similar early and late after PTCA (Fig. 2).
In patients who showed a worsening response during DSE before revascularization, WMSI was 1.92 ± 0.32 at rest, remained similar during low dose dobutamine (1.93 ± 0.35) and increased to 2.16 ± 0.5 at high dose dobutamine (Fig. 2). After revascularization, no significant change in rest WMSI was observed in these patients, early or late after revascularization. However, WMSI increased at low dose and high dose dobutamine and was significantly different from pre-revascularization at the peak dose of dobutamine (WMSI 2.16 ± 0.5 before PTCA vs. 1.60 ± 0.57 late after PTCA; p < 0.05).
Patients with sustained improvement during dobutamine had a decrease in WMSI during dobutamine before PTCA (WMSI 1.86 ± 0.61 at rest, 1.54 ± 0.37 at low dose and 1.52 ± 0.45 at peak dose; p = 0.004 by ANOVA) (Fig. 2). After revascularization, a small improvement in global LV function at rest was observed in these patients but did not reach statistical significance (1.86 ± 0.61 before, 1.62 ± 0.61 early and 1.65 ± 0.60 late after revascularization). The WMSI during low dose as well as peak dose dobutamine was similar to pre-revascularization values (Fig. 2).
Patients with no change in function during dobutamine on the pre-revascularization study had no change in rest WMSI after revascularization (Fig. 2). Furthermore, no significant difference in WMSI was observed in these patients during dobutamine, before or after revascularization (Fig. 2).
2.4 Changes in WMSI During DSE in Patients With and Without Recovery of Rest Function
Fig. 3shows the changes in WMSI at rest and during serial DSE in patients with and without late recovery of rest function. In patients with recovery of function, the majority of improvement occurred early after revascularization (WMSI 2.0 ± 0.66 before PTCA vs. 1.49 ± 0.53 early after PTCA vs. 1.35 ± 0.44 late after PTCA; p < 0.0001 by ANOVA). Before PTCA, WMSI improved with low dose dobutamine and worsened at high dose dobutamine (low dose 1.65 ± 0.59 vs. high dose 2.0 ± 0.63; p = 0.0006). The types of response to DSE before PTCA included biphasic response in 10 patients, worsening in 2, sustained improvement in 2 and no change in wall motion in 1. After revascularization, WMSI at low and high dose dobutamine was higher than before revascularization. At high dose DSE, global function was markedly different compared with before revascularization (peak dose WMSI 2.0 ± 0.63 before PTCA vs. 1.20 ± 0.36 late after PTCA; p < 0.0001 by ANOVA) (Fig. 3) and was similar early and late after revascularization.
There were 19 patients who did not have recovery of rest function late after revascularization (Fig. 3). In these patients, before revascularization, WMSI improved slightly during low dose DSE and worsened at high dose DSE (WMSI at rest 2.14 ± 0.76 vs. low dose 1.99 ± 0.76 vs. high dose 2.11 ± 0.77; p = 0.019 by ANOVA). After revascularization, function at rest and during low dose DSE was similar to pre-revascularization (Fig. 3). At high dose DSE, however, LV function was significantly improved after revascularization (WMSI at peak dose 2.11 ± 0.77 before PTCA vs. 1.85 ± 0.79 early after PTCA vs. 1.95 ± 0.78 late after PTCA; p = 0.004 by ANOVA).
To further elucidate which patients without recovery of rest function had improvement in their function during DSE after revascularization, changes in WMSI at peak dose dobutamine were compared between patients with demonstrable ischemia before revascularization (biphasic and worsening responses; n = 6) and those without inducible ischemia (sustained improvement and no change responses; n = 13). In patients without inducible ischemia, WMSI at peak dose DSE was unchanged from before PTCA to late after PTCA (2.06 ± 0.87 vs. 2.06 ± 0.86), whereas it decreased significantly in patients with demonstrable ischemia before revascularization (2.21 ± 0.56 vs. 1.72 ± 0.54; p = 0.02). The maximal rate–pressure product achieved in this subgroup was similar before and late after PTCA.
Fig. 4depicts individual changes in WMSI at peak DSE, before and late after PTCA. In all patients who had recovery of rest function, WMSI decreased at peak dobutamine by >0.25 (2-grade improvement in two segments). In patients without recovery of rest function, WMSI decreased by >0.25 in five of six patients who had inducible ischemia before revascularization and in only one of 13 patients without inducible ischemia before PTCA.
To our knowledge, the present study is the first to demonstrate that revascularization of patients with chronic myocardial dysfunction leads to significant improvement in contractile function during inotropic stimulation, even in the absence of recovery of rest function. Improvement in function in response to DSE occurs predominantly in patients with demonstrable ischemia before revascularization (biphasic and worsening responses). Patients who show recovery of rest function have the most marked improvement in contractile function during DSE. However, those without recovery of rest function also demonstrate improvement in contractile function during inotropic stimulation, particularly when there is inducible ischemia before revascularization. Although recovery of rest function was seen early after revascularization in the majority of patients, 27% showed late recovery and demonstrated improved function during DSE early after revascularization, consistent with concomitant myocardial stunning.
3.1 Response of Hibernating Myocardium to Dobutamine
Myocardial hibernation is a condition characterized by impaired rest LV function in the presence of severe, stable coronary artery disease whereby recovery of function occurs after revascularization [1–6, 12, 13]. Several studies have shown that contractile reserve to inotropic stimulation is preserved but limited in the majority of patients with myocardial hibernation, due to impairment of coronary flow reserve [5, 7, 8, 14]. A biphasic response during DSE has been shown to be the most predictive factor for recovery of function, followed by a worsening response during dobutamine . The presence of sustained improvement to DSE before revascularization, although a marker of residual viability, is a poor predictor of recovery of ventricular function after revascularization, because no ischemia is elicited even during moderate to high stress [5, 10].
There are currently no studies evaluating the serial change in the response of the dysfunctional myocardium to inotropic stimulation after revascularization. In the present study, a significant increase in contractile function during DSE was observed, predominantly in patients with biphasic and worsening responses before revascularization. This is most likely secondary to an increase in coronary flow reserve after revascularization and a reduction in ischemic burden. The most marked improvement in contractile function during DSE was observed in patients showing a biphasic response before revascularization. In contrast, patients demonstrating sustained improvement before revascularization maintained similar contractile reserve after revascularization. Similarly, those with no change in wall motion during DSE did not show significant improvement in function at rest or during DSE after revascularization.
Of interest are the changes in cardiac function during DSE in patients with a worsening response before revascularization. Although rest function did not improve in these patients as a group, cardiac function during DSE increased significantly after revascularization, particularly at high dose dobutamine. These areas most likely represent dysfunctional myocardium with exhausted coronary reserve before revascularization, which improves on revascularization. Recent observations with rest-redistribution thallium-201 scintigraphy in segments with worsening response further support this hypothesis . The lack of significant improvement of rest function in the majority of these patients may be related to the presence of subendocardial infarction or an admixture of viable and necrotic myocardium, enough to satisfy a “threshold phenomenon” for rest contraction . However, during inotropic stimulation, improved thickening is observed in these areas with residual viability. It is important to note that because no augmentation in myocardial function was seen with low dose dobutamine before revascularization, these patients would not have been detected as having viability if only low dose DSE was performed.
3.2 Recovery of Rest Function Versus Recovery of Function During Stress
The magnitude of improvement in contractile function during DSE was highest for patients who had recovery of rest function (40% change in WMSI at peak DSE). Of interest are the changes in contractile reserve during DSE in patients who did not have recovery of rest function. Global function during high dose dobutamine in these patients improved after revascularization, but to a lesser degree (8% change in WMSI at peak DSE), the majority of which occurred in patients with demonstrable ischemia before revascularization (22% change in WMSI at peak DSE). Although the reason for this interesting observation is not clear, these findings are consistent with the presence of an admixture of viable and nonviable myocardium, subtended by significant coronary stenosis. Although rest function did not improve after revascularization because of myocardial tethering or other mechanisms [5, 15], relief of ischemia with revascularization most likely restored contractile reserve to inotropic stimulation in the residual viable myocardium. This may account in part for improvement of symptoms in some patients who do not show recovery of rest function after revascularization. Importantly, this raises the question as to the appropriate end point for recovery of function after revascularization in patients with suspected hibernation: evaluation of rest function versus function during stress. Further investigations are needed in this regard.
3.3 Myocardial Stunning After Reperfusion of Hibernating Myocardium
Currently, it is well accepted that myocardial hibernation occurs in patients with stable, severe coronary artery disease. However, the pathophysiology of myocardial hibernation is still not well elucidated. Whether this condition represents adaptations of the myocardium to chronic reduction in rest flow, the end result of repetitive myocardial stunning or a combination of mechanisms is still unclear . Recently, using positron emission tomography and rest thallium-201 scintigraphy, rest coronary flow has generally been mildly affected [10, 17, 18], whereas coronary flow reserve was severely impaired .
The time course of recovery of function after revascularization in patients with myocardial hibernation has been also variable. Although earlier studies have demonstrated more rapid improvement in function after revascularization [1, 19], other clinical and experimental data have shown a gradual recovery of rest function after revascularization [5, 20–22]. Among the reasons for the discrepant findings is the inclusion in several studies of patients with unstable ischemic syndromes where myocardial stunning may be prevalent. In the present group, no patients with unstable syndromes were included. Although the majority of function improved within the first week after revascularization, improvement in function was delayed in 27% of patients. The persistence of LV dysfunction early after restoration of blood flow with preserved contractile reserve and eventual recovery of rest function is compatible with concomitant myocardial stunning in patients with myocardial hibernation.
3.4 Study Limitations
We studied a select group of patients referred for revascularization; therefore, the prevalence of different responses to DSE may differ in the general population with ischemic heart disease. However, neither the decision for revascularization nor patient selection was influenced by the DSE study. Coronary angiography was not repeated to determine the presence or absence of restenosis. Absence of an ischemic response during DSE after revascularization, however, suggests absence of flow-limiting restenosis in our patients. In addition, none of the patients complained of recurrent angina during the follow-up period. Echocardiographic wall motion was analyzed qualitatively because of limitations of existing quantitative methods. The interpretation, however, was performed without knowledge of clinical data, timing of the study or changes in rest function after PTCA.
Although bypass surgery offers more complete revascularization, for a variety of reasons we chose to study patients undergoing PTCA. The rate of procedure-related myocardial infarction is lower and easier to diagnose with angioplasty. Early after bypass, a number of factors may influence wall motion, such as anemia, changes in preload and use of inotropic agents, and thus hinder the early assessment of recovery of function after revascularization. In addition, cardiac translation is greater after bypass, which not only renders the assessment of wall motion more difficult but also makes it harder keep the reader unaware of the status of revascularization.
At late follow-up, we evaluated patients >6 weeks after revascularization, with all patients having their follow-up by 3 months. Although the likelihood of recovery after 3 months is conceivable, it is less likely. Furthermore, the recovery rate observed is similar to that recently observed with prospective studies using echocardiography or radionuclide techniques [4, 10, 23, 24]. In addition, a longer follow-up interval may result in an increased incidence of restenosis. Thus, the timing of follow-up in the present study is likely the most appropriate.
In myocardial hibernation, the majority of improvement in function at rest and during inotropic stimulation was seen in patients who showed a biphasic response to DSE before revascularization. However, patients without improvement in function during low dose dobutamine, who demonstrated worsening of function at high dose (worsening response), had a significant augmentation in cardiac function during DSE after revascularization, further emphasizing the need for high dose in addition to low dose dobutamine in the assessment of myocardial viability. Patients who had recovery of rest function had the most marked improvement in function during dobutamine. However, those without recovery of rest function also demonstrated improvement in function during dobutamine, particularly if they showed evidence of ischemia before revascularization. This may account in part for amelioration of symptoms in patients without improvement of rest function after revascularization.
We thank Eula Landry for assistance in the preparation of the manuscript.
↵1 Present address: Section of Cardiology, University of Texas Southwestern, Dallas, Texas 75216.
☆ This study was supported in part by a grant from the John S. Dunn, Sr., Trust Fund, Houston, Texas and was presented in part at the 6th Annual Scientific Session of the American Society of Echocardiography, Toronto, Canada, June 1995.
☆☆ To discuss this article on-line, visit the ACC Home Page at www.acc.org/membersand click on the JACC Forum
- analysis of variance
- dobutamine stress echocardiography
- left ventricular
- percutaneous transluminal coronary angioplasty
- wall motion score index
- Received March 14, 1997.
- Revision received July 11, 1997.
- Accepted July 21, 1997.
- The American College of Cardiology
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