CLINICAL STUDIES
Recovery of contractility of viable myocardium during inotropic stimulation is not dependent on an increase of myocardial blood flow in the absence of collateral filling
Francesco Barillà, MD*,
Giuseppe De Vincentis, MD ,
Enrico Mangieri, MD*,
Massimo Ciavolella, MD, PhD* ,
Gaetano Pannitteri, MD*,
Francesco Scopinaro, MD,
Giuseppe Critelli, MD* and
Pietro Paolo Campa, MD*
* 2nd Section of Cardiology, Institute of Cardiac Surgery, University "La Sapienza," Rome, Italy
Section of Nuclear Medicine, University "La Sapienza," Rome, Italy
Manuscript received March 23, 1998;
revised manuscript received October 14, 1998,
accepted November 18, 1998.
Reprint requests and correspondence: Dr. Francesco Barillà, 2nd Section of Cardiology, University of Rome "La Sapienza," Policlinico Umberto I, Viale Del Policlinico 155, 00161 Rome, Italy
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Abstract
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OBJECTIVES
The purpose of this study was to determine whether contractile recovery induced by dobutamine in dysfunctioning viable myocardium supplied by nearly occluded vessels is related to an increase in blood flow in the absence of collaterals.
BACKGROUND
Dobutamine is used to improve contractility in ventricular dysfunction during acute myocardial infarction. However, it is unclear whether a significant increase in regional blood flow may be involved in dobutamine effect.
METHODS
Twenty patients with 5- to 10-day old anterior infarction and  90% left anterior descending coronary artery stenosis underwent 99mTc-Sestamibi tomography (to assess myocardial perfusion) at rest and during low dose (5 to 10 µg/kg/min) dobutamine echocardiography. Rest echocardiography and scintigraphy were repeated >1 month after revascularization. Nine patients had collaterals to the infarcted territory (group A), and 11 did not (group B).
RESULTS
Baseline wall motion score was similar in both groups (score 15.9 ± 1.3 vs. 17.4 ± 2.0, p = NS), whereas significant changes at dobutamine and postrevascularization studies were detected (F[2,30] = 409.79, p < 0.0001). Wall motion score improved significantly (p < 0.001) in group A both at dobutamine (–5.3 ± 2.2) and at postrevascularization study (–5.5 ± 1.9), as well as in group B (–3.9 ± 2.8 and –4.5 ± 2.4, respectively). Baseline 99mTc-Sestamibi uptake was similar in both groups (62.9 ± 9.7% vs. 60.3 ± 10.4%, p = NS), whereas at dobutamine and postrevascularization studies a significant change (F[2,30] = 65.17, p < 0.0001) and interaction between the two groups (F[2,30] = 33.14, p < 0.0001) were present. Tracer uptake increased significantly in group A both at dobutamine (+10.9 ± 7.9%, p < 0.001) and at postrevascularization study (12.1 ± 8.7%, p < 0.001). Conversely, group B patients showed no change in tracer uptake after dobutamine test (–0.4 ± 5.8, p = NS), but only after revascularization (+8.8 ± 7.2%, p < 0.001).
CONCLUSIONS
The increase in contractility induced by low dose dobutamine infusion in dysfunctional viable myocardium supplied by nearly occluded vessels occurs even in the absence of a significant increase in blood flow.
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Abbreviations and Acronyms
| | ECG | = electrocardiogram | | LAD | = left anterior descending artery | | LDD | = low dose dobutamine | | LV | = left ventricular | | MI | = myocardial infarction | | PET | = positron emission tomography | | SPECT | = single-photon emission computed tomography | | WMS | = wall motion score |
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The inotropic agent dobutamine has been used by our group and by others to assess viability in poorly contracting myocardium (1–6). However, it is unclear whether a significant increase in regional blood flow in the area supplied by a critically narrowed coronary artery may be a component of dobutamine-induced recovery of contractile function (7).
Evidence has been provided in the animal model (8,9) that dobutamine infusion improves contractility without increasing subendocardial blood flow in severely hypoperfused myocardium, and clinical studies have shown that dobutamine may ameliorate contractile dysfunction in myocardium supplied by stenotic coronary arteries, in spite of a decreased perfusion in the same regions (10).
Some authors emphasized the role of collaterals in protecting ischemic myocardium and in limiting infarct size (11–13), although previous studies failed to detect a relationship between the presence of collaterals and myocardial viability (14).
We hypothesized that collateral blood flow in asynergic regions subtended by occluded or severely narrowed coronary arteries could play a role in increasing perfusion during dobutamine-induced inotropic improvement of dysfunctional but viable myocardium. As dobutamine administration is known to improve contractility during the acute phase of myocardial infarction (MI), without extension of the ischemic injury (15–17), a prospective study was undertaken to determine the relation between regional myocardial perfusion and viability during low dose dobutamine (LDD) infusion, in patients with left ventricular (LV) dysfunction after recent MI, with and without angiographic evidence of collaterals. The pattern of myocardial blood flow changes was analyzed through 99mTc-Sestamibi uptake, known to closely parallel changes in myocardial blood flow over a wide range of flows (18). Postrevascularization echocardiographic and single-photon emission computed tomography (SPECT) studies were used as a reference.
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Methods
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Patients and protocol.
Among patients referred to our Institution because of acute MI, 20 patients, 18 men and two women, aged 39 to 73 years (mean 56 ± 12) were selected, since they fulfilled the following inclusion criteria: 1) recent (5 to 10 days old) anterior MI, documented by electrocardiogram (ECG) and enzyme changes, with residual regional LV dysfunction, as documented by echocardiography and angiography; 2) severe (90% cross-sectional) left anterior descending artery (LAD) stenosis; 3) absence of significant stenoses in coronary arteries providing collateral filling; 4) no evidence of previous MI at the inferior, posterior or lateral wall; 5) absence of symptomatic congestive heart failure or other significant complications during hospitalization, and 6) revascularization procedure performed during hospitalization. Thirteen patients had received thrombolytic therapy. Seventeen patients developed Q waves in at least two precordial leads, whereas the remaining three patients showed non–Q wave MI.
Two-dimensional echocardiography and SPECT were performed within 8 days after MI, at baseline, during LDD infusion carried out 3 h later and 40 ± 10 days after revascularization. This sequence of imaging testing was approved by the Hospital Human Rights Committee. Informed consent was obtained from each patient.
Cardiac catheterization.
Selective coronary angiography and biplane LV angiography were performed in all patients within 10 days after MI and within 1 to 2 days of LDD study. Two blinded observers evaluated the degree of coronary lesions and the extent of visible collaterals, which were graded according to the guidelines recommended by the Thrombolysis in Myocardial Infarction trial classification (12,14). Only well developed collateral flow with visualization and dense opacification of the entire distal vessel (grade 3) was taken into account.
Data acquisition.
Echocardiography was performed after a 2-day washout period of nitrates, and beta-adrenergic and calcium-channel blocking agents, using a 2.5-MHz transducer and a commercially available scanner (Hewlett-Packard Sonos 1000). Images were recorded on VHS videotape. Parasternal long-axis, parasternal short-axis (at basal, middle and apical levels) and apical four- and two-chamber views were used. Images were digitized on-line in a quad screen cine loop format (Pre-Vue III, Nova Microsonics), and used to evaluate the inotropic response and the correct timing of tracer injection.
Low dose dobutamine study was carried out at the infusion rate of 5 µg/kg/min for 5 min, and increased to 10 µg/kg/min for another 5 min if no response in wall motion and systolic thickening was noted with the first dose. Recording of images as well as tracer injection were carried out at the end of the last step of dobutamine infusion, which was continued at the same flow rate for 3 min further after tracer injection during its distribution to the myocardium. Blood pressure and 12-lead ECG were monitored throughout the study. To avoid misinterpretation (19), improvements occurring within 1 cm of the boundary of the involved myocardium were not taken into account.
For baseline radionuclide study, 370 MBq (10 mCi) of 99mTc-Sestamibi was administered intravenously, and the patient encouraged to have a fatty meal, to speed up hepatobiliary elimination of the tracer. Ninety minutes later, SPECT imaging was performed using a single-head gamma camera (Starcam 2000, General Electric, Herts, England), centered on the 99mTc 140-keV photopeak and equipped with a high resolution collimator. Data were recorded in a 64 x 64 matrix across a 180° circular orbit, starting at 45° right anterior oblique position, acquiring 32 views lasting 20 s each. Three hours after the first tracer injection, LDD study was carried out, and 1,110 MBq (30 mCi) of the tracer was administered in the same way as described above. Single-photon emission computed tomography imaging was carried out 1 h later using the same protocol as for baseline study. Postrevascularization SPECT was carried out under resting conditions with a dose of 370 MBq (10 mCi) of 99mTc-Sestamibi, using the same protocol as for baseline study. From raw radionuclide data, short-axis, vertical long-axis and horizontal long-axis tomograms were reconstructed by filtered back-projection using a Butterworth filter with a cutoff of 0.4 cycles/min, an order of 3.5 and no attenuation correction. For each set of images, 3-pixel thick slices were reconstructed along each axis, to incorporate a substantial amount of myocardium in each territory, as well as to optimize alignment with echocardiographic segments.
Data analysis.
Echocardiographic images were analyzed off-line by two independent observers, unaware of angiographic and SPECT results. The LAD territory was divided into nine segments: anteroseptal, anterior and anterolateral, at the chordal, midpapillary muscle and apical levels. Wall motion and systolic thickening were graded semiquantitatively using a scoring system as follows: 1 = normal wall thickening; 2 = hypokinesia; 3 = akinesia; 4 = dyskinesia. A score 2 in at least two different views was considered suggestive of regional systolic dysfunction, whereas improvement of contractile function was defined when a score change  1 occurred.
Single-photon emission computed tomography analysis was performed by two investigators who were blinded to angiographic and echocardiographic results. The LAD territory was divided into nine sectors representing the anteroseptal, anterior, anterolateral and apical wall. Each sector was qualitatively scored on a 3-point scale: 0 = absent or markedly reduced activity; 1 = definitely reduced activity; and 2 = normal activity. Quantitative evaluation of SPECT images was also performed on the representative slices on each axis by means of a computer-assisted circumferential profile analysis (20,21). Each profile was plotted using 20 points, and the activity within each angular sector (18°) was calculated as a percentage of total heart counts and compared with 99mTc-Sestamibi reference profiles obtained at our laboratory from a gender-specific database composed of healthy volunteers imaged with 99mTc-Sestamibi at rest and exercise. An uptake 2 SD below normal (always <80% peak activity) was considered an abnormal vascular territory. Both dobutamine and postrevascularization improvement were defined as an increment in 99mTc-Sestamibi uptake >12% (i.e., >1 SD above the average uptake value observed in normal volunteers), as compared with baseline. Abnormal uptake was classified as mild to moderate when 99mTc-Sestamibi activity was 50% of maximal activity, and severe when tracer activity was <50%.
Interobserver and intraobserver variability.
Data were checked for interobserver reproducibility by randomly selecting 10 patient studies for reinterpretation by a second investigator, and comparing the results with the initial determinations. The agreement was good for both echocardiographic (r = 0.93, p < 0.001) and SPECT data (r = 0.92, p < 0.001). Intraobserver variability was assessed by having the initial operator reanalyze 10 randomly selected patient studies on a different occasion. The agreement between the two analyses was also good for both echocardiographic (r = 0.95, p < 0.001) and SPECT data (r = 0.96, p < 0.001).
Statistical analysis.
After intrapatient normalization, ordinal data were expressed in percentages, and were compared by means of chi-square test. Quantitative data are presented as mean value ± 1 SD. To evaluate the effect of collateral circulation on contractile response after i) LDD infusion, and ii) myocardial revascularization, echocardiographic and scintigraphic data were analyzed by means of analysis of variance with repeated measures, with collateral circulation (yes vs. no) as between-subject factor, and time of echocardiographic and scintigraphic evaluation (at baseline, during LDD infusion and after revascularization) as repeated measure factor. Multiple comparisons were performed by applying the appropriate t test with Bonferroni’s correction. The analysis was performed by using BMDP statistical software. A p value <0.05 was considered statistically significant.
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Results
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Angiographic and revascularization data.
In all patients the coronary lesion was located at the proximal LAD artery, and was always graded 90% (total occlusion in five patients). In seven patients the apical segment was supplied by the right coronary artery, which in no case showed a significant obstruction. Left ventricular ejection fraction was 40% in 17 patients, and 25% in the others.
Based on the presence or the absence of collateral filling, patients were divided into group A (nine patients) and group B (11 patients), respectively. No significant difference in age, gender, prevalence of diabetes, hypertension, cigarette smoking, angina or extent of coronary artery disease was present between the two groups.
Coronary revascularization was accomplished within 20 days of MI by coronary angioplasty in 12 patients (six patients from each group), and by coronary artery bypass grafting in eight (three from group A, five from group B).
Echocardiographic results.
During LDD infusion, neither significant changes in heart rate or systolic blood pressure, nor arrhythmias or ST-T changes occurred. Analysis of variance with repeated measures applied to echocardiographic data showed no significant difference in wall motion score (WMS) between the two groups (main effect of grouping factor F[1,15] = 0.52, p = NS). On the contrary, a significant difference was observed among baseline, LDD and postrevascularization study (main effect of repeated measures F[2,30] = 409.79, p < 0.0001). This difference was not affected by the presence or absence of collaterals (interaction F[2,30] = 1.41, p = NS) (Table 1).
Multiple comparisons performed by two-group t test with Bonferroni’s correction showed no significant difference in WMS between the two groups at baseline, LDD and postrevascularization study (p = NS).
Paired t test with Bonferroni’s correction showed a significant improvement of WMS in both groups, comparing LDD study (group A: –5.3 ± 2.2, p < 0.001; group B: –3.9 ± 2.8, p < 0.001) as well as postrevascularization study (group A: –5.5 ± 1.9, p < 0.001, group B: –4.5 ± 2.4, p < 0.001) to baseline values (Fig. 1 to 3).
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Figure 1 Bar histograms comparing echocardiographic (top) and scintigraphic results (bottom) at baseline, during low dose dobutamine infusion and postoperatively (POST-REV), in patients with (group A) and without (group B) collaterals. The lack of significant changes in myocardial 99mTc-Sestamibi uptake after dobutamine infusion in patients without collaterals is clearly visible, in spite of a recovery of both function and perfusion detected after revascularization.
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Figure 2 Example of echocardiographic and scintigraphic images obtained in a patient with collaterals (group A) at baseline, during low dose dobutamine infusion and after revascularization (POST-REV). In the top row, a left ventricular end-systolic frame obtained at echocardiographic study in the four-chamber view is shown. In the bottom row, a set of tomographic slices reconstructed along the short axis from left ventricular apex to base (a d) is shown. The decrease in left ventricular end-systolic dimensions at both dobutamine and postrevascularization echocardiographic studies in comparison with the basal study is visible. The functional changes were associated with an increase in 99mTc-Sestamibi uptake detected at dobutamine scan in the areas of the previous infarction in comparison with basal scan, and confirmed after revascularization.
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Figure 3 Example of echocardiographic and scintigraphic images obtained in a patient without collaterals (group B) at baseline, during low dose dobutamine infusion and after revascularization (POST-REV) (image composed as in Fig. 2). The decrease in left ventricular end-systolic dimensions at both dobutamine and postrevascularization echocardiographic studies in comparison with the basal study is visible. Differently from the patient shown in Figure 2 (a patient with collaterals), no change in 99mTc-Sestamibi uptake in the infarcted area is visible at dobutamine scan in comparison with basal scan. A significant increase in tracer uptake was nevertheless detected after revascularization.
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Radionuclide results.
Analysis of variance with repeated measures applied to scintigraphic data showed no significant difference in average tracer uptake between the two groups (main effect of grouping factor F[1,15] = 1.38, p = NS). On the contrary, a significant difference was observed among baseline, LDD and postrevascularization study (main effect of repeated measures F[2,30] = 65.17, p < 0.0001); this difference was affected by the presence or absence of collaterals (interaction F[2,30] = 33.14, p < 0.0001) (Table 1).
Multiple comparisons performed by two-group t test with Bonferroni’s correction showed no difference in quantitative SPECT analysis between the two groups at baseline, LDD and postrevascularization study (p = NS).
Paired t test with Bonferroni’s correction showed an increase of tracer uptake both at LDD study (+10.9 ± 7.9%, p < 0.0001) and after revascularization (+12.1 ± 8.7%, p < 0.001) in comparison with baseline values in group A. Conversely, in group B, tracer uptake slightly but not significantly decreased at LDD study (–0.4 ± 5.8%, p = NS), and improved significantly after revascularization (+8.8 ± 7.2%, p < 0.001) in comparison with baseline values (Fig. 1 to 3).
A significant difference in tracer uptake was found in group B patients when comparing postrevascularization with LDD study results (p < 0.005).
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Discussion
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The results of the present study confirm that hypoperfused viable myocardium supplied by nearly occluded arteries can increase contractility in response to LDD infusion, despite the lack of significant improvement in regional myocardial perfusion. Although the presence of collaterals can contribute to matching, the increased oxygen demand induced by LDD infusion in territories distal to a severe coronary stenosis, their presence does not seem to be necessary for the drug to be effective. Thus, in the absence of angiographically visible collaterals, such a phenomenon may lead to an apparent mismatch between increased contractility and almost unchanged relative myocardial blood flow.
Previous investigations.
Intracoronary infusion of dobutamine in the animal resulted in an increase of maximum work of hypoperfused myocardium without altering global hemodynamics, even in the presence of decreased subendocardial blood flow (8,9). An improvement of myocardial blood flow distal to an induced coronary stenosis, in response to dobutamine infusion, was also described (22). However, coronary perfusion pressure was deliberately held constant in the latter study, thus not adequately representing the clinical setting, in which dobutamine-induced arteriolar vasodilation can result in a reduction of perfusion pressure distal to a coronary lesion, with a further possible reduction of subendocardial blood flow.
A correlation between function and perfusion with dobutamine infusion in the clinical setting was reported by Coma-Canella et al., who found an increase in regional contractility only when dobutamine induced a mild to moderate ischemia, whereas the contractile function was worsened with severe ischemia (10).
Additional investigation recently supported the concept that different patterns of baseline perfusion, as well as of perfusional changes during LDD infusion, are possible in dysfunctioning yet viable myocardium (7). No significant correlation between myocardial blood flow and WMS, both at rest and during dobutamine infusion, was observed in different types of dysfunctioning myocardium. Wall motion improvement was not consistently associated with an increase in myocardial blood flow and vice versa. Similarly, Lee et al. showed contractile reserve to be only in part dependent on the level of myocardial blood flow at rest and during inotropic stimulation in a mixed patient population with and without previous MI (23). Though the presence and the functional efficacy of collateral filling was not specifically addressed in these studies, possibly a variable prevalence of collaterals was at least in part responsible for the inconsistency of the results obtained.
Elhendy et al. recently showed that the presence of collaterals failed to identify a different behavior of viable myocardial areas at both LDD echocardiography and after revascularization (24), although without evaluating myocardial blood flow, either invasively or noninvasively. However, previous investigations by Di Carli et al. had already shown the lack of correlation between myocardial viability assessed by means of positron emission tomography (PET) and the presence of collaterals (14).
Pathophysiologic explanations.
A body of experimental data demonstrated that distal to critical coronary stenoses the subendocardial vasodilator reserve is exhausted (25–27). In such a condition, a further reduction of perfusion pressure, induced either pharmacologically (28,29) or through metabolic vasodilation (30,31), results in an uneven distribution of myocardial blood flow, which is improved in the subepicardial layers, and unchanged or paradoxically reduced in subendocardial areas.
As shown by the results of the present report, the majority of 99mTc-Sestamibi defects observed at baseline in patients with collaterals filled in when the tracer was injected during recovery of contractility. In the presence of an exhausted flow reserve, this would imply that collaterals improve blood flow distal to the coronary stenosis, in response to the increased oxygen demand induced by LDD administration in hypoperfused myocardium. Conversely, in patients without collaterals, a mismatch between improved contractility and unchanged 99mTc-Sestamibi activity was evident. Thus, it appears reasonable to argue that an increase in regional blood flow is not involved in the recovery of contractile function induced by LDD. Indeed, in the presence of an inhomogeneous increase of flow induced by LDD, a coronary steal could have been responsible for ischemia, as observed by Mayer et al. (32). Also, more recently, a flow redistribution from the subendocardium toward the subepicardium as a consequence of intracoronary dobutamine infusion has been reported in animal investigations (9,33).
The results obtained in the present study after revascularization demonstrate that in patients without collaterals the lack of improvement of tracer activity in territories susceptible to contractile recovery does not necessarily imply irreversible myocardial damage. Indeed, in these patients the majority of segments identified as viable at echocardiography exhibited complete recovery of contractility after revascularization, and this was coincident with a more evident increase in 99mTc-Sestamibi uptake, as compared with patients with collaterals, in whom the increase in tracer uptake with LDD was similar to that achieved after revascularization.
The results of the present study might apparently seem to run counter to existing data on the diagnostic effectiveness of LDD echocardiography and scintigraphy in the evaluation of myocardial viability. However, many segments without collaterals presented with a baseline tracer uptake >50%, which is generally regarded as representing viable, though hypoperfused, tissue, and were therefore viable from a scintigraphic point of view.
Study limitations.
It is conceivable that patients early after acute MI will have continuous changes in regional myocardial perfusion, LV geometry and regional wall motion. Additionally, the development of collaterals occurs very early after MI. Therefore, all patients underwent coronary angiography, echocardiography and scintigraphy within a few days, and 99mTc-Sestamibi SPECT was performed as a single-day protocol (34–36).
It is possible that the absolute amount of activity in a segment was related to improvement of contractile function with dobutamine, rather than to increased blood flow, such as described by others (20,37). However, dobutamine effects on wall motion and thickening are very short-lasting, and were certainly over at the time of imaging. Additionally, improved wall motion was observed to the same extent both in the presence and in the absence of increased tracer uptake.
The main limitation of the present study is certainly due to the impossibility of measuring absolute blood flow through 99mTc-Sestamibi uptake, in the absence of a quantitative evaluation by PET. Despite a close relation between PET results and those obtained with Sestamibi as well as 201Tl (38), a possible increase in blood flow to infarcted areas, although to a lesser extent than in normally perfused areas, in response to LDD infusion cannot be excluded. However, as the increase in tracer uptake induced by LDD in normal areas was presumably similar in both groups, the lower tracer uptake in areas not supplied by collaterals should reflect a truly different behavior. In any case, such a wide difference in the pattern of relative tracer uptake between collateral-dependent and -independent areas can hardly be related to similar dobutamine effectiveness.
Conclusions.
The present study gives some insights into the role played by collateral circulation in the flow response to inotropic stimulation, in the presence of critically narrowed epicardial coronary arteries and consequently of almost exhausted precapillary flow reserve. Certainly, the interplay between anterograde and retrograde filling and the increase in myocardial oxygen demand induced by dobutamine infusion has still to be clarified. Furthermore, the evidence of a mismatch between functional improvement induced by inotropic agents and relatively unchanged myocardial blood flow in acute ischemic heart failure warrants further clinical investigations.
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Acknowledgments
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The authors are indebted to M. Cristina Acconcia, MD, and to Prof. Massimo Donnetti, for their valuable advice in the analysis of data.
The authors wish to thank the staff of the Coronary Care Unit of the 2nd Section of Cardiology, Institute of Cardiac Surgery, whose cooperation and assistance made this study possible.
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Footnotes
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This study was partially supported by Grant 5/15/02/003 from the Ministero Università e Ricerca Scientifica e Tecnologica, Italy.
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Abstract
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