CLINICAL STUDIES
Myocardial viability on echocardiography predicts long-term survival after revascularization in patients with ischemic congestive heart failure
Roxy Senior, MD, DM, FRCPa,
Sanjiv Kaul, MD, FACC* and
Avijit Lahiri, MD, MRCP, FACCa
a Department of Cardiovascular Medicine, Northwick Park and St. Mark’s Hospitals and Institute of Medical Research, Harrow, United Kingdom
* Cardiovascular Division, University of Virginia, Charlottesville, Virginia, USA
Manuscript received July 31, 1998;
revised manuscript received January 25, 1999,
accepted February 15, 1999.
Reprint requests and correspondence: Dr. Avijit Lahiri, Department of Cardiology, Northwick Park Hospital, Harrow, Middlesex HA1 3UJ, United Kingdom
nphcardicac{at}compuserve.com
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Abstract
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OBJECTIVES
This study was conducted to evaluate the effect of revascularization on survival in patients with congestive heart failure (CHF) due to ischemic left ventricular (LV) systolic dysfunction based on the presence of myocardial viability (MV).
BACKGROUND
There are insufficient data regarding the survival benefit of revascularization in patients with CHF due to ischemic LV systolic dysfunction.
METHODS
Follow-up was obtained in 87 consecutive patients with CHF due to ischemic LV systolic dysfunction (New York Heart Association [NYHA] class II-IV; LV ejection fraction <0.35) who underwent low-dose dobutamine echocardiography (DE). MV within each of 12 myocardial segments representing the LV was defined as having either: 1) normal function or mild dyssynergy at rest; 2) severe resting dyssynergy that improved on DE, or 3) worsening of function on DE except in the case of akinesia.
RESULTS
At a mean follow-up of 40 ± 17 months, 37 patients had received revascularization on the basis of clinical grounds, and there were 22 (25%) cardiac-related deaths. Multivariate Cox regression analysis revealed that when patients with at least five segments showing MV underwent revascularization, mortality was reduced by an average of 93% (confidence interval of 22% to 99%), which was associated with improvement in NYHA class as well as LV ejection fraction. Patients with less than five segments showing MV who underwent revascularization (and thus, showing mostly scar), and those with at least 5 segments demonstrating MV who were treated medically, had a much higher mortality.
CONCLUSIONS
Revascularization produces a clear survival benefit in patients with CHF due to ischemic LV systolic dysfunction who have a significant region of the LV demonstrating MV. These data may have wide-ranging implications in the management of patients with coronary artery disease whose main clinical presentation is CHF.
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Abbreviations and Acronyms
| | ACE | = angiotensin converting enzyme | | CAD | = coronary artery disease | | CHF | = congestive heart failure | | DE | = dobutamine echocardiography | | ECG | = electrocardiography | | LV | = left ventricle; left ventricular | | NYHA | = New York Heart Association | | MV | = myocardial viability | | SWT | = systolic wall thickening |
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In some patients with coronary artery disease (CAD), the main symptom may be dyspnea rather than angina. In many instances, these patients may also manifest signs of congestive heart failure (CHF). They are usually treated with diuretics, digoxin and more recently, with ACE inhibitors. Because they do not complain of angina, workup for reversible ischemic left ventricular (LV) dysfunction is many times not even instituted. With the aging population, chronic ischemic LV dysfunction has reached epidemic proportions, and is now the leading cause of CHF in the western hemisphere (1,2).
It is now recognized that revascularization provides both symptomatic relief and mortality benefit in patients with angina and ischemic LV systolic dysfunction (3–7). Ischemia in these patients can be documented on exercise electrocardiogram (ECG) (8,9). Most patients with CHF, however, are unable to exercise to work loads that can manifest ischemia on the ECG. Baseline abnormalities on the ECG also preclude interpretation of minor exercise-induced changes in many instances. Thus, recognition of viable but potentially ischemic myocardium is problematic in this cohort of patients. Without evidence for ischemia, physicians are reluctant to consider revascularization as an option, because LV systolic dysfunction in these patients is presumed to be due to multiple infarctions.
Echocardiography is a reliable clinical means for assessing regional LV function. If regional LV function is normal or only mildly reduced, myocardial viability (MV) is known to be present (10). When resting regional LV function is severely reduced, however, it is not possible to differentiate MV from scar. The response of severely dysfunctional myocardium to dobutamine has been shown to predict MV in patients post–myocardial infarction (10–13), and those with chronic ischemic LV dysfunction (14–18). The purpose of our study was to assess the interaction between the amount of MV (defined by regional LV function at rest and during dobutamine) and revascularization in terms of its effect on long-term outcome in patients with chronic CAD whose main clinical presentation is CHF. The hypothesis tested was that revascularization would not only improve symptoms and regional LV function, but would also provide a survival benefit if sufficient MV was present. Conversely, providing revascularization to a severely dysfunctional LV that did not have enough MV would not be beneficial.
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Methods
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Patient selection.
Eighty-seven consecutive outpatients at Northwick Park Hospital were included in this study. All patients gave written informed consent to participate in the study. To be included in the study, three inclusion criteria needed to be met: 1) CHF (NYHA class II-IV) for at least three months that was treated medically; 2) LV ejection fraction  0.35, and 3) clinical evidence of CAD (usually prior infarction, and in some cases documented ischemia on exercise testing). Patients with significant valvular disease, unstable angina, myocardial infarction within three months, sustained ventricular tachycardia or atrial fibrillation were excluded from the study. All patients underwent clinical assessment, rest echocardiography, low-dose dobutamine echocardiography (DE), coronary angiography and prospective follow-up.
Echocardiography.
Echocardiographic images were acquired in the standard parasternal long and short axis as well as apical four- and two-chamber views. LV ejection fraction at rest was estimated from the apical views using the modified Simpson’s method previously validated in our laboratory (19). Dobutamine was infused intravenously starting at 5 µg/kg/min, and increased to 10 and then 15 µg/kg/min, with each dose maintained for 5 min (13). Although imaging was performed continuously, data were acquired only at baseline and during the last minute of each dobutamine dose.
Images were analyzed in a quad-screen cine-loop format (14) by two experienced observers blinded to all other clinical information. Systolic wall thickening (SWT) was graded in each of 12 myocardial segments (Fig. 1) as: 1 = normal; 2 = mild hypokinesia; 3 = severe hypokinesia; and 4 = akinesia (20) using a consensus opinion. SWT index was calculated by summing the grades of all segments that were visualized and dividing this sum by the number of segments visualized. The segments ascribed to each of the three vascular vascular territories are mentioned in the legend to Figure 1.
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Figure 1 The 12-segment model used for echocardiographic assessment of resting function and function during DE. Segments 1, 2, 6, 7 and 11 belong to the left anterior descending artery vascular territory. Segments 3 and 8 belong to the left circumflex artery territory. Segments 4, 5, 9 and 10 belong to the right coronary artery territory. Segment 12 belongs to the left anterior descending artery territory, unless it is abnormal in conjunction with other segments of the right coronary artery and not the left anterior descending artery territory, in which case it belongs to the right coronary artery territory.
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For MV to be considered present within a myocardial segment, one or more of the following criteria had to be met: 1) normal (grade 1) or mildly reduced (grade 2) systolic function at rest (10,18); 2) improvement in systolic function during DE by  1 grade when systolic function was severely reduced (grade 3 [14]); or, 3) worsening of systolic function on DE (indicating inducible ischemia, and thus also MV [18]), except when akinesia (grade = 4) was present at rest (10).
Coronary angiography.
CAD was defined as 50% luminal diameter narrowing of a major epicardial coronary artery or its major branch. Each patient was classified as having one-, two- or three-vessel disease. In addition, a coronary jeopardy score was calculated based on dividing the coronary tree into six segments and giving each segment with a 75% stenosis, or any segment distal to such a stenosis, a score of 2. In patients with a left dominant system, the right coronary artery was assigned no score. The maximal possible score in any patient was 12 (21).
Follow-up.
All patients underwent clinical assessment at a mean of 21 months after entering the study. Survival status was determined at a mean of 40 months by contacting the patient or next of kin. The cause of death was established by review of hospital records or from the patient’s physician. Cardiac deaths were defined as those resulting from acute myocardial infarction, refractory CHF or occurring suddenly and not being attributed to other known causes.
Statistical methods.
Continuous variables are expressed as mean ± 1 SD, and categorical variables are expressed as proportions. Survival data were assessed by Cox proportional hazard models (22) to estimate the interaction of revascularization with the extent of MV as well as with other potential prognostic factors, and to characterize the effects of these interactions on mortality. Univariate Cox regression analysis was initially performed using clinical, echocardiographic and angiographic variables. Multivariate Cox regression analysis was then performed by entering into the model variables that had a p value of <0.10 on univariate analysis. All variables with a p value of <0.05 were allowed to remain in the final model.
A receiver-operator characteristics curve was plotted to define the sensitivity and specificity of different cutoff points for the number of viable segments that needed to be revascularized to show survival benefit (23). Patients were then classified into groups based on the best cutoff point and the type of treatment offered (revascularization vs. medical management). Baseline clinical characteristics (including medical therapy), and echocardiographic as well as angiographic data, were compared between these groups using analysis of variance or Fisher exact test. Kaplan-Meier life table analysis was performed to assess event-free survival (24), which was compared between the four groups using the Mantel-Cox test. A p value of <0.05 (two-sided) was considered significant.
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Results
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Patient characteristics are listed in Table 1. More than three fourths of the patients were male and had a history of myocardial infarction. Only one fourth had chest pain, despite the majority (81%) having multi-vessel CAD. Almost 90% were taking diuretics and ACE inhibitors. On average, only one fourth of the 12 myocardial segments in any patient demonstrated normal (grade 1) or mildly reduced (grade 2) systolic function; three fourths demonstrated severe resting dysfunction (grade 3), which was consistent with the low resting LV ejection fraction in these patients. Less than half of the dysfunctional segments in these patients showed improvement on DE. Most segments showed no response (improvement or worsening) to DE. Despite severe LV dysfunction, however, on an average more than half of the segments showed MV based on the combined assessment of resting and dobutamine-induced wall thickening.
Of the 87 patients, 37 (43%) underwent revascularization, of whom most (89%) underwent multiple coronary artery bypass grafting. Percutaneous coronary angioplasty of the left anterior descending coronary artery was performed in four patients (11%), one of whom also had the procedure performed on the left circumflex coronary artery. The mean interval between DE and revascularization was 11 ± 4 weeks. The DE results were not known to the clinicians who determined the treatment option. One half of the 50 patients who did not receive revascularization had a plausible reason for not undergoing surgery: 13 were considered to have poor distal vessels on angiography, 6 had severe pulmonary disease and 6 refused surgery. Of the other half, surgeons were reluctant to operate on 10 because of poor LV ejection fraction and a high LV end-diastolic pressure, and 15 did not receive surgery because of lack of funds.
At a mean follow-up of 40 ± 17 months, there were 22 (25%) cardiac-related deaths: 5 from acute myocardial infarction, 14 from progressive CHF and 3 occurred suddenly. On Cox regression, the univariate predictors of survival were the number of segments demonstrating MV, number of viable segments in the right and left circumflex coronary territories, occurrence of revascularization and the interaction between MV and the occurrence of revascularization when the number of segments showing MV was at least five (Table 2). The last variable was the most important independent predictor of survival on multivariate Cox regression analysis. The only additional variable that was predictive of survival on multivariate analysis was the baseline NYHA class (Table 2).
The receiver-operator characteristic curve showing the sensitivity and specificity of different cutoff points for the number of segments with MV that needed to be revascularized to note a survival benefit is depicted in Figure 2. In keeping with the results of Cox regression analysis, a cutoff point at at least four versus at least five segments with MV showed the best sensitivity and specificity (75% and 91%, respectively) for survival after revascularization.
According to these results, we divided our patients into four groups based on MV (present in 5 of the 12 myocardial segments) and type of treatment offered (revascularization vs. medical management): Group 1 (n = 31) had MV and underwent revascularization; Group 2 (n = 32) had MV but were managed medically; Group 3 (n = 6) had no MV but underwent revascularization; and Group 4 (n = 18) had no MV and were treated medically. There were no differences in any of the variables between the four groups at the time of entry into the study (Table 3).
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Table 3 Patient Characteristics Based on Presence of Myocardial Viability (5 of 12 segments) and Treatment Offered (Revascularization or Medical)
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By 21 ± 8 months, 7 patients had died and 10 did not return for follow-up. Significant improvement in NYHA functional class (1.5 ± 0.6 vs. 2.5 ± 0.6 at baseline p < 0.001) and LV systolic function (SWT index of 2.6 ± 0.9 vs. 3.1 ± 0.6 at baseline, p < 0.01) were noted in the Group 1 patients, while no changes were observed in the other three groups. In the Group 1 patients, there was a reduction in diuretic use from 87% to 30% (p < 0.001) and nitrate intake from 48% to 9% (p < 0.001), while reduction in use of these drugs was not seen in the other groups. The use of ACE inhibitors remained unchanged in all groups. At a mean follow-up of 40 ± 17 months, of the 22 patients who died, 1 (3%) belonged to Group 1, 10 (31%) to Group 2, 3 (50%) to Group 3 and 8 (44%) to Group 4 (Table 3). Group 1 mortality was significantly (p < 0.001) less compared with the other three groups. Figure 3 illustrates the Kaplan-Meier survival curves of the four groups of patients.
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Figure 3 Event-free survival curves for the four patient groups. See text for details. Solid diamond = revascularization with myocardial viability; solid triangle = medical therapy with myocardial viability; open triangle = medical therapy without myocardial viability; open diamond = revascularization without myocardial viability.
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Discussion
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The new finding of our study is that patients with CAD and chronic LV systolic dysfunction whose main clinical presentation is CHF show improvement in NYHA class, LV systolic function and long-term outcome after revascularization if they have sufficient MV on echocardiography. If such patients are treated by conventional medical therapy, their mortality is high, presumably from progressive ischemic LV dysfunction or an acute ischemic event. Conversely, if sufficient MV is lacking in the presence of severe LV systolic dysfunction, revascularization provides no benefit. Thus, echocardiography may have an important role in patients with CHF for selecting those who may benefit from revascularization.
The problem of CHF.
There are ample data to support the use of revascularization in patients with CAD and LV systolic dysfunction who have angina. Such patients show marked symptomatic relief as well as significant improvement in long-term survival (3–6,25,26), and their regional LV systolic function generally improves (4–6). The systolic dysfunction can occur from either chronic reduction in resting myocardial blood flow or repetitive ischemia, or both (27). In either case, successful revascularization removes the cause of dysfunction.
Many patients with CAD present with symptoms other than angina. At times it is dyspnea on exertion from transient LV systolic dysfunction caused by exercise-induced ischemia. More often, the dyspnea is associated with chronic LV systolic dysfunction and CHF, with angina not being a major symptom. With people living longer lives, and the prevalence of CAD being higher in them, the incidence of chronic ischemic LV dysfunction is increasing rapidly, so that the epidemiology of CHF has changed in recent years from causes other than CAD to predominantly CAD (1,2).
Admission (and readmission) for CHF is now the leading cause of hospitalization in the western hemisphere (28). Many of these patients have reversible ischemic LV dysfunction, and if revascularized, would show both symptomatic improvement and benefit from a longer life. The cost of revascularization may offset the cost of repeated hospitalizations and improve the quality of life. With modern surgery and other forms of revascularization, elderly patients are tolerating interventions much better (29). If surgery is not an option, aggressive medical therapy to alleviate ischemia and its sequelae, such as with carvedilol, may also provide survival benefit (30). The challenge is to recognize the presence of reversible LV systolic dysfunction in these patients.
Comparison with previous studies.
There are remarkable similarities between our results and those of Ragosta et al. (6) and Pagley et al. (7) using 201thallium imaging. Similar to us, they found only a minority of patients with chronic ischemic LV dysfunction lacking evidence for MV. Using a 15-segment model of the LV, they found that if 7 dyssynergic segments exhibited MV, LV ejection fraction was likely to improve after revascularization (6). Survival benefit was seen only in patients undergoing revascularization. Conversely, patients with sufficient MV who did not undergo revascularization had a poor outcome (7).
Dobutamine echocardiography has also been used to assess MV in chronic ischemic LV dysfunction. In all studies, patients with MV had poor outcome on medical therapy compared with revascularization (31–33). Williams et al., however, reported less events in medically treated patients with no MV compared with those with MV (31). The difference between their study and ours could be explained by the differences in the types of events. Whereas we considered only cardiac-related death as events, they included other soft points as well. Our results are very similar to those of Afridi and colleagues, who demonstrated improved survival in patients with CAD and severe LV dysfunction who had both MV and revascularization (32). Like us, they found lack of MV and revascularization to be associated with poor outcome. Like Afridi et al. and us, Meluzin et al. also showed that the beneficial effect of revascularization was related to the amount of MV (33).
The major difference between our study and all previous studies assessing the role of MV in LV dysfunction due to CAD is that although these studies also included patients with CHF, their major clinical presentation was angina. We specifically studied patients whose main presentation was CHF. Nonetheless, these studies combined with ours make a strong argument for assessing MV in patients with ischemic LV dysfunction irrespective of the presenting symptom. Such an approach can guide management.
For scoring regional LV function, we selected a model in which each myocardial segment is equivalent in weight (20). Thus, when half the segments are involved, half the LV myocardium is involved. The major difference between this and some other models is the segmentation of the apex. In our model, the apex is divided into two segments. Consequently, some adjustments need to be made when interpreting our results in the context of other segmentation schemes.
Study limitations.
Similar to previous studies (5–7,31,33), this is a single-center study where selection bias is unavoidable. The patients were selected from an outpatient setting and may not be as sick as those who seek repeated hospitalizations for CHF. The number of patients in the group who underwent revascularization in the absence of MV is small. Also, the results may not be applicable to populations where multi-vessel disease is less frequent. A randomized design would undoubtedly be ideally suited for a study such as this, but it is difficult, if not impossible, to prospectively randomize patients with very poor LV systolic function for surgery versus medical management.
In our study, the results of DE were not divulged to the physician making the decision whether to revascularize or not. Although no differences were noted between patients undergoing revascularization and those receiving medical management, selection bias may have favored taking one group to surgery over another. Factors such as quality of vessels on angiography, pulmonary status and the reluctance to operate on patients with poor LV ejection fraction played a role in our study. A significant number of patients also did not receive surgery because of lack of funds.
We only used low-dose dobutamine in our study. We were, therefore, unable to study the value of the "biphasic" response on the prediction of survival. The "biphasic" response indicates the presence of a physiologically significant coronary stenosis proximal to viable myocardium (10), and revascularization of myocardium showing this response is highly predictive of functional recovery after revascularization (16). However, a "biphasic" response can only be seen in segments that first demonstrate an improvement in thickening, a criterion for MV in our study. Thus, segments likely to ultimately show a "biphasic" response were considered viable in our study. Segments likely to demonstrate ischemia on DE (worsening of function except in the presence of akinesia) were also considered viable.
Conclusions.
Patients with CHF due to LV systolic dysfunction from CAD who have sufficient MV on echocardiography have a marked survival benefit from revascularization compared with those with MV who do not undergo revascularization or those without sufficient MV who undergo revascularization. This survival benefit is also associated with improvement in NYHA class and global systolic LV function. These data may have wide-ranging implications in the management of patients with ischemic LV systolic dysfunction whose main clinical presentation is CHF.
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Acknowledgments
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We thank Caroline Dore, PhD, for assistance in the statistical methods.
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Footnotes
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This work was supported in part by grants from National Public Health Cardiac Research Fund, Dupont Pharmaceuticals, North Billerica, Massachusetts and Michael Tabor Grant, Harrow, UK. Dr. Kaul was supported by a grant (HL-48890) from the National Institutes of Health, Bethesda, Maryland, an Established Investigator Award from the American Heart Association, Dallas, Texas and a travel grant from Dupont Pharmaceuticals, North Billerica, Massachusetts.
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Abstract
Methods