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(Chest. 2003;124:1250-1258.)
© 2003 American College of Chest Physicians

Aspirin Does Not Adversely Affect Survival in Patients With Stable Congestive Heart Failure Treated With Angiotensin-Converting Enzyme Inhibitors*

Valérie Aumégeat, MD; Nicolas Lamblin, MD; Pascal de Groote, MD; Eugène P. Mc Fadden; Alain Millaire, MD, PhD; Christophe Bauters, MD and Jean-Marc Lablanche, MD

* From the Service de Cardiologie C, Hôpital Cardiologique, CHRU Lille, Bd Prof J Leclercq, 59037 Lille Cedex, France.

Correspondence to: Pascal de Groote, MD, Service de Cardiologie C, Hôpital Cardiologique, CHRU, Bd du Prof J Leclercq, 59037 Lille Cedex, France; e-mail: pdegroote{at}chru-lille.fr


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Background: Experimental studies and retrospective analyses of mortality trials with angiotensin-converting enzyme inhibitors (ACE-Is) have suggested that aspirin may reduce the beneficial effect of these drugs. The aim of this study was to assess a possible detrimental effect of aspirin on survival in stable patients with left ventricular systolic dysfunction who had congestive heart failure and had been treated with ACE-Is.

Methods and results: We performed a retrospective analysis in 755 consecutive stable patients with left ventricular systolic dysfunction. A Cox regression model was used to select independent predictors of survival and to test for a possible interaction between aspirin and ACE-Is with an adjustment to differences in clinical characteristics in subgroups of patients. Of the 755 patients, 328 (43.4%) had proven ischemic cardiomyopathy, 693 patients (91.8%) were receiving ACE-Is, and 317 patients were receiving aspirin (mean [± SD] dose, 183 ± 65 mg/d; 74% of the patients receiving <= 200 mg/d). During a median follow-up period of 1,996 days, there were 273 cardiac-related deaths, 14 urgent transplantations, 71 nonurgent transplantations, and 46 noncardiac-related deaths, and 3 patients were lost to follow-up. The cardiovascular mortality rates were 11.5% and 19.0%, respectively, at 1 and 2 years. There were no interactions among aspirin, ACE-Is, and survival in the overall population (p = 0.21), or in subgroups of patients with ischemic cardiomyopathy (p = 0.41) or with nonischemic cardiomyopathy (p = 0.74).

Conclusions: In this population of stable patients with left ventricular systolic dysfunction, our retrospective analysis did not demonstrate any interaction between the use of aspirin and survival in patients receiving ACE-Is.

Key Words: angiotensin-converting enzyme inhibitors • aspirin • heart failure • prognosis


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
During the last decade, several studies have suggested that aspirin could have a possible negative therapeutic interaction with angiotensin-converting enzyme inhibitors (ACE-Is) in patients with congestive heart failure (CHF). The evidence for this hypothesis is based both on experimental studies and on retrospective analyses of trials designed to test the effect of various therapeutic agents in patients with heart failure.1 2 3 4 5 6 Investigators of the Studies of Left Ventricular Dysfunction (SOLVD)3 suggested, in a retrospective analysis, that while aspirin therapy had an overall beneficial effect on mortality, it might attenuate the documented benefit of enalapril on survival. This hypothesis has been supported by experimental data.1 2 7 8 However, other studies9 10 have provided conflicting results. Data from the Captopril and Thrombolysis Study (CATS),11 from the Bezafibrate Intervention Project Study (BIP) registry,12 or from the ACE-I Myocardial Infarction Collaborative Group13 do not support the hypothesis that aspirin has a negative effect on survival in patients treated with ACE-Is.

Another possible confounding factor relates to the doses of aspirin that were prescribed. In the vast majority of retrospective analyses of large trials, information regarding the dose of aspirin was not provided. It is possible that these conflicting results could be related to the different doses of aspirin used. An analysis published in 199814 involving patients with either hypertension or CHF concluded that small doses of aspirin did not interact with ACE-Is.

We performed a retrospective analysis in a population of stable patients with CHF in order to investigate a possible interaction between aspirin and ACE-Is. The unique feature of this study is that some characteristics of our population, such as etiology, left ventricular ejection fraction (LVEF), peak oxygen consumption (O2), and the doses of aspirin and ACE-Is, were prospectively recorded at baseline.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 Conclusion
 References
 
We performed a retrospective analysis in consecutive stable patients with CHF related to left ventricular systolic dysfunction (ie, LVEF <= 45%) who were referred to our institution for a prognostic evaluation. All the patients had been ambulatory and symptomatically stable during the preceding 2 months. Patients with recent (ie, for < 3 months) acute coronary syndromes or with recent (ie, for < 6 months) coronary revascularizations were excluded from the study. Patients underwent echocardiography and performed a cardiopulmonary exercise test. The cardiopulmonary exercise testing was performed on an upright electromagnetically braked bicycle (Hellige Meditronic 35, Freiburg, Germany; and 1996 Ergo-Metrics 900, Ergoline, Bitz, Germany) using a continuous protocol (10 W/min). Patients had to cycle at the rate of 60 revolutions per minute at each stage, and exercise was terminated because of dyspnea or leg/general fatigue. The heart rate was continuously recorded on a 12-lead ECG (Case 15; GE Medical Systems; Chicago, IL). BP was measured every 2 min and at peak workload with a mercury sphygmomanometer. The data for gas exchange were collected on a breath-by-breath basis using a computerized system (CPX system; MedGraphics Corp; St. Paul, MN). Both analyzers were calibrated using standard gas mixtures prior to each exercise test. Peak O2 was defined as the average value obtained during the last 30 s of exercise. All the patients underwent Doppler echocardiography for the determination of LVEF and other standard measurements (CFM 750; Vingmed; Horten, Norway).

The etiology of the left ventricular dysfunction was carefully determined by the examination of hospital charts and/or the results of coronary angiography. The presence of ischemic cardiomyopathy was defined in patients with a proven history of myocardial infarction (ie, significant q waves on the ECG and/or a significant increase in creatinine kinase levels during a previous hospitalization) and/or stenosis of > 50% in one of the major coronary arteries. Patients who did not fulfill these criteria were considered to have nonischemic cardiomyopathy. If coronary angiography was not performed or if ECG was not contributive, patients were considered as having undetermined cardiomyopathy, except for young patients (ie, those < 30 years old) without any risk factor for atherosclerosis. These patients were considered to have nonischemic cardiomyopathy.

The generic names and doses of the medications taken by the patient at entry into the study were recorded. During the follow-up period, information on changes in medications were obtained during outpatient visits, by contact with the general practitioner, the cardiologist, or the patient, and by review of hospital charts. If a death occurred during a hospitalization, the medications that were being used by the patient just before hospital admission were considered to be the last treatment. For sudden cardiac death without hospitalization, we postulated that the medications recorded at the last visit constituted the last treatment if the patient had been stable before the sudden death and if the time that had elapsed between the last visit and the sudden death was < 1 month. Otherwise, the treatment was considered to be unknown.

Statistical Analysis
Results are presented as the mean ± SD. Differences between groups were assessed by unpaired Student t test followed by the Student-Newman-Keuls test. Discrete variables were compared using a {chi}2 analysis.

Follow-up was performed by outpatient visits or by contact with the general practitioner or the cardiologist. The major end points were cardiovascular-related death, including cardiovascular-related death and urgent cardiac transplantation (ie, United Network for Organ Sharing status 1), and cardiovascular events, including cardiovascular-related death and cardiac transplantation. A Kaplan-Meier method was performed to estimate the cumulative survival of the population or those in the different subgroups. A comparative log-rank test was used to compare the survival rates of different subgroups. A stepwise multivariate Cox proportional hazards analysis was performed to determine independent predictors of cardiac survival and event-free cardiac survival and to test for possible interactions among aspirin, ACE-Is, and survival. Because of the retrospective design of the study, an adjustment was performed with the parameters significantly different in the subgroups of patients who were receiving and not receiving aspirin. Quantitative variables were entered as continuous variables. Parameters were entered in the model when p < 0.1 in the univariate analysis. Statistic analyses were performed with a statistical software package (SPSS, version 9; SPSS Inc; Chicago, IL). A p value of < 0.05 was considered to be statistically significant.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 Conclusion
 References
 
Study Population
From November 1990 to June 1997, 755 consecutive stable patients with CHF related to left ventricular systolic dysfunction were referred to our institution for a prognostic evaluation.

Etiology
Coronary angiography was performed in 694 patients, 29 patients refused angiography, 16 patients with a history of myocardial infarction did not have an angiography, and angiography was not performed in 16 young (ie, < 30 years old) patients without risk factors for arteriosclerosis. These 16 young patients were presumed to be free of coronary artery disease. Thus, 328 patients (43.4%) had proven ischemic cardiomyopathy, 398 patients (52.7%) had nonischemic cardiomyopathy, and 29 patients were classified as having undetermined cardiomyopathy (3.8%).

Treatment
Six hundred ninety-three patients (92%) were receiving ACE-Is. In the remaining 62 patients, therapy with ACE-Is was started during the follow-up period in 14 patients, 15 patients had ACE-I related cough, and 23 patients had moderate left ventricular dysfunction at entry in the study (ie, LVEF >= 40%) or improvement during the follow-up (the initiation of therapy with ACE-Is was left to the discretion of the cardiologist). In 10 patients (of whom 5 died), there was no information available on why they were not receiving ACE-Is. The baseline characteristics of the 693 patients receiving therapy with ACE-Is are presented in Table 1 . The type of ACE-I and the mean doses of each ACE-I are presented in Table 2 . The exact doses of the various drugs were known for all but one patient at the time of the cardiopulmonary exercise test. We divided the overall population into three subgroups according to the doses of ACE-I (according to the maximal doses used in several ACE-I studies) as follows: small doses (146 patients); intermediate doses (321 patients); and full doses (225 patients).


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  		Table 1.. Clinical Characteristics of the Study Population Receiving ACE-Is and Subgroups of Patients*

 

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  		Table 2.. Different Kinds and Doses of ACE-Is Used*

 
Table 3 presents the number of patients receiving therapy with ACE-Is and aspirin or oral anticoagulants at the entry of the study and at the end of the follow-up period. The mean dose of aspirin was 183 ± 65 mg/d, ranging from 100 to 500 mg/d (74% of patients received <= 200 mg/d). The clinical characteristics of patients who were or who were not receiving aspirin are summarized in Table 1 . Patients receiving aspirin were older (p = 0.0001) and were predominantly male (p = 0.0001). Ischemic cardiomyopathy and sinus rhythm were more frequent in group of patients receiving aspirin. The differences in treatment between these two subgroups are presented in Table 1 . There were no significant differences with respect to New York Heart Association (NYHA) class, LVEF, or peak O2.


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  		Table 3.. Number of Patients Receiving ACE-Is and Aspirin and/or Oral Anticoagulants During the Study

 
Information concerning the treatment at the end of the follow-up period was available in 694 patients (92%) of the total of 755 patients. It was not possible to precisely determine the treatment used in 8 living patients, in 3 patients who were lost to follow-up, and in 50 patients who died during the follow-up period (of whom 43 had a cardiac-related death). Most of the patients (479 patients; 69%) received the same doses of ACE-Is, with reduced doses given to 24 patients (3%) and increased doses given to 150 patients (22%). Therapy with ACE-Is was introduced in 14 patients and was stopped in 30 patients (4%), of whom 21 patients began receiving angiotensin II type I receptor blockers. At the end of the follow-up period, 46 patients (6%) were receiving angiotensin II type I receptor blockers. The doses of aspirin were unchanged in 176 patients (61%), were reduced in 54 patients (17%), and were increased in 12 patients (4%). Therapy with aspirin was introduced in 22 patients and was stopped in 58 patients (20%), of whom 28 patients began receiving oral anticoagulants and 6 patients began receiving ticlopidine or clopidogrel. Therapy with oral anticoagulants were stopped in 11 patients and was introduced in 49. During the follow-up period 47 patients received a combination of aspirin and oral anticoagulants (Table 3) .

Survival
The median follow-up period was 1,996 days. The minimal follow-up period was 5 years. During this follow-up period, there were 273 cardiac-related deaths, 14 urgent transplantations, 71 nonurgent transplantations, and 46 noncardiac-related deaths, and 3 patients were lost to follow-up. The cardiovascular mortality rates were 11.5%, 19%, 25%, 30%, and 35%, respectively, at 1, 2, 3, 4, and 5 years.

Table 4 summarizes the results of the univariate analyses in the study population. Using the Cox model, after adjustment for significantly different variables in the subgroups of patients, there were no interactions among therapy with aspirin, therapy with ACE-Is, and survival either in the whole population (p = 0.21) or in patients with ischemic cardiomyopathy (p = 0.41) or nonischemic cardiomyopathy (p = 0.74). Figure 1 shows the survival curves according to the use of aspirin and/or the use of oral anticoagulants.


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  		Table 4.. Univariate Predictors of Survival in Patients Receiving ACE-Is

 


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  		Figure 1.. Survival curves in different subgroups of patients divided according to the antithrombotic treatment. Top: patients receiving or not receiving aspirin. Middle: patients receiving or not receiving oral anticoagulant agents (AC). Bottom: patients receiving or not receiving aspirin and/or oral anticoagulant agents.

 
Table 5 summarizes the results of the univariate analyses in patients receiving ACE-I subdivided into subgroups according to etiology and antithrombotic treatment. There was no difference in survival in patients with nonischemic cardiomyopathy, whatever the antithrombotic treatment used. However, in patients with ischemic cardiomyopathy, there was a trend for a better survival in patients receiving aspirin (p = 0.04) and in patients not receiving oral anticoagulants (p = 0.06). Table 6 summarizes the mortality rates according to modifications of the treatment during the follow-up period. Mortality rates were similar, whatever the modification of the treatment, except in patients who had a decrease in the dose of ACE-I, but the numbers of patients and cardiac events were limited in this subgroup.


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  		Table 5.. Univariate Predictors of Survival in Patients Receiving ACE-Is, and Relationships Among Etiology, Aspirin, and Anticoagulants

 

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  		Table 6.. Number of Cardiac-Related Deaths and Mortality Rates in Subgroups of Patients Divided According to Modifications of the Treatment During the Follow-up Period*

 
The multivariate Cox analysis selected the following three independent predictors of cardiac survival: LVEF (adjusted relative risk [RR], 0.96; 95% confidence interval [CI], 0.95 to 0.97; p < 0.0001); percentage of maximal predicted O2 (adjusted RR, 0.98; 95% CI, 0.97 to 0.99; p < 0.0001); and NYHA classification (adjusted RR, 1.75; 95% CI, 1.33 to 2.31; p = 0.0002 [NYHA classes I + II vs NYHA class III]). Treatment with either aspirin or/and oral anticoagulants was not an independent predictor of cardiac survival. Results were similar when cardiac mortality and all transplantations were used as an end point.


   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
Conclusion
 References
 
In our population of stable patients with CHF related to left ventricular systolic dysfunction, we found no evidence of a negative therapeutic interaction between aspirin and ACE-Is. Our results confirm those of previous studies (ie, CATS,11 BIP,12 the meta-analysis performed by the ACE-I Myocardial Infarction Collaborative Group,13 or the Cooperative Cardiovascular Project cohort15 ), but are in conflict with the results of SOLVD,3 the Cooperative New Scandinavian Enalapril Survival Study (CONSENSUS) II,4 and the analysis from the Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries (GUSTO) I and the Evaluation in PTCA to Improve Long-Term Outcome with Abciximab GP IIb/IIIa Blockade (EPILOG) trials.6 Despite the large number of patients studied in the meta-analysis of the ACE-I Myocardial Infarction Collaborative Group (which included patients from CONSENSUS II), the controversy persists. In the editorial comment accompanying that article, Hall16 interpreted these results cautiously, discussing a possible bias related to the unequal number of patients receiving and not receiving aspirin. He suggested that with a greater number of patients not receiving aspirin, the difference in favor of this subgroup might be significant (30-day mortality rate, -6% vs -10%). In the analysis of patients from the GUSTO-1 and the EPILOG trials, Peterson et al6 demonstrated a significant negative interaction between aspirin and ACE-I. But again in these studies, different subgroups had unequal numbers of patients. In GUSTO-1, only 14% of patients received both drugs compared to 82% receiving aspirin and < 1% receiving ACE-Is. In the recent meta-analysis from the ACE Inhibitors Collaborative Group,17 which included patients from the Survival and Ventricular Enlargement trial, the Acute Infarction Ramipril Efficacy trial, the Trandolapril in Patients with Reduced Left Ventricular Function after Acute Myocardial Infarction trial, and the Heart Outcomes Prevention and Evaluation trial, but also patients from the SOLVD studies, the authors did not find any interactions among the use of ACE-Is, the use of aspirin, and outcomes.

Tables 7 and 8 summarize the major results of the different studies published concerning the interaction between ACE-Is and aspirin. Compared to previous studies, ours has several specific features. First, it is a single-center study with the same kind of management used for all patients with CHF. Although it is a retrospective analysis, the data were collected prospectively, and the population represents consecutive patients referred to our institution. Thus, there is less likelihood of a selection bias, as might be observed in mortality trials. In addition, the number of patients (three patients) lost to follow-up was very low. Second, for the vast majority of the patients, the presence of coronary artery disease was assessed by coronary angiography, which was not required in other studies to define the cardiomyopathy. Thus, we knew exactly the coronary status of our patients. Third, all our patients had CHF that was related to left ventricular systolic dysfunction. The CONSENSUS II,4 the CATS,11 the GUSTO-1/EPILOG trials,6 and the meta-analysis of the ACE-I Myocardial Infarction Collaborative Group13 involved patients with acute myocardial infarction with or without left ventricular systolic dysfunction. In these studies, if patients had heart failure, it was CHF, which has a different pathophysiology than acute chronic heart failure, as in our patients. In the GUSTO-1 study, no patient had CHF, and in the EPILOG study there were only 394 patients with LVEF <= 45%, of whom 164 had used a combination of aspirin and ACE-Is. Our patients with ischemic cardiomyopathy had stable coronary artery disease. Patients with recent acute coronary syndromes or recent coronary revascularization were not included in the study because cardiopulmonary exercise testing is always performed with patients in a stable condition. In the BIP registry, the 464 patients with heart failure were defined with an NYHA classification of grade 2 or greater.12 It is possible that in some patients, dyspnea was related to left ventricular diastolic dysfunction or to noncardiac diseases. Similarly, in several other studies, systematic echocardiography was not required to define CHF.18 19 20 In the Heart Outcomes Prevention and Evaluation study,17 patients with atherosclerosis who were at risk for an ischemic event were included in the study, but patients with CHF were excluded. All of our patients had systolic dysfunction with a LVEF of <= 45%.


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  		Table 7.. Summary of the Different Studies Concerning the Interaction Between ACE-Is and Aspirin*

 

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  		Table 8.. Summary of the Different Studies Concerning the Interaction Between ACE-Is and Aspirin Including Follow-up, Number of Deaths, Mortality Rates, and Interaction

 
Quarterly, all of our patients underwent an echocardiographic study and performed a cardiopulmonary exercise test to determine precisely well-known prognostic parameters, such as LVEF or peak O2. That improved the adjustments in our multivariate analysis.

Finally, treatment at entry into the study was precisely recorded (except for one patient), and this information was available in 92% of the population at the end of the follow-up period. As expected, the doses of ACE-Is were unchanged in 69% of the patients and were increased in 22%. The replacement of therapy with ACE-Is by therapy with angiotensin type I receptor blockers was rare. Because of the limited number of patients receiving these drugs (6%), it was not possible to analyze the interaction with aspirin. The mean dose of aspirin at entry in the study was 183 ± 65 mg/d, with 74% of patients receiving < 200 mg/d. The doses of aspirin used in our patients were relatively low, and this could explain the discrepancy between our results and those of previous studies. Because of the small number of patients receiving higher doses of aspirin, we could not conclude whether the lower dose used is the potential explanation for these discrepancies. In the CATS and BIP studies, doses of aspirin of <= 200 mg/d were used, and no negative interactions have been demonstrated.11 12 Unfortunately, the doses of aspirin in other large mortality trials6 20 were often unreported. In the United States, the dose of aspirin used in patients with coronary artery disease is generally > 200 mg/d (ie, 325 mg/d). Some experimental studies have demonstrated that 100 mg/d aspirin induced a significant endothelium-dependent arterial vasodilatation.21 In patients with hypertension, aspirin counteracts the vasodilating properties of ACE-Is when administered in doses of > 100 mg/d.22 Finally, one analysis14 has suggested that a dose of 100 mg/d does not interfere with the beneficial effect of therapy with ACE-Is. However, it has been demonstrated23 that 6 weeks of treatment with aspirin at a dose of 325 mg/d did not diminish forearm vasodilatation during exercise in stable patients with CHF who were treated with enalapril. In contrast, 8 weeks of treatment with 325 mg/d aspirin reduced exercise capacity in CHF patients receiving enalapril. This negative interaction seems to be related to the effect of ACE-Is on the alveolar capillary membrane.7 In the EPILOG trial6 and in the study by Lapane et al20 in very old patients, the dose of aspirin was >= 325 mg. The conclusions of these two studies were conflicting.

It is also possible that the negative interaction between aspirin and ACE-Is could be related to the different kinds of ACE-Is used. In our study, the numbers of patients in the different subgroups were limited, but we did not find any interaction between aspirin and the different ACE-Is or the doses of ACE-Is used. Experimental studies in patients with CHF or coronary disease have reported conflicting results regarding the effects of ACE-Is on vasodilatation. For example, quinapril has been shown to induce a significantly greater arterial vasodilatation than enalapril.24 25

The multivariate analysis selected well-known independent predictors of survival, namely, NYHA classification, LVEF, and percentage of maximal predicted O2. This fact demonstrates that our population was a representative population of patients with CHF, and that this analysis seems valid. It is important to note that these parameters were similar in patients who were or were not receiving aspirin (Table 1) . The mortality rate was also consistent with the reported mortality rates in similar patients who had been treated with ACE-Is.

Concerning oral anticoagulants, we found a trend toward better survival in patients not receiving this medication. This result was related to the retrospective nature of the study. Patients receiving oral anticoagulants had more severe CHF than did other patients. The difference in survival reflected the severity of illness in the population rather than a deleterious effect of oral anticoagulants. The result of our multivariate analysis supports this conclusion, since treatment with oral anticoagulants was not selected as an independent predictor of cardiac survival.

Study Limitations
The most important limitation of this study, as in all previously published studies, is its retrospective design. However, it is a single-center study of consecutive patients with an extremely high follow-up rate. There were some differences in clinical characteristics and treatment in patients receiving and not receiving aspirin, but the multivariate analysis was adjusted to these different parameters. The number of patients was limited, and we cannot exclude a possible negative interaction between aspirin and ACE-Is. However, our study was powered to detect a difference in survival after 5 years of follow-up of at least 9% between patients receiving and not receiving aspirin. In the SOLVD, the absolute difference in mortality between these two subgroups of patients was 10.3%. Moreover, we demonstrated in our study population that there were few modifications of the treatment during the follow-up period. The impact of the different ACE-Is could not be assessed because of the small number of patients in some subgroups. Similarly, the effect of changes in the medication during the follow-up period could not be analyzed since the vast majority of the patients had received the same treatment. Finally, we cannot exclude a possible intermittent administration of other nonsteroidal anti-inflammatory drugs to our patients. However, the number of patients receiving these drugs was probably limited.


   Conclusion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
References
 
Small doses of aspirin do not seem to affect survival in patients with stable CHF who have been treated with ACE-Is. In practice, we recommend that aspirin (< 200 mg/d) be used only in the subgroup of stable patients with CHF who have established coronary artery disease or peripheral atherosclerosis. The results of ongoing trials evaluating antithrombotic therapy in patients with stable CHF will provide more definitive data regarding antiplatelet therapy in stable patients with heart failure.


   Footnotes
 
Abbreviations: ACE-I = angiotensin-converting enzyme inhibitor; BIP = Bezafibrate Intervention Project Study; CATS = Captopril and Thrombolysis Study; CHF = congestive heart failure; CI = confidence interval; CONSENSUS = Cooperative New Scandinavian Enalapril Survival Study; EPILOG = Evaluation in PTCA to Improve Long-Term Outcome with Abciximab GP IIb/IIIa; GUSTO = Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries; LVEF = left ventricular ejection fraction; NYHA = New York Heart Association; RR = relative risk; SOLVD = Studies of Left Ventricular Dysfunction; O2 = oxygen consumption

Received for publication March 6, 2002. Accepted for publication March 6, 2003.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 

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