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Right arrow Electrophysiology - arrhythmias

Ann Thorac Surg 2002;74:1727-1732
© 2002 The Society of Thoracic Surgeons

Review

Effect of beta blockers after coronary artery bypass in postinfarct patients: what can we learn from available literature?

Stephen A. Geraci, MDa, Constance K. Haan, MDb*

a Section of Cardiovascular Medicine, Department of Medicine, University of Wisconsin-Madison, Madison, Wisconsin,, USA
b Division of Cardiothoracic Surgery, Department of Surgery, University of Florida Health Science Center, Jacksonville, Florida, USA

* Address reprint requests to Dr Haan, Division of Cardiothoracic Surgery, University of Florida Health Science Center, 655 W. 8th St, Jacksonville, FL, 32209, USA.
e-mail: connie.haan{at}jax.ufl.edu


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
Studies have shown that beta adrenergic antagonist therapy benefits patients with coronary disease through reduced mortality rate after acute myocardial infarction and reduced incidence of postoperative atrial fibrillation after coronary artery bypass grafting. The long-term benefit of this therapy in survivors of myocardial infarction who are subsequently revascularized, however, has not been defined or studied rigorously. We reviewed the published data to clarify the role of beta blockade in patients who had surgical revascularization after myocardial infarction. We found that patients who received beta blockers after myocardial infarction had a reduced mortality rate and fewer cardiac events in most clinical situations, a benefit which likely extends to patients who have had subsequent surgical revascularization.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
Treatment with betaadrenergic blocking drugs has a well-established role in many cardiovascular conditions. There is substantial evidence documenting their benefit in chronic coronary artery disease [1, 2], early in acute coronary syndromes [3, 4], and after myocardial infarction (MI) [5, 6]. In several placebo-controlled trials, long-term administration of beta blockers decreased the total mortality rate in these patients through a reduction in both sudden and nonsudden cardiac death. Similarly, they are effective as prophylaxis against perioperative cardiovascular morbidity and mortality after noncardiac surgical procedures [7–9].

The American College of Cardiology and the American Heart Association Task Force on Practice Guidelines has reported on the benefit of beta blocker therapy and made strong recommendations in its Guidelines for the Management of Patients with Acute Myocardial Infarction [5]. Beta blockers are designated class I (clearly indicated and beneficial) for all but low-risk postinfarction patients who have no clear contraindication to their use, with a recommendation for treatment to begin within a few days of the event (if not initiated acutely) and to continue indefinitely. Even low-risk patients may derive benefit from beta blockers, with a class IIa (probably useful) recommendation in this group. Although the Task Force statement admits that no study has determined definitively that long-term beta blocker therapy should be administered to survivors of MI who have subsequently undergone successful revascularization, it also states that there is no reason to believe that these agents act differently in coronary patients who have had revascularization.

There are, however, diverging points of view as to their benefit after coronary artery bypass operations. Some physicians believe that, once revascularized, the patient is at sufficiently low risk as to not require long-term beta blockers. Others argue that the substrate of previously infarcted myocardium and the high frequency of incomplete revascularization (especially of small but diseased coronary arteries) leave these patients at risk, which could be reduced further by long-term treatment with beta blockers.

In a retrospective analysis, Viskin and colleagues [10] described the failure of physicians to prescribe beta blockers after myocardial infarction and the relatively low rate of application of recommendations from randomized trials into clinical practice. In that study, a poor correlation was found between failure to prescribe post-MI beta blockers and clear contraindications to their use. Rather, they found that many patients not receiving beta blockers would have derived the greatest benefit from such therapy, including those with left ventricular dysfunction, heart failure, and advanced age. Only 11% of study participants received dosages equivalent to 50% or more of those proven effective by randomized controlled studies. Therefore, even when data are clear, beta blockers are underprescribed.

The translation of scientific study into evidence-based practice and implementation of guidelines remains incomplete. The goals of decreasing variation and improving use of recommended therapies will require continued effort. There are, however, gaps in the evidence that must be filled in order to build and improve evidence-based practice. The aim of this paper is to attempt to fill one important gap by clarifying the role of postinfarction beta blockade after coronary artery bypass grafting (CABG).


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
We conducted a search of the available literature using the PubMed search engine of the National Library of Medicine database. We searched for studies on beta blocker therapy and its benefit in coronary artery disease and after MI and on beta blocker therapy in relation to revascularization procedures, especially CABG. Key words used for this search included "beta adrenergic blockade," "myocardial infarction," and "coronary revascularization." The analysis included careful attention to patient numbers, inclusion and exclusion criteria, and relationships of treatments to outcomes of interest. Studies dealing with atrial fibrillation prophylaxis after CABG were excluded from analysis. A critical review of the identified literature was conducted to draw conclusions about the applicability of beta blocker therapy to the postinfarction, postrevascularization coronary disease patient and thereby derive specific recommendations for their use in this population.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
Because of the paucity of available literature specifically addressing the question of interest, the literature review was expanded to examine the effects of beta blockers on related populations. A total of 22 papers were identified as being relevant to the primary review objective (Table 1). Only one prospective study of post-CABG beta blocker effects on hard cardiovascular clinical endpoints was identified [11]. Furthermore, only one retrospective study specifically addressed postinfarction CABG patients as the primary study group [12]. Eleven papers reported on the related issues of beta blocker use generally in post-MI patients, perioperatively in the general CABG population, and periprocedurally with percutaneous interventions. Several original investigations and reviews included subgroups of patients who had had an acute MI requiring surgical revascularization.


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  		Table 1. Applicable Studies on Beta Blocker Therapy

 
The articles reviewed are grouped and organized, in the text and the table, according to their study population by timing of use of beta blockade—ie, postinfarction use, use in patients who had nonsurgical revascularization, preoperative and intraoperative CABG use, postoperative use, use in coronary artery disease where CABG patients were included, and postinfarct postoperative use. Our intention was to extrapolate from the available literature on beta blockers the impact on outcomes in specific, related populations with coronary artery disease.

Studies of chronic postinfarction beta blocker therapy
Several studies have documented long-term reductions in mortality and second infarct rates in MI survivors treated with beta blockers, with the sentinel studies published almost 2 decades ago. The Norwegian Timolol Trial began treatment with oral timolol 1 to 4 weeks after index infarction and documented a 39% relative risk reduction in all-cause mortality rate and a 29% reduction in second infarcts over almost 3 years of follow-up [13]. The Beta Blocker in Heart Attack Trial found a 27% relative reduction in total mortality and a similar decrease in sudden death over 2 years in patients treated with propranolol compared with placebo [14]. In addition, ISIS-1 [3] and Hjalmarson and associates [15] showed significant differences in reinfarction rate when acute intravenous beta blockers were added to long-term oral therapy.

Using a reverse-logic design, data from Kaiser Permanente (Northern California) were examined to quantify the effect of beta blockers on mortality rate in patients who were not revascularized after MI [16]. Active treatment was a much stronger predictor of survival in patients who did not undergo coronary angiography (and therefore did not undergo revascularization) than in those who did. Thus, the benefit of beta blockers in the general post-MI population is clear and well-evidenced.

Beta blockers and percutaneous coronary interventions
Coronary patients revascularized by nonsurgical means (ie, percutaneous coronary interventions) also show benefit from beta blocker therapy. Revascularization by percutaneous coronary intervention (PCI) and postprocedure medical therapy was reviewed retrospectively by Hasdai and coworkers [17]. The 3831 study subjects who were followed up for more than 18 years were not postinfarction patients, and the study evaluated only symptoms and medication regimens for 6 months after PCI. Sharma and associates [18] prospectively studied 1675 patients who had coronary intervention and correlated preprocedure beta blocker therapy with lower cardiac enzyme release after PCI and lower mortality at intermediate-term (15 ± 3 months) follow-up. Once again, these were not patients with a recent MI.

Silber and colleagues [19] described the role of beta blockers as part of an ideal secondary prevention regimen in individuals identified to have coronary artery disease by virtue of referral for PCI (ie, post-MI, previous PCI, or bypass operation patients). The authors discussed the undertreatment of patients with coronary heart disease after revascularization but did not address outcomes in the post-MI postoperative subgroup and cited no data addressing this question specifically.

Perioperative beta blockers
Beta blocker therapy has been studied in each aspect of perioperative CABG care—in preoperative, intraoperative, and postoperative settings. Weightman and associates [20] looked at the association between preoperative drug therapy and in-hospital mortality rate in patients who had coronary artery procedures. They found that postoperative death was more likely after nitrate therapy and less likely after beta blocker treatment.

Two studies that were collaborative efforts between physicians in Cologne, Germany and the University of Texas-Houston examined intraoperative use of beta blockade as a method of myocardial protection. Geissler and associates [21] studied the patient subgroup that had emergency CABG in the presence of acute myocardial ischemia and the use of high-dose beta blockade as an alternative to cardioplegia. Mehlhorn and colleagues [22] described the use of myocardial beta blockade as an alternative to cardioplegic arrest in the broader population of patients who had coronary artery operations. Both studies measured left ventricular function by transesophageal echocardiography and cardiac metabolism and structure using myocardial biopsy. Although both papers concluded that high-dose beta blockade with continuous coronary perfusion may be a useful alternative for myocardial protection during coronary artery surgery, neither measured long-term outcomes (mortality rate or cardiac events) after CABG. These findings suggest that beta blockers may be of benefit in several subgroups of patients who have CABG.

Beta blockade after coronary artery bypass grafting
Studies of post-CABG beta blocker use are more variable in both design and results. Hirsch and associates [23] reviewed the literature on acute ischemic syndromes after CABG. They found that although administration of beta blockers to preoperative and postoperative CABG patients has increased in recent years, this finding may be attributed to then-published trials demonstrating the drug’s ability to reduce the frequency of postoperative atrial fibrillation. Relatively few studies had addressed the short- and long-term effects of beta blockers on post-CABG ischemia, and the long-term beneficial effect in preventing ischemia remains unclear from that review.

Sjoland and colleagues [24] published a randomized, placebo-controlled trial of the effects of metoprolol treatment on exercise capacity and signs of myocardial ischemia for 2 years after CABG. There was no significant difference in the rate of clinical events (MI, unstable angina, need for intervention with CABG or PCI, or the frequency and severity of angina pectoris) between the two treatment groups, but the event rates were small (eg, 4 of 311 patients who had acute MI). Because the patients in need of beta blockade for clinical reasons (eg, need for open treatment) were excluded from main study participation, only 26% of the patients who had CABG during the study period were enrolled. Furthermore, only two thirds of the patients participating in the metoprolol trial performed an exercise test at 2 years of follow-up, and 31% of the patients were withdrawn from blinded treatment prematurely, which reduced the active treatment study group with fully reported data to approximately 12% of all CABG patients at their center.

In the only prospective trial to address the effect of beta blockers on hard cardiac endpoints, Johan Herlitz and the Division of Cardiology in Goteborg, Sweden conducted a study of the effect of long-term treatment with metoprolol after coronary bypass grafting on death and cardiac events [11]. In a randomized, double-blind, placebo-controlled trial, they evaluated the impact of prophylactic treatment with beta blockers on survival and ischemic events (MI, development of unstable angina, and need for CABG or PCI) during a 2-year follow-up period. The investigators concluded that prophylactic beta blockers did not reduce death or cardiac events after CABG. There are, however, several notable issues of concern with regard to that study. Only 12% of enrolled patients had an acute MI. The study was stopped prematurely because of lower event, lower inclusion, and higher withdrawal rates than predicted. The included patients differed dramatically from those excluded in the following respects: they were healthier, and generally had a better course overall, as evidenced by shorter time in the intensive care unit, shorter time on a respirator, less frequent postoperative complications, and lower perioperative cardiac enzyme levels. Enrolled patients also had shorter extracorporeal circulation time, shorter occlusion (cross-clamp) time, higher number of anastomoses, and more frequent use of mammary artery grafts. By intention to treat, nearly half the patients included in the placebo group were withdrawn from blinded therapy and treated with open-label beta blockers. There was also drug withdrawal in many patients from subgroups subsequently shown to benefit from beta blockade (eg, those with left ventricular dysfunction). By best estimate, less than 4% of eligible patients who had CABG in this sample and met other presently-accepted guidelines for beta blocker therapy received active treatment, and a large percentage of control patients crossed over to open label beta blockers, greatly reducing the study’s power to detect a treatment effect. Thus, no published post-CABG beta blocker studies support a lack of benefit from active therapy.

Beta blocker therapy in coronary artery disease
Several studies did not specifically focus on post-CABG patients but included these subjects in their study cohorts. Sarasin and coworkers [25] performed a prospective study in Switzerland on the use of beta blockers in patients who had MI. It assessed the effect of standardized guidelines on prescription patterns. After guideline implementation, beta blocker prescriptions increased from 38% to 63% (p < 0.001). Although it was not possible to determine the extent of overlap between patients in the control and implementation periods who had both previous MI and prior CABG, one independent predictor of beta blocker prescription was previous CABG (odds ratio = 8.7; 95% CI = 2.5, 30).

In another study of the effect of clinical practice guidelines, Iliadis and associates [26] assessed patients with unstable angina. The rates of CABG and PCI were similar between the two cohorts, defined as patients admitted before versus after institution of the clinical guidelines published by the Agency for Health Care Policy and Research [1]. Guideline implementation was associated with greater use of aspirin and coronary angiography and earlier and more frequent administration of beta blockers. Significantly lower rates of recurrent angina and fewer myocardial infarctions or deaths were seen in the post-guideline group. Overall beta blocker use increased only marginally (16% overall, with 32% of patients receiving new beta blocker prescriptions as defined by these investigators). Surgically revascularized patients were not examined separately for beta blocker benefit.

A report on MI treatment in the United States between 1990 and 1993 from the National Registry of Myocardial Infarction (NRMI) also describes low beta blocker prescription rates [27]. Of patients who had thrombolytic therapy for MI, 17.4% received intravenous beta blockers and 36.3% received these agents orally. Rates were even lower among patients not given thrombolytic therapy, with only 5.5% receiving intravenous and 29.5% receiving oral beta blockers. Bypass operations were performed in 13.3% of MI patients treated with fibrinolytic agents and 10.9% of MI patients who did not receive thrombolytic treatment. The patients who received beta blockers and had CABG were not analyzed separately, and conclusions on this therapeutic combination cannot be drawn.

The Cooperative Cardiovascular Project (CCP), which was sponsored by the Health Care Financing Administration to evaluate care of Medicare patients with the diagnosis of acute MI, is an observational database. Cooperative Cardiovascular Project analyses are retrospective, not randomized, and only determined discharge prescriptions. No method of identifying drug dose, compliance, or duration of therapy after discharge exists. However, the CCP has served as a useful vehicle for many findings regarding postinfarction patients, their treatment, and associated outcomes. Included among the patients in the CCP are patients with coronary artery disease who had surgical revascularization It is worth noting, however, that most patients were not analyzed separately in most publications.

Beta blockers reduced the 1-year mortality rate in elderly diabetics to an extent similar to that in nondiabetics [28]. Krumholz and coworkers [29] developed a model for predicting 1-year mortality rates after MI from the CCP. The entire study sample of 103,164 patients had a 1-year mortality rate of 22% among hospital survivors. They found that 41% of the survivor group were discharged on beta blockers versus 23% of the nonsurvivors. Of the survivors, 9% had had CABG during the hospital stay compared with 2% of the group that died. However, the article provided no information on the proportion of patients who had CABG after MI and received beta blocker therapy, so no recommendations can be made based on this subgroup.

In another CCP paper, Gottlieb and colleagues [30] showed that only 41% of low-risk patients with normal ejection fractions received beta blockers and that the most severely ill patients were even less likely to receive these agents. The high-risk patients included those with diabetes mellitus, chronic obstructive pulmonary disease, a history of congestive heart failure, and older age. Each group showed a decrease in relative risk of death at 2 years after MI when given beta blocker therapy.

Tolbert and associates [31] confirmed these CCP findings and added blacks, smokers, patients with bundle branch block or atrial fibrillation, previous stroke, resuscitated cardiac arrest, and concurrent calcium-channel blocker therapy to the list of those at high risk who receive added benefit from discharge beta blocker prescriptions. However, the subgroup of patients who received CABG after MI was not analyzed separately.

Studies on beta blockers in postinfarction coronary artery bypass grafting patients
Only one study specifically addressed postinfarction CABG patients as the primary study group. Chen and colleagues [12] retrospectively examined the effect of beta blocker therapy on survival in elderly CCP patients who had coronary revascularization after MI. They found that, after adjusting for demographic and clinical factors, patients over age 65 years were less likely to have beta blocker therapy initiated after CABG (OR = 0.44; 95% CI = 0.41, 0.47) or after PCI (OR = 0.89; 95% CI = 0.85, 0.93) relative to the nonrevascularized group. After adjusting for confounding variables, beta blocker treatment was associated with a significantly lower 1-year mortality rate in patients who had CABG or PCI, an effect similar in direction and magnitude to that in the nonrevascularized group. As noted, this retrospective, nonrandomized database fails to provide level I or II evidence, yet it constitutes the strongest evidence to date for beta blocker use specifically in the post-MI, post-CABG patient.


   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
There are several recurring themes in the literature on the effect of beta blocker therapy after MI, with or without revascularization. First, beta blocker administration clearly benefits (through improved primary outcomes or secondary surrogate endpoints) patient populations that are similar to the target postinfarct, post-CABG cohort. Patients with previous MI, those who had nonsurgical revascularization, and those who had CABG in general fared better when these agents were included in their medical regimen. Second, there is underprescription of beta blockers despite the preponderance of evidence for benefit in most of these populations. There seems, in fact, to be an underreporting of benefit, as large groups of patients were excluded from analyses because of stringent, and perhaps questionable, beta blocker contraindication criteria. There may be an excessive application of contraindications as justification for withholding drug therapy, because patients previously thought to be inappropriate for beta blocker treatment (eg, those with left ventricular systolic dysfunction or stable chronic lung disease) have subsequently been shown to derive additional benefit from this therapy through reductions in rates of mortality and cardiac events. Finally, no published studies support the contrary position, that beta blockers lack benefit (or are harmful) in postinfarction CABG patients.

Our ability to contribute to the literature in evidence-based medicine and surgery was limited by the paucity of studies that were designed to answer the question we asked. We attempted, therefore, to look at the outcomes of patients who received beta blockers, after MI or with acute coronary syndromes, who had undergone CABG, to gain insight from these subgroups of the patient samples being analyzed.

We conclude, based on the available science, that beta blockers likely confer a positive benefit in terms of improved survival and fewer complicating cardiac events after MI, even in the face of traditional contraindications to their use. There is no substantive evidence that suggests that patients who undergo surgical coronary revascularization fail to enjoy this benefit. Retrospective observations suggest beta blockers further reduce mortality in post-MI CABG patients.

We propose that future prospective studies be conducted that allow for direct analysis of the effect of beta blockers after CABG, beyond atrial fibrillation prophylaxis, specifically in the large cohort of postinfarction patients. Furthermore, we suggest that efforts be made to develop better long-term monitoring of outcomes after CABG, linking surgical and medical databases for following up patients throughout the course of their cardiac care. This would enable tracking of the cost-benefit of interventions and therapies, identification and quantification of treatment interactions, and will enhance our ability to understand the long-term effects of multimodality therapy in this large and important segment of the population, postinfarction CABG patients.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

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