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| REVIEW ARTICLE |
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| Year : 2023 | Volume
: 24
| Issue : 1 | Page : 41-49 |
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Beta-blockers in the prevention and treatment of ischemic heart disease: Evidence and clinical practice
Omer Khan1, Murti Patel2, Anna N Tomdio2, Jeffrey Beall1, Ion S Jovin2
1 Department of Medicine, Hunter Holmes McGuire VA Medical Center, Richmond, Virginia, USA
2 Department of Medicine, Hunter Holmes McGuire VA Medical Center; Department of Medicine, Virginia Commonwealth University, Richmond, Virginia, USA
| Date of Submission | 22-Aug-2022 |
| Date of Acceptance | 02-Oct-2022 |
| Date of Web Publication | 23-Feb-2023 |
Correspondence Address:
Dr. Ion S Jovin
Department of Medicine, Virginia Commonwealth University, Hunter Holmes McGuire VA Medical Center, 1201 Broad Rock Boulevard Suite 4a-123, Richmond, Virginia 23249
USA
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/heartviews.heartviews_75_22
 Abstract | | |
Coronary artery disease (CAD) is the most prevalent cardiovascular disease characterized by atherosclerotic plaque buildup that can lead to partial or full obstruction of blood flow in the coronary arteries. Treatment for CAD involves a combination of lifestyle changes, pharmacologic therapy, and modern revascularization procedures. Beta-adrenoceptor antagonists (or beta-blockers) have been widely used for decades as a key therapy for CAD. In this review, prior studies are examined to better understand beta-adrenoceptor antagonist use in patients with acute coronary syndrome, stable coronary heart disease, and in the perioperative setting. The evidence for the benefit of beta-blocker therapy is well established for patients with acute myocardial infarction, but it diminishes as the time from the index cardiac event elapses. The evidence for benefit in the perioperative setting is not strong.
Keywords: Acute coronary syndrome, beta-blocker, coronary artery disease
How to cite this article:
Khan O, Patel M, Tomdio AN, Beall J, Jovin IS. Beta-blockers in the prevention and treatment of ischemic heart disease: Evidence and clinical practice. Heart Views 2023;24:41-9 |
How to cite this URL:
Khan O, Patel M, Tomdio AN, Beall J, Jovin IS. Beta-blockers in the prevention and treatment of ischemic heart disease: Evidence and clinical practice. Heart Views [serial online] 2023 [cited 2023 Mar 26];24:41-9. Available from: https://www.heartviews.org/text.asp?2023/24/1/41/370263 |
| Beta-Blockers | |  |
Beta-blockers are a class of medications that inhibit the binding of norepinephrine and epinephrine to beta receptors. While there are three types of beta-receptors found throughout the body, beta-1 and beta-2 receptors are of the greatest clinical interest. Beta-1 receptors are found in the heart, eyes, and kidneys. Beta-2 receptors are also found in the heart but are primarily found in the lungs, gastrointestinal tract, liver, uterus, skeletal muscle, and blood vessels. Beta-3 receptors are mainly found in adipose tissue, with some presence in cardiovascular tissue.[1] When beta-1 receptors are inhibited, they decrease heart rate, decrease myocardial oxygen demand, increase diastolic filling time, and increase coronary perfusion, resulting in anti-ischemic effects in cardiac tissue [Figure 1]. | Figure 1: The effects of beta-blockers on beta-1 receptors in cardiac tissue
Click here to view |
Cardioselective beta-blockers include acebutolol, atenolol, bisoprolol, esmolol, metoprolol, and nebivolol. Only some cardioselective beta-blockers approved by the Food and Drug Administration are used in the treatment of multiple disorders. Although nebivolol is cardioselective, it promotes the release of nitric oxide, leading to a reduction in blood pressure. Labetalol and carvedilol are nonselective beta-blockers that also inhibit alpha-1 receptors, which decreases systemic vascular resistance while preventing reflex tachycardia through beta-1 inhibition. [Table 1] provides a summary of beta-blockers used in clinical practice.
| Beta-Blockers and Cardiovascular Disease | | |
Cardiovascular disease (CVD) is the leading cause of death globally, with an estimated 17.9 million people deaths in 2019, representing about 32% of all deaths.[2] Coronary artery disease (CAD) is the most common type of CVD that killed over 350,000 people in the United States in 2017.[3] Beta-blocker therapy in the treatment of patients with CVD has been used for decades. However, new guidelines to treat hypertension have relegated beta-blockers to a form of second-line treatment behind other anti-hypertensive drugs such as angiotensin-converting enzyme inhibitors, angiotensin receptor blocks, and calcium channel blockers unless the patient has a compelling indication such as CAD or heart failure.[4],[5],[6],[7],[8] This is primarily due to beta-blockers having a greater effect on heart rate than on vasculature tone, as previously described.
Despite benefits in patients with CVD, beta-blocker use in patients with concurrent asthma or chronic obstructive pulmonary disease (COPD) was historically cautioned due to concerns for respiratory complications. As a result, patients were often precluded from receiving beta-blockers and their anti-ischemic benefits. When beta-2 receptors are inhibited, smooth muscle in the airways constricts, leading to increased resistance to airflow and possible bronchospasm.[9],[10],[11] The available literature about beta-blocker use in asthma and COPD has conflicting results. Some evidence suggests beta-blockers contribute to improving health outcomes in patients with COPD by reducing COPD exacerbations.[12],[13] However, other studies have shown an increased risk for hospitalization for COPD exacerbation in patients taking beta-blockers compared to placebo.[14] More recently, a large systematic review and meta-analysis that included observational studies and randomized controlled trials evaluated the effects of beta-blockers in patients with COPD and CVD. This analysis concluded that beta-blocker use was associated with a reduction in hospital and all-cause mortality in patients with COPD and CVD. In addition, the use of cardioselective beta-blockers (beta-1 selective agents) was associated with a reduced risk of COPD exacerbation.[15] Although the available literature is mixed, beta-blockers are generally considered safe in patients with asthma and COPD, it is prudent to use cardioselective beta-blockers in these patients to minimize pulmonary complications.
In recent years, the use of beta-blockers in the treatment of all patients with CAD has been debated.[16],[17] This article aims to review clinical studies to assess the efficacy of beta-blocker therapy in patients presenting with acute coronary syndrome (ACS), stable coronary heart disease, and in the perioperative setting. Using the PubMed platform, a search was conducted using the following keywords: beta-blockers, CAD, ACS, stable coronary heart disease, and perioperative beta-blockers.
| Beta-Blockers In Patients With Acute Coronary Syndrome | | |
ACS is an umbrella term that includes ST-Segment-elevation myocardial infarction (STEMI), Non-STEMI (NSTEMI), and unstable angina (UA). There are several treatment modalities, including medical management with anti-ischemic, antiplatelet, anticoagulant, and lipid-lowering therapies or the same therapies (medical management) plus coronary revascularization. The anti-ischemic effects of beta-blockers make them a foundational component of the treatment and secondary prevention of ACS.[18],[19]
The first clinically significant beta-blockers were synthesized in the 1960s, with the first studies to evaluate the mortality benefit in ischemic heart disease being published in the 1970s. In a multicenter, double-blind, placebo-controlled trial, patients who were diagnosed with myocardial infarction were randomized to receive either practolol or placebo. Results showed a significant reduction in total mortality and sudden deaths after anterior myocardial infarction in patients who received long-term practolol treatment. Practolol has been withdrawn from the market as the study also identified severe adverse reactions associated with long-term practolol treatment, including oculomucocutaneous syndrome and sclerosing peritonitis. The authors postulated that the favorable results of the trial were due to the beta-adrenoceptor blockage rather than to a specific property of practolol itself and they recommended using an alternative beta-blocker.[20]
The Beta-Blocker Heart Attack Trial was a multicenter, randomized, double-blind, placebo-controlled trial published in 1982 that compared propranolol to placebo in patients who had at least one documented myocardial infarction. The results showed that propranolol decreased total mortality as well as mortality related to CVD and arteriosclerotic heart disease in patients who had recently survived an acute myocardial infarction (AMI). The beneficial effects of propranolol were observed for up to 36 months after initiation.[21]
Patients with ST-segment-elevation myocardial infarction
A STEMI occurs when one or more coronary arteries are acutely occluded. In general, the cause of this occlusion is due to plaque fissuring or rupture, resulting in an obstructing thrombus. Some of the major risk factors for STEMI include diabetes mellitus, dyslipidemia, family history of CAD, hypertension, obesity, and smoking.[22],[23],[24] In addition, cocaine use increases the risk of coronary vasoconstriction, leading to a STEMI regardless of risk factors.[25] In the acute phase of STEMI, left ventricular function can be reduced dramatically, leading to an increased risk of heart failure and mortality.[26] Initial treatment of a STEMI focuses on rapid reperfusion through primary coronary intervention, if possible, or through therapy with fibrinolytic.[18]
Early intravenous (IV) administration of beta-blockers in the acute setting of STEMI is recommended in clinical practice guidelines (Class IIA recommendation and Level A evidence).[18] However, based on the publication of the clopidogrel and metoprolol in Myocardial Infarction (COMMIT) Trial, early IV administration of beta-blockers may require more caution. In this randomized, placebo-controlled trial, the study aimed to assess the value of emergent beta-blocker therapy in patients with AMI. Patients were treated with metoprolol or placebo. The two co-primary outcomes were: (1) composite of death, reinfarction, or cardiac arrest (including ventricular fibrillation), and (2) death from any cause during the scheduled treatment period.[27]
Neither of the co-primary outcomes was significantly reduced by allocation to metoprolol. In addition, there was an increase in death in the metoprolol group attributed to cardiogenic shock. On average, the reduction in arrhythmia-related deaths and an increase in shock-related deaths were of similar magnitude. Due to the increased risk of cardiogenic shock and potential for hemodynamic instability, the results of the COMMIT trial resulted in a recommendation for careful consideration of immediate (days 01) beta-blocker therapy in an acute STEMI.[27],[28]
The Effect of METOprolol in CARDioproteCtioN During an AMI trial was a randomized, controlled study aimed to determine if the early use (i.e., before reperfusion therapy) of IV beta-blockers in anterior STEMI patients would reduce infarct size in patients treated by the primary percutaneous coronary intervention (PCI). The primary outcome was infarct size by magnetic resonance imaging (MRI). Prespecified secondary outcomes were the extent of myocardial salvage on MRI, infarct size quantified by MRI in patients with a pre-PCI Thrombolysis in Myocardial Infarction (TIMI) Grade Flow of 0 (no perfusion) to 1 (penetration without perfusion), and infarct size estimated by peak and area under the curve release of creatine kinase (CK) through 72 h. The major prespecified safety secondary outcome was the incidence of major adverse cardiac events (MACE), defined as a composite of death, malignant ventricular arrhythmias, advanced atrioventricular block, cardiogenic shock, and reinfarction during the first 24 h after STEMI.[29]
Infarct size by MRI showed improvement in the IV metoprolol group when compared to the placebo group in the group of patients with a pre-PCI TIMI Grade Flow of 0 to 1. In the group of patients with a pre-PCI TIMI Grade Flow of 2 to 3, the IV metoprolol group did not show a significant improvement in infarct size. In addition, the IV metoprolol group showed improvement in enzymatic infarct size with reduced CK release and improved left ventricular ejection fraction (LVEF) 1 week after STEMI. No increases in adverse effects or cardiogenic shock were observed in the IV metoprolol group.[29]
The early beta-blocker administration before primary PCI in patients with ST-Elevation Myocardial Infarction (EARLY-BAMI) trial was a randomized, placebo-controlled study aimed at assessing the effect of IV metoprolol on myocardial infarct size in STEMI patients eligible for primary PCI before reperfusion therapy. The primary outcome was myocardial infarct size assessed by MRI at 30 days. Secondary outcomes were enzymatic infarct size and ventricular arrhythmias. The safety outcomes were symptomatic bradycardia, symptomatic hypotension, and cardiogenic shock.[30]
In the IV metoprolol group, mean infarct size did not show significant changes between the two groups. In addition, no major differences were observed in LVEF or enzymatic infarct size. There were no significant changes in MACE rates at 30 days. Rates of cardiogenic shock, bradycardia, and hypotension did not change significantly between the two groups. However, the study showed a statistically significant reduction in malignant arrhythmias in the IV metoprolol group.[30]
To assess the role of esmolol in STEMI patients, the beta-blocker therapy in-AMI trial, a prospective, randomized, placebo-controlled study, was conducted. Patients were treated with IV esmolol or placebo. The primary outcome was a maximum change in troponin T from baseline to 48 h. Secondary outcomes included concentrations of CK, CK-MB, N-terminal brain natriuretic peptide (NT-proBNP) at 48 h, echocardiographic ejection fraction at 48 h, 6 weeks, and 6 months, 6-min walking test at 6 weeks and 6 months, and assessment of the quality of life at 48 h, 6 weeks, and 6 months. The safety outcomes included incidences of cardiogenic shock, symptomatic bradycardia, symptomatic hypotension, repeat angina, target vessel revascularization, rehospitalization, cerebral insult, and mortality.[31]
In the IV esmolol group, the maximum change in cardiac biomarkers, which include troponin T, CK, and CK-MB within 48 h was significantly lower than in the placebo group. In addition, peak cardiac biomarkers were lower in the IV esmolol group when compared to the placebo group. Peak NT-proBNP levels increased from baseline in the IV esmolol group. LVEF at 6 months was not significantly different. The 6-min walking test showed improvement at 6 weeks and 6 months. The frequency of ventricular extrasystoles was reduced in the IV esmolol group without increasing the risk of cardiogenic shock. MACE rates were similar in both groups.[31]
In the treatment of patients after an acute STEMI, beta-blocker therapy continues to be recommended, although not in the acute setting. Moreover, in a meta-analysis of early IV beta-blocker therapy in patients with ACS, Chatterjee et al. showed that beta-blockers do not increase the risk of cardiogenic shock.[32]
In addition, prior studies have shown that intervention with beta-blockers shows a reduction in malignant arrhythmias while showing some evidence of improving LVEF and reducing infarct size. Currently, clinical guidelines still recommend early beta-blocker intervention in stable patients with STEMI.
Patients with non-ST-segment elevation myocardial infarction
An NSTEMI occurs when there is an imbalance between myocardial oxygen supply (perfusion) and demand. Most frequently, in the setting of an NSTEMI, the decreased myocardial perfusion is caused by a nonocclusive thrombus. The elevation of cardiac biomarkers is what separates NSTEMI from UA when. The risk factors and treatment are the same as those for STEMI, except for the emergent nature of STEMI, given the acute vessel occlusion. The use of beta-blockers within 24 h of presentation with NSTEMI is a Class 1 recommendation with Level C evidence.[19]
Due to limited data on the use of beta-blockers in patients with NSTEMI, Miller et al. examined this issue using data from the Can Rapid risk stratification of UA patients Suppress ADverse outcomes with early implementation of the ACC/AHA initiative. Clinical endpoints included all-cause mortality during hospitalization, postadmission infarction, in-hospital heart failure, and cardiogenic shock.[33]
Patients treated with beta-blockers within 24 h of symptom onset had lower rates of adjusted and unadjusted in-hospital mortality. In addition, rates of reinfarction and cardiogenic shock were lower. No difference in risk of congestive heart failure was found. This study suggested positive outcomes in the use of beta-blockers in the acute setting and over the long term, including improved in-hospital mortality, rates of reinfarction, and cardiogenic shock. The study acknowledged that prior beta-blocker use was strongly associated with acute beta-blocker use, which makes it difficult to determine if beta-blocker therapy was initiated due to a new ischemic event. In addition, data on the dose, type, or method of administration were not collected.[33]
Another study by Emery et al. evaluated early beta-blocker therapy in patients with NSTEMI. Specifically, the study aimed to evaluate early beta-blocker therapy administered within 24 h of NSTEMI presentation and attempted to determine the impact of early beta-blocker therapy on long-term outcomes. In addition, the study aimed to characterize early beta-blocker therapy in patients presenting with or without heart failure.[34]
In this study, patients who did not receive early beta-blockers were significantly less likely to receive beta-blockers later, regardless of Killip[35] class. Patients who received early beta-blocker therapy were significantly more likely to receive other forms of treatment, including dual antiplatelet therapy, statins, and PCI. In addition, early beta-blocker therapy independently correlated with lower hospital mortality, 6-month mortality, arrhythmias, and cardiogenic shock.[34]
Recently, Nicolau et al. analyzed short-term and long-term clinical outcomes in propensity-matched patients who were admitted to the coronary care unit and who were started or not started on oral beta-blockers within 24 h of NSTEMI presentation.[36] In-hospital mortality rates were found to be lower in patients who received oral beta-blockers within the first 24 h of hospitalization. Furthermore, mean survival times in the long-term follow-up were higher in patients who received oral beta-blockers within the first 24 h of hospitalization. In the high-risk population, cardiogenic shock was significantly decreased in the propensity-matched population. In this study, it was determined that early use of oral beta-blockers in NSTEMI patients leads to improved in-hospital and long-term mortality while decreasing the incidences of cardiogenic shock during the in-hospital phase.[36]
In patients with NSTEMI, current clinical guidelines recommend early beta-blocker therapy. Although clinical studies analyzing the efficacy of beta-blocker therapy in NSTEMI patients are limited when compared to the number of studies on STEMI patients, studies have associated early beta-blocker therapy in NSTEMI patients with lower mortality rates, lower rates of cardiogenic shock, and lower rates of reinfarction.[33],[34],[35],[36]
In the meta-analysis by Chatterjee et al., the authors showed that the use of IV beta-blockers within 12 h of presentation had a statistically significant impact on reducing the risk of myocardial reinfarction.[32]
Patients with unstable angina
UA, like NSTEMI, is a result of decreased myocardial perfusion generally due to plaque progression or thrombosis that results in partial occlusion of the coronary arteries. Cardiac biomarkers are not elevated. Risk factors and treatment are similar to NSTEMI and STEMI.[22],[23],[24] Current guidelines have a Class 1 recommendation with Level C evidence for the use of early beta-blocker therapy.[19]
The Holland Interuniversity Nifedipine/Metoprolol Trial was a randomized, placebo-controlled study that attempted to evaluate the efficacy of nifedipine (a calcium channel blocker) and metoprolol in the treatment of UA. The primary outcome of this study was the recurrence of ischemia or progression to myocardial infarction within 48 h. The groups were divided into placebo, nifedipine, metoprolol, or a combination of nifedipine and metoprolol.[37]
Patients who did not receive prior beta-blocker therapy showed a beneficial effect when treated with metoprolol or when treated with metoprolol and nifedipine. However, patients who were treated with nifedipine only had higher incidences of myocardial infarction. In patients who had received beta-blocker therapy in the past, the addition of nifedipine to the treatment regimen showed favorable outcomes.[37]
To determine the efficacy of esmolol in treating UA, Wallis et al. conducted a small study on patients with known CAD who had daily episodes of chest pain. In this study, patients either received a continuous infusion of esmolol or oral propranolol. Episodes of chest pain were significantly reduced in patients receiving esmolol or propranolol.[38]
A randomized, placebo-controlled study by Brunner et al. analyzed the safety and efficacy of oral carvedilol in patients with new-onset UA. Patients underwent 48-h Holter monitoring to assess ischemic episodes.[39] The study found a significant reduction in ischemic episodes and the mean number of ischemic episodes in patients treated with carvedilol. Due to the reduction in blood pressure and heart rate, the ischemic burden decreased. However, the study acknowledged the risk of hypotension and bradycardia and recommended close monitoring of patients at risk.[39]
Similar to NSTEMI, early beta-blocker therapy continues to be recommended, but the lack of large, frequent clinical trials remains a concern.
Beta-blockers in patients with stable coronary heart disease
Patients with stable coronary heart disease include a broad group of patients, including long-term survivors of ACS, patients with symptomatic stable angina, and asymptomatic patients who have undergone revascularization.[40] Newer European Society of Cardiology guidelines recommends categorizing CAD as ACS or chronic coronary syndrome (CCS). CCS includes patients with CAD and stable anginal symptoms, patients with new onset of heart failure, patients with stabilized symptoms less than 1 year after ACS or revascularization, patients with angina and suspected vasospasm or microvascular disease, and patients with detected CAD at screening.[41]
Although beta-blocker therapy is considered a standard form of treatment in ACS, Bangalore et al. sought to assess the significance of beta-blocker therapy in patients with stable coronary heart disease. In this prospective, observational study, Bangalore et al. analyzed three groups of patients with stable coronary heart disease: (1) Patients with a prior history of myocardial infarction, (2) patients with no history of myocardial infarction, and (3) patients with risk factors for CAD. Using the Reduction of Atherothrombosis for Continued Health registry, patients were included in the propensity-matched analysis to address confounding factors associated with beta-blocker use at baseline. The primary outcome was a composite of cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke. The secondary outcome was the primary outcome and hospitalization for atherothrombosis or revascularization.[42]
In the group with a history of myocardial infarction and risk factors for CAD, event rates were not significantly different in patients with beta-blocker use when compared to patients without beta-blocker use for the primary outcome. Event rates for the secondary outcome were not significantly different. In the group with stable coronary heart disease and no history of myocardial infarction, event rates were not significantly different in patients with beta-blocker use compared to patients without beta-blocker use for the primary outcome. Overall, beta-blocker use was not associated with a decrease in cardiovascular events, including in the group with a history of myocardial infarction.[42]
In a prospective cohort study, Bauters et al. analyzed data on patients with stable coronary heart disease. Those using beta-blockers and those not using beta-blockers were matched on propensity scores for beta-blocker use at baseline. The primary outcome was cardiovascular mortality after a 2-year follow-up.[43]
In the propensity-matched cohort, the cardiovascular mortality rate among patients with beta-blocker use was significantly lower. Noncardiovascular mortality was similar in both groups. In summary, the use of beta-blockers in patients with stable coronary heart disease was associated with a lower risk of cardiovascular mortality.[43]
Studies on beta-blocker therapy in patients with stable coronary heart disease are very limited. A study by Motivala et al. suggested that beta-blocker therapy at discharge among patients 65-year-old or older with stable coronary heart disease and no prior history of myocardial infarction, LVEF <40%, or systolic heart failure undergoing elective PCI do not gain a survival benefit.[44]
In a study by Andersson et al., it was determined that beta-blocker therapy among patients with stable coronary heart disease is only associated with a lower risk of cardiac events in patients who had a recent myocardial infarction.[45] A recent meta-analysis found no significant impact of beta-blockers on mortality but showed some promise in cardioselective beta-blockers improving mortality rates.[46] Still, beta-blockers are widely used for relieving anginal symptoms and reducing ischemic burden due to their negative inotropic and chronotropic effects.
[Table 2.1], [Table 2.2], [Table 2.3], [Table 2.4] provide a summary of the key findings from the aforementioned studies.
Beta-blocker therapy in the perioperative setting
Due to several physiological changes that occur in the perioperative setting, postoperative cardiac complications, especially ACSs, which occur more frequently in patients with preexisting coronary disease, remain a concern. During this period, the physiological stress response can significantly alter homeostatic mechanisms that affect the cardiovascular system. The anti-ischemic effects of beta-blockers play a role in CAD and heart failure [Figure 1]. However, the benefit or lack thereof of beta-blockers in the perioperative setting is still a matter of debate.
Mangano et al. attempted to answer this question a couple of decades ago. In this randomized controlled trial, patients with or at risk for CAD were treated with IV atenolol or placebo before and immediately after noncardiac surgery, followed by oral atenolol during the hospitalization period. The study found that atenolol reduced mortality rates compared to placebo in patients undergoing noncardiac surgery.[47] Similarly, a study by Poldermans et al. showed a perioperative mortality benefit and reduced risk of myocardial infarction in high-risk patients undergoing vascular surgery.[48]
As the usage of beta-blocker therapy in the perioperative setting grew, the Perioperative Ischemic Evaluation trial reported contradictory results. In this large, randomized controlled trial, patients undergoing noncardiac surgery were treated with oral extended-release metoprolol or placebo before surgery and were continued on a daily dose for 30 days. The primary outcome was a composite of cardiovascular death, nonfatal myocardial infarction, and nonfatal cardiac arrest.[49]
The study concluded that perioperative extended-release metoprolol reduced the risk of myocardial infarction, cardiac revascularization, and atrial fibrillation in the 30-day treatment period. However, there was a significant increase in death, stroke, bradycardia, and hypotension.[49]
In the perioperative setting, beta-blocker therapy has shown mixed results. Multiple meta-analyses suggest perioperative cardiac risk reduction, but findings are conflicting on mortality benefits in addition to concerns about an increased risk of stroke, bradycardia, and hemodynamic instability.[50],[51],[52],[53] ACC/AHA and ESC/ESA guidelines recommend that patients undergoing noncardiac surgery and on long-term beta-blocker therapy should continue their perioperative beta-blocker therapy. In addition, perioperative beta-blocker therapy can potentially benefit patients with three or more Revised Cardiac Risk Index (RCRI) risk factors, but patients with a long-term indication for beta-blocker therapy, but no other RCRI risk factors may not benefit from initiation of beta-blocker therapy. Initiation of beta-blocker therapy on the day of surgery is not recommended and should begin at least one day before surgery.[54],[55]
| Conclusion | | |
For the past decades, beta-blocker therapy has helped improve the lives of many patients with CVD and especially with CAD. However, in the era of reperfusion therapy for AMI, the efficacy of beta-blocker therapy, especially in the longer term, has been brought into question. This may be because large infarcts that lead to cardiogenic shock and cardiomyopathy with heart failure are seen less often in the era of rapid reperfusion. In addition, many studies on beta-blocker therapy focused on STEMI patients, with data being extrapolated from those studies to patients with other forms of ACS, such as NSTEMI and UA. Furthermore, there are no randomized, controlled trials of beta-blocker therapy in patients with stable coronary heart disease. Due to mixed findings on beta-blocker therapy in the perioperative setting, questions remain on its efficacy in reducing cardiac complications in patients who are not already taking beta-blockers.
Future studies should consider the type of beta-blocker being used, its method of administration, and the timing of administration in the setting of ACS and perioperative settings while considering modern methods of treatment.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1]
[Table 1], [Table 2]
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