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Acute myocardial infarction: Role of beta blocker therapy

Acute myocardial infarction: Role of beta blocker therapy
Literature review current through: Aug 2023.
This topic last updated: Dec 02, 2020.

INTRODUCTION — For patients with acute myocardial infarction (MI), beta blocker therapy reduces infarct size and early mortality when started early and lowers the risk of death when continued long term. (See "Overview of the acute management of ST-elevation myocardial infarction" and "Overview of the acute management of non-ST-elevation acute coronary syndromes" and "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk" and "Overview of the nonacute management of ST-elevation myocardial infarction" and "Overview of the nonacute management of unstable angina and non-ST-elevation myocardial infarction".)

This topic will discuss the use of beta blockers in patients with acute MI and focus on those without heart failure or reduced left ventricular systolic dysfunction [1]. Other relevant issues regarding beta blockers are discussed elsewhere. (See "Major side effects of beta blockers" and "Ventricular arrhythmias during acute myocardial infarction: Prevention and treatment" and "Primary pharmacologic therapy for heart failure with reduced ejection fraction".)

MECHANISM OF ACTION — Potentially beneficial effects of beta blockers in patients with acute myocardial infarction (MI) include [2]:

Decreased oxygen demand due to the reductions in heart rate, blood pressure, and contractility, and the consequent relief of ischemic chest pain.

Decreased risk of ventricular fibrillation as suggested by experimental studies demonstrating an increase in the ventricular fibrillation threshold and by clinical trials showing a relative risk reduction in sudden cardiac death (eg, 30 to 47 percent) [3-5].

Decreased automaticity, increased electrophysiologic threshold for activation, and slowing of conduction.

Bradycardia prolongs diastole and therefore improves coronary diastolic perfusion and reduces after-depolarizations and triggered activity.

Reduction in remodeling and improvement in left ventricular hemodynamic function, depending upon infarct size and the timing of treatment [6-8]. (See "Pharmacologic therapy of heart failure with reduced ejection fraction: Mechanisms of action", section on 'Beta blockers'.)

Improved left ventricular diastolic function with a less restrictive filling pattern [9]. (See "Treatment and prognosis of heart failure with preserved ejection fraction".)

Slowing of the yearly rate of progression of coronary atherosclerosis in patients with and without MI, as demonstrated by intravascular ultrasound evaluation of atheroma volume [10].

Inhibition of platelet aggregation and thromboxane synthesis [11].

One or more of the above mechanisms may contribute to a reduction in reperfusion injury. (See "Reperfusion injury of the heart", section on 'Definition'.)

INDICATIONS — We treat all patients with acute myocardial infarction (MI) with beta blocker therapy. The evidence supporting the benefit of beta blockers has been obtained primarily from randomized trials that included predominantly patients with ST-elevation myocardial infarction (STEMI). There have been no randomized trials specifically addressing the efficacy of these drugs in non-ST elevation MI (NSTEMI). Observational studies have attempted to evaluate patients with STEMI and those with NSTEMI.

Many of the relevant studies were performed before the routine use of long-term antiplatelet and statin therapy. Thus, it is possible that the absolute magnitude of the mortality benefit from beta blocker described below may be smaller due to the beneficial impact of these preventative medications as well as the use of reperfusion therapies.

Evidence from studies of STEMI patients — The use of beta blockers has been relatively well studied in patients with STEMI treated with no reperfusion, fibrinolytic therapy, or primary percutaneous coronary intervention.

No reperfusion – Randomized trials performed before the use of reperfusion therapy with either fibrinolysis or PCI consistently showed a reduction in cardiovascular mortality of 10 to 25 percent in patients treated with propranolol, metoprolol, or atenolol (figure 1) [12-16]. A 1985 meta-analysis of these studies found a 25 percent reduction in mortality at one year [17]. These patients did not routinely receive statin therapy or a P2Y12 receptor blocker, both of which are now standard of care.

Fibrinolytic therapy – There is no high quality evidence demonstrating a beneficial impact of long-term beta blocker use in patients treated with fibrinolytic therapy. Thus, much of the evidence is indirect, coming from the benefit shown in patients not receiving reperfusion.

The individual studies that evaluated the long-term impact of beta blockade in patients treated with fibrinolysis were limited by small size [18,19], early termination [20], observational design [21], or relatively short duration follow-up [22]. A 1999 meta-analysis, which included trials of patients (n = 24,974) who did or did not receive fibrinolytic therapy, found that beta blockers reduced the odds of death by 23 percent (95% CI 15-31) when taken long term, a result comparable to that seen in patients who received no reperfusion [23].

Primary PCI – The evidence presented above, supporting long-term beta blocker use in patients treated with or without fibrinolysis, provides the basis for a similar recommendation in patients who undergo primary percutaneous coronary intervention (PCI). Some experts have suggested that the benefit of beta blockers in this subpopulation may be reduced by the improvement in outcome afforded by revascularization. There have been no randomized trials and few observational studies of long-term beta blocker therapy patients treated with primary PCI [24-26]. Three large observational studies have come to differing conclusions:

One observational study evaluated mortality in over 20,000 STEMI patients (2005 to 2010) [27]. In a propensity-matched analysis of 2650 patients who received and 1325 who did not receive a beta blocker at discharge, treatment was associated with a lower incidence of all-cause death (2.8 versus 4.1 percent; adjusted hazard ratio 0.46, 95% CI 0.27-0.78) during a median follow-up of about one year. In addition, the result was consistent across all subgroups, including those at relatively low risk, such as those with left ventricular ejection fraction >40 percent and those with single-vessel disease.

In a meta-analysis of 10 observational studies of patients (n = 16,645) with preserved left ventricular ejection fraction who underwent PCI, there was no difference in one-year mortality group between those receiving or not receiving beta blocker [28].

A second study evaluated outcomes in 88,522 STEMI and 81,993 NSTEMI patients (2007 to 2013) who did not have heart failure or left ventricular systolic dysfunction [29]. The overall one-year mortality was 5.2 percent. After adjustment, there was no significant difference in mortality between those with and without beta blocker use in either STEMI or NSTEMI groups.

INITIAL THERAPY — For patients without contraindications, we treat all patients with an oral beta blocker within the first 24 hours after diagnosis. There is no consistent evidence of benefit from the use of intravenous beta blocker use prior to primary percutaneous coronary intervention. We reserve the intravenous route principally for patients with refractory angina and/or hypertension who have ongoing ischemia prior to percutaneous coronary intervention (PCI) in whom there is no hemodynamic instability, risk for shock, heart failure, or other contraindications.

Left ventricular dysfunction/heart failure — Some of the studies discussed directly below were performed before the availability of angiotensin converting enzyme inhibitors and generally did not assess patients with asymptomatic left ventricular dysfunction or heart failure [13,15,16]. They were also performed before the strong beneficial effects of beta blockers in heart failure were demonstrated. The use of beta blockers in patients with heart failure due to systolic dysfunction is discussed elsewhere. (See "Primary pharmacologic therapy for heart failure with reduced ejection fraction".)

Fibrinolytic therapy — While, in the aggregate, the available evidence does not support routine, early initiation of intravenous beta blockade in patients treated with fibrinolytic therapy, we do recommend oral therapy. This recommendation for these patients is based on the overall benefit of beta blockers. (See 'Indications' above.)

Three randomized trials (1989, 1991, and 1993) of ST-elevation myocardial infarction (STEMI) patients treated with fibrinolytic therapy compared early and deferred beta blocker therapy and found no clear evidence of a mortality benefit with early beta blocker [22,30,31]. In these studies, deferred therapy occurred within 24 hours to up to six days.

The findings were somewhat similar in the randomized COMMIT/CCS2 trial of almost 46,000 MI patients (93 percent with ST elevation or left bundle branch block), one-half of whom received fibrinolytic therapy [32]. In this trial, patients were randomly assigned to placebo or to three 5 mg intravenous boluses of metoprolol tartrate followed by oral metoprolol extended release (succinate) 200 mg/day for 30 days. There was no overall mortality benefit from early intravenous beta blocker therapy. However, hemodynamic stability appeared to be an important determinant of the response to beta blockers. There was a significant increase in mortality in patients who presented with hemodynamic compromise that was balanced by a trend toward reduced mortality in patients who were hemodynamically stable. Importantly, patients with hemodynamic compromise and who received beta blockers did not go through a period of up-titration of the drug, raising the possibility that a more careful use of early intravenous beta blocker may improve outcomes.

Some evidence of benefit of early intravenous administration comes from the following studies:

The TIMI-IIB trial randomly assigned 1434 patients to either early intravenous (IV) therapy (metoprolol tartrate, 15 mg IV given in three equal doses at two-minute intervals if tolerated, followed by 50 mg orally twice daily for the first day and 100 mg orally twice daily thereafter) or to delayed oral beta blockade (metoprolol, 50 mg twice daily on day six and 100 mg twice daily thereafter) [30].

Immediate beta blocker therapy may reduce the incidence of intracerebral hemorrhage [30,33]. This effect was suggested in a review of data from 60,329 patients treated with alteplase in the National Registry of Myocardial Infarction [33]. Immediate beta blocker use was associated with a lower incidence of intracerebral hemorrhage (0.67 versus 1 percent for no immediate beta blocker; odds ratio 0.69, 95% CI 0.57-0.84). This apparent benefit was seen in all age groups and in both men and women.

Pooled data from controlled trials involving over 29,000 patients undergoing early, short-term IV administration of a beta blocker showed a 13 percent relative risk reduction in acute mortality [34].

Primary PCI — The evidence presented below does not support the routine use of intravenous beta blocker prior to primary percutaneous coronary intervention (PCI). It should also be kept in mind that clinical experience has shown that intravenous therapy has worsened outcomes in patients with hemodynamic instability or evidence of Killip Class II or III (table 1) heart failure. It must be given cautiously or avoided in these patients.

Two randomized trials, each with significant limitations, have evaluated the role of intravenous beta blocker before primary PCI:

In METOCARD-CNIC, 270 patients with Killip class II or less (table 1) anterior STEMI were randomly assigned to receive intravenous metoprolol (up to three 5 mg boluses of metoprolol tartrate given two minutes apart) or not before reperfusion and all patients received oral metoprolol within 24 hours [35]. The primary end point of infarct size on magnetic resonance imaging performed five to seven days was significantly smaller in the group that was treated early (25.6 versus 32.0 grams; p = 0.012). In addition, left ventricular ejection fraction was higher in the treated group at five to seven days and at six months (adjusted treatment difference 2.67 percent; p = 0.045 and 3.49 percent; p = 0.025) [36]. There was no difference in the safety end point. Limitations of the study include lack of a placebo control and exclusion of patients with inferior MI.

In the EARLY-BAMI trial, 683 patients with STEMI were randomly assigned to intravenous metoprolol (two sequential 5 mg boluses) or placebo before PCI [37]. The first bolus was given in the ambulance. The primary end point of myocardial infarct size (percent of LV), as assessed by cardiac magnetic resonance imaging at 30 days, was performed in 342 patients. There was no difference in infarct size between the two groups (15.3 versus 14.9 percent, respectively). Supporting this finding of no difference was a lack of difference in the secondary end point of peak and area under the creatinine kinase curve. Limitations of the study include failure to achieve the necessary sample size for the primary endpoint, the possibility that the groups with and without measurement of the primary end point were not well balanced, and a smaller than estimated infarct size than predicted, which may have made it harder to find a true difference. There was no difference in the rate of adverse events between the two groups.

Observational studies have also not shown convincing evidence of benefit from early intravenous beta blocker use:

An apparent benefit from preprocedural intravenous administration of a beta blocker was also shown in a retrospective analysis from the CADILLAC trial of 2082 patients [38]. At 30 days, patients who had received a preprocedural beta blocker had a significantly lower mortality than those who had not (1.5 versus 2.8 percent); the lower mortality was limited to patients who had not been receiving an oral beta blocker before admission. (See "Primary percutaneous coronary intervention in acute ST elevation myocardial infarction: Determinants of outcome".)

The optimal timing of beta blocker therapy was evaluated in a study of patients enrolled in the TIMI II trial [31]. A subset of 1390 patients who were eligible for intravenous beta blockade were randomly assigned to 15 mg of IV metoprolol tartrate (followed by oral metoprolol) or oral metoprolol begun on day six. There was no significant difference between the two groups in the in-hospital left ventricular ejection fraction or in mortality at 6 and 42 days. However, by day six, the early therapy group had significant reductions in nonfatal reinfarction (16 versus 31 patients) and recurrent ischemic episodes (107 versus 147 patients).

Patients who do not receive a beta blocker during the first 24 hours because of early contraindications should be re-evaluated for beta blocker candidacy for subsequent therapy.

Choice of drug and route of administration — For most patients, we prefer an oral rather than intravenous beta blocker. A cardioselective oral beta blocker, such as metoprolol or atenolol, is preferred in the setting of an acute myocardial infarction (MI). We use oral metoprolol tartrate 25 to 50 mg every 6 to 12 hours or atenolol 25 to 50 mg twice daily, initially, titrating upward as needed. Short-acting beta blockers are preferred early to allow for more rapid adjustment of dose based on the patient’s blood pressure and heart rate response. Near the time of discharge, we prefer to switch to longer-acting beta blockers.

For the uncommon patient in whom intravenous therapy may be chosen, such as those with ongoing ischemia prior to PCI in whom there is no hemodynamic instability including heart failure, we suggest the following regimens [16] (see 'Primary PCI' above):

Intravenous metoprolol tartrate can be given in 5 mg increments by slow intravenous administration (5 mg over one to two minutes), repeated every five minutes for a total initial dose of 15 mg (three doses). Patients who tolerate this regimen should then receive early oral therapy with either metoprolol succinate 25 to 50 mg daily (dependent on heart rate and blood pressure post-IV infusion) with careful up-titration to as much as 200 mg daily or metoprolol tartrate 25 to 50 mg 2 to 4 times daily beginning 15 to 30 min after the last intravenous dose. We attempt to achieve a discharge heart rate of approximately 70 beats per minute.

Intravenous atenolol can be given in a 5 mg dose followed by another 5 mg five minutes later. Patients who tolerate this regimen should then receive maintenance oral therapy with atenolol 50 mg every 12 hours daily beginning one to two hours after the last intravenous dose. Intravenous atenolol is not available in the United States or Canada.

Esmolol (50 mcg/kg per min increasing to a maximum of 200 to 300 mcg/kg per min), an ultra-short-acting beta blocker, can be given to assess tolerance to beta blockade in patients with borderline or questionable left ventricular function.

Bradycardia and hypotension are the most common limitations to achieving the full dose. In this setting, the rate of administration should be slowed or oral therapy initiated. However, a rigid "cookbook" regimen should not be used since there is a variable sympathetic response to acute MI.

Patients with hypertension — Some experts have recommended the use of intravenous beta blocker therapy for patients with acute MI and hypertension. Due to our concerns regarding this application of intravenous beta blockade, we prefer intravenous nitroglycerin, starting at a low dose, for such patients. (See 'Primary PCI' above.)

Special situations (eg, malignant hypertension or dissecting aortic aneurysm) may require the judicious use of intravenous beta blockade in such patients.

LONG-TERM THERAPY — While all patients with acute myocardial infarction (MI) should receive long-term beta blocker therapy, the optimal duration, dose, and agent are not known. We recommend the use of a long-acting, once daily beta blocker to improve treatment adherence.

Duration — The evidence summarized below supports the use of beta blockers for as long as three years after acute MI. The evidence supporting a longer duration or indefinite therapy is limited. Multiple randomized trials evaluating the optimal duration of beta blocker after acute MI are ongoing.

It should be kept in mind that many patients with prior MI have a clear indication for continued beta blocker therapy such as heart failure with reduced ejection fraction, asymptomatic left ventricular systolic dysfunction, hypertension, or angina. (See "Choice of drug therapy in primary (essential) hypertension" and "Beta blockers in the management of chronic coronary syndrome", section on 'Summary and recommendations' and "Primary pharmacologic therapy for heart failure with reduced ejection fraction".)

We suggest continuing beta blocker indefinitely in patients who had high-risk features at presentation such as cardiogenic shock, heart failure, or chronic kidney disease. For patients without these high-risk features, we suggest that practitioners discuss the potential benefits and risks of continued therapy beyond three years with patients and have them participate in decision making. (See 'Contraindications' below.)

In addition, it is reasonable to discontinue beta blocker therapy, using a tapering protocol carried out over a few weeks, in patients with unacceptable side effects, for whom the financial burden is unacceptable, or in those for whom the use of multiple medications is problematic (polypharmacy). There are no known life-threatening side effects (such as proarrhythmia or malignancy) of long-term beta blocker therapy [39].

Older studies with follow-up of as long as four years suggested a mortality benefit from long-term beta blocker therapy but also raised the possibility that the benefits declined with time [21,23,25,40].

A 2020 observational study confirmed benefit for up to three years but not longer [41]. In this study, nearly 29,000 patients who underwent coronary revascularization for acute MI, who were discharged on beta blocker, and who were event free from death, recurrent MI, or heart failure for one year were followed long term. Mortality was compared in patients who continued beta blocker for one year or longer with those who received therapy for less than one year. All-cause death was lower in patients who continued with beta blocker for one year or longer (adjusted hazard ratio [HR] 0.81, 95% CI 0.72-0.91). The lower risk of all-cause death in those treated for longer than one year lost statistical significance beyond three years after MI (adjusted HR 0.87, 95% CI 0.73-1.03).

Dose — The optimal long-term dose for each beta blocker is not known. Our approach is to attempt to prescribe doses used in randomized trials.

While it makes sense to recommend the doses used in the randomized trials, that approach has not been adopted widely by the medical community. The practice of using a lower dose than used in the trials is supported by a 2015 multicenter registry (OBTAIN) study that evaluated the relationship between dose and survival in 6682 acute MI survivors who were discharged on a beta blocker [42]. Discharge beta blocker dose was compared with target doses used in the randomized trials, grouped as >0 to 12.5 percent, 12.5 to 25 percent, >25 to 50 percent, and >50 percent of target dose. The following was noted after 2.1 years median follow-up:

91.5 percent of all patients were discharged on a beta blocker, with a mean dose 38.1 percent of the target dose. Metoprolol and carvedilol accounted for 92 percent of the drugs used, with target doses of 200 mg/day and 50 mg per day, respectively.

Lower mortality was observed with all doses compared with non-beta blocker therapy.

The primary end point of the study was mortality at two years. Compared with the >50 percent dose, the adjusted hazard ratios for the mortality for the 0 to 12.5, 12.5 to 25, and 25 percent groups were 0.86, 0.80, and 0.96, respectively. None of these were statistically significant.

This study raises the possibility that doses lower than those used in clinical trials may lead to similar or better outcomes. However, the study has significant limitations and we recommend doses uses in randomized trials.

Agent — For long-term administration, we believe that the benefit from beta blockers is a class effect and that agents without intrinsic sympathomimetic activity (ISA) are preferred [43-45]. In a 1999 meta-analysis of randomized controlled trials, there was no significant difference in benefit with cardioselective compared to nonselective drugs, but there was an almost significant trend toward less benefit with drugs that have ISA [23].

We start with a beta-1-selective agent in most patients. Usual initial doses are metoprolol tartrate (immediate release preparation) 25 to 50 mg two to four times daily or metoprolol succinate (extended release preparation) 25 to 200 mg daily or atenolol 50 to 100 mg divided twice daily. When possible, we use the longer-acting preparation. For patients in whom there is a concern for intolerance to these doses, lower initial doses should be used; in this setting, up-titration should occur as promptly as possible.

For patients who are initially treated with metoprolol tartrate, we give the drug twice daily long term or switch to metoprolol succinate.

Patients with heart failure with reduced ejection fraction (HFrEF) should be treated long-term with carvedilol, extended-release preparation metoprolol succinate, or bisoprolol. (See "Primary pharmacologic therapy for heart failure with reduced ejection fraction".)

Heart rate goal — We suggest reducing the heart rate to between 55 and 70 beats per minute while maintaining a systolic pressure above 90 mmHg, based on a small amount of published evidence and our clinical experience.

An inverse relationship between short-term and long-term mortality and the degree of heart rate reduction with beta blockade after MI was suggested in the 1980s [46]. This hypothesis was confirmed in a 2007 meta-regression analysis of 17 trials including nearly 31,000 MI patients who were placed on either a beta blocker (14 trials) or a rate slowing calcium channel blocker (three trials) [47]. There was a statistically significant and progressive reduction in the odds ratio for all-cause and cardiac death and non-fatal MI as the resting heart rate was slowed from 5 to 15 beats per minute compared to baseline. However, the optimal degree of heart rate lowering is unknown.

CONTRAINDICATIONS

Absolute contraindications — Potential absolute contraindications to the immediate use of beta blocker therapy include the following groups:

Hemodynamically compromised individuals, including those with hypotension with or without shock [43,44].

Patients with active bronchospasm, heart block greater than first degree (unless the patient has a permanent pacemaker), those with first degree heart block and a PR interval >0.30 seconds, or severe bradycardia. The rate at which a patient is labelled as having severe bradycardia is somewhat age dependent, as heart rate tends to decrease normally with age. While there is little evidence upon which to guide recommendations for the use of beta blockers in patients with bradycardia, we do not start such therapy in patients with a heart rate <40 beats per minute (bpm). Above 40 BPM, our threshold for starting beta blockers is lower in younger patients. Some of our experts use a higher threshold than 40 bpm.

Patients with overt heart failure, including pulmonary edema. However, there is a strong indication for carefully initiated oral beta blocker therapy (beginning at very low doses) in such patients whose heart failure has been brought under control prior to discharge. (See "Primary pharmacologic therapy for heart failure with reduced ejection fraction".)

The role of beta blocker therapy in patients with myocardial infarction (MI) precipitated by cocaine use is controversial. (See "Cocaine: Acute intoxication".)

Patients with comorbidities — A survival benefit from beta blockade is seen in patients with relative or potential contraindications to such therapy such as chronic obstructive pulmonary disease (COPD)/asthma, reduced left ventricular (LV) ejection fraction, treated heart failure, diabetes mellitus, and peripheral artery disease [21,48-55].

COPD/asthma — Beta blockers are safe and effective in MI patients with mild to moderate pulmonary disease, as illustrated by the following data from observational studies:

In a study of 54,962 MI patients over the age of 65 years who had no contraindications to beta blocker therapy, beta blockers were associated with a lower one-year mortality in patients with COPD or asthma who were not on beta agonist therapy (adjusted relative risk 0.85 compared to no beta blockers); the lower mortality was similar to that seen in patients without COPD or asthma [51]. In contrast, beta blockers had no difference in survival in patients who were using a beta agonist or who had severe COPD or asthma.

In a review of over 200,000 MI patients from the Cooperative Cardiovascular Project, survival among patients with COPD was significantly higher in those treated with a beta blocker (83 versus 72 percent without a beta blocker) at two years (figure 2) [21].

In a cohort study of 1063 patients with mild or moderate COPD who sustained a first MI, mortality was lower in those who started or were previously taking a beta blocker (adjusted hazard ratio 0.50, 95% CI 0.36-0.69 and 0.59, 95% CI 0.44-0.79, respectively) during nearly three years of follow-up [56].

Diabetes mellitus — Concern about the possibility of masking hypoglycemic symptoms or worsening glycemic control has made some physicians reluctant to prescribe beta blockers to patients with diabetes during an acute MI. However, these concerns have been overstated, and analysis of outcomes of diabetic subgroups in several postinfarction beta blocker trials documents an overall benefit from the use of beta blockers that is at least equivalent to and may be greater than that seen in patients without diabetes. (See "Acute myocardial infarction: Patients with diabetes mellitus", section on 'Beta blockers'.)

Peripheral artery disease — Although there has been a concern involving the use of beta blockers in patients with intermittent claudication, there appears to be no adverse effect of beta-1 selective blockers on claudication symptoms [57-59]. The use of beta blockers in patients with peripheral artery disease, including abdominal aortic aneurysm, is discussed elsewhere. (See "Management of claudication due to peripheral artery disease".)

Patients treated with antiarrhythmic drugs — Beta blockers are effective in patients treated with antiarrhythmic drugs (figure 3 and figure 4) [34,39,60]. This was illustrated in a pooled analysis of patients in the CAMIAT and EMIAT trials of amiodarone in acute MI [60]. The relative risks for all-cause mortality, cardiac death, arrhythmic deaths, and resuscitated cardiac arrest were lower for patients receiving beta blockers along with amiodarone than for those without a beta blocker, with or without amiodarone. This interaction was significant for cardiac death and for arrhythmic death or resuscitated cardiac arrest (relative risk 0.59 and 0.39) (figure 5A-B) [60]. Antiarrhythmic drugs other than amiodarone have not been similarly studied. (See "Ventricular arrhythmias during acute myocardial infarction: Prevention and treatment".)

In patients treated with beta blocker therapy in whom amiodarone is initiated, there is an increased risk of bradycardia. We advise close monitoring of the heart rate in these patients. For patients with HR <70 beats per minute, we recommend lowering the beta blocker dose at the time of initiation of amiodarone. (See "Amiodarone: Adverse effects, potential toxicities, and approach to monitoring", section on 'Adverse cardiac effects' and "Amiodarone: Clinical uses", section on 'Dose adjustment'.)

RECOMMENDATIONS OF OTHERS — Our approach to the use of beta blockers in patients with acute myocardial infarction (MI) is similar to that made in the 2015 European Society of Cardiology guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation [61].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Non-ST-elevation acute coronary syndromes (non-ST-elevation myocardial infarction)" and "Society guideline links: ST-elevation myocardial infarction (STEMI)".)

SUMMARY AND RECOMMENDATIONS

Beta blockers should be given to all myocardial infarction (MI) patients with heart failure (HF) and a left ventricular ejection fraction ≤40 percent. However, in patients with active HF, initiation should be delayed until the HF is under control. (See 'Left ventricular dysfunction/heart failure' above.)

For all patients who have sustained an acute MI without HF and preserved left ventricular systolic function and who have been treated with standard-of-care risk factor interventions, as well as dual antiplatelet therapy, we suggest treatment with an oral beta blocker (Grade 2C). (See 'Indications' above.)

For all patients with acute MI, we recommend initiation of oral beta blockers within the first 24 hours, as long as no contraindications are present (Grade 1B). (See 'Indications' above and 'Absolute contraindications' above.)

Patients who do not receive a beta blocker during the first 24 hours because of early contraindications should be reevaluated for beta blocker candidacy prior to discharge. If on reevaluation the preexisting contraindication is no longer present, a beta blocker should be administered. (See 'Primary PCI' above.)

The optimal duration of beta blocker therapy is not known. We treat most patients for a minimum of three years. In high risk patients, such as those who present with cardiogenic shock, heart failure, or chronic kidney disease, we treat for longer than three years. (See 'Long-term therapy' above.)

We attempt a target heart rate of between 55 and 70 beats per minute while maintaining a systolic pressure above 90 mmHg. (See 'Heart rate goal' above.)

Absolute contraindications to the initiation of beta blocker therapy include cardiogenic shock, active bronchospasm, severe bradycardia or heart block greater than first degree (unless the patient has a permanent pacemaker), and patients with overt heart failure. Patients with treated heart failure or bronchospastic lung disease, peripheral artery disease, or diabetes mellitus should receive beta blocker therapy; however, these individuals should be monitored for the development of adverse side effects. (See 'Contraindications' above.)

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Topic 96 Version 50.0

References

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