Role of Beta Blockers On AMI

Acute myocardial infarction: Role of beta blocker therapy
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Official reprint from UpToDate

www.uptodate.com 2015 UpToDate

Authors
Robert S Rosenson, MD
Guy S Reeder, MD
Harold L Kennedy, MD, MPH
Section Editor
Christopher P Cannon, MD
Deputy Editor
Gordon M Saperia, MD, FACC
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2015. | This topic last updated: Jun 23, 2014.
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. The evidence supporting the benefit of beta blockers has been obtained
primarily from randomized trials that included predominantly patients with ST-elevation MI (STEMI). There have been no randomized trials
specifically addressing the efficacy of these drugs in non-ST elevation MI (NSTEMI); however, there is no observational evidence to suggest
different outcomes in patients with NSTEMI. (See "Overview of the acute management of ST elevation myocardial infarction" and "Overview of
the acute management of unstable angina and non-ST elevation myocardial infarction" and "Secondary prevention of cardiovascular disease".)
This topic will discuss the use of beta blockers in patients with acute MI. Other relevant issues regarding beta blockers are discussed
elsewhere. (See "Major side effects of beta blockers" and "Use of beta blockers and ivabradine in heart failure with reduced ejection fraction"
and "Rationale for and clinical trials of beta blockers in heart failure due to systolic dysfunction" and "Prophylaxis against ventricular
arrhythmias during and after acute myocardial infarction" and "Clinical features and treatment of ventricular arrhythmias during acute
myocardial infarction".)
MECHANISM OF ACTION Potentially beneficial effects of beta blockers in patients with acute myocardial infarction (MI) include [1]:
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) [2-4].
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 [5-7]. (See "Cardiac remodeling: Clinical assessment and therapy".)
Improved left ventricular diastolic function with a less restrictive filling pattern [8]. (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 [9].
Inhibition of platelet aggregation and thromboxane synthesis [10].
One or more of the above mechanisms may contribute to a reduction in reperfusion injury. (See "Ischemic reperfusion injury of the heart",
section on 'Definition'.)
INDICATIONS Unless contraindicated, all patients with acute myocardial infarction (MI) should receive beta blocker therapy. While the
evidence is robust for patients with ST-elevation MI (STEMI) treated without fibrinolysis or percutaneous coronary intervention (PCI), this
recommendation also applies to STEMI patients who are treated with reperfusion as well as those with non-ST elevation MI (NSTEMI) [11,12].
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.
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) [13-17]. A 1985
meta-analysis of these studies found a 25 percent reduction in mortality at one year [18].
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
[19,20], early termination [21], observational design [22], or relatively short duration follow-up [23]. 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 [24].
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 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.
The largest observational study of STEMI patients who underwent primary PCI evaluated over 20,000 such individuals [25]. In a propensitymatched 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
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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. Prior smaller observational studies provided inconsistent evidence of
benefit [26-28].
INITIAL THERAPY For patients without contraindications, we treat all patients with an oral beta blocker within the first 24 hours after
diagnosis. While some studies supporting this recommendation for early beta blocker tested intravenous beta blocker, we are concerned about
the potential for development of hemodynamic instability. We reserve the intravenous route principally for patients with refractory angina who
have ongoing ischemia prior to percutaneous coronary intervention (PCI) in whom there is no hemodynamic instability including heart failure.
The finding of benefit from early initiation is consistent with some of the mechanisms by which beta blockers might improve clinical outcomes.
(See 'Mechanism of action' above.)
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 [23,29,30]. 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 [31]. 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 uptitration 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) [29].
Immediate beta blocker therapy may reduce the incidence of intracerebral hemorrhage [29,32]. This effect was suggested in a review of
data from 60,329 patients treated with alteplase in the National Registry of Myocardial Infarction [32]. 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 [11].
Primary PCI The evidence presented below raises the possibility that intravenous beta blocker therapy improves short-term (and possible
long-term) outcomes when given before primary percutaneous coronary intervention (PCI) in patients with STEMI [33].
However, based on our clinical experience that 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, we do not recommend its routine use. Potential candidates for early,
intravenous beta blocker include those with ongoing ischemia and no evidence of hemodynamic compromise, including heart failure.
The best evidence for early initiation in patients treated with current recommended therapies (eg, statins, dual antiplatelet therapy) comes from
the METOCARD-CNIC trial [34]. 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. 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) [35]. In addition, 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.
An apparent benefit from preprocedural intravenous administration of a beta blocker was shown in a retrospective analysis from the
CADILLAC trial of 2082 patients [36]. 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 [30]. (See "Trials of conservative
versus early invasive therapy in unstable angina and non-ST elevation myocardial infarction", section on 'TIMI IIIB trial'.) 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).
In an observational study of 2537 patients enrolled in primary angioplasty trials, those who received beta blocker therapy before primary
angioplasty, compared to those who did not, had lower adjusted in-hospital mortality (odds ratio [OR] 0.41, 95% CI 0.20-0.84) and
nonsignificantly lower one-year mortality (OR 0.72, 95% CI 0.47-1.08). The dose and route of administration of beta blocker was not reported.
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.
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Choice of drug 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 patients 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 [17] (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
maintenance oral therapy with metoprolol succinate 50 mg daily beginning 15 min after the last intravenous dose.
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 twice 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.)
LONG-TERM THERAPY The optimal duration of beta blocker therapy after myocardial infarction (MI) is not known. We believe the
evidence supports the use of beta blockers in patients with MI for as long as three years. The evidence supporting a longer duration, or
indefinite therapy, is limited. We suggest doing so in patients with 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 with patients and have them participate in decision making. (See 'Contraindications' below.)
We believe 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 [37].
Many patients have been continued on this therapy indefinitely based on a 1999 meta-analysis of over 50,000 patients that showed a 23
percent reduction in death at a mean follow-up of 1.4 years [24]. In addition to the relatively short duration of follow-up, application of the
conclusions of this meta-analysis is limited as reperfusion and medical (aspirin and statin) therapies were underutilized routinely. The findings
in this meta-analysis were supported by a large observational study published in 1998 [22].
A more contemporary evaluation of the potential benefit from long-term beta blocker use was made in a 2012 observational study of over
14,000 patients with known prior MI enrolled in the international REACH registry [38]. Patients were enrolled in 2003 and 2004 and followed
prospectively for up to four years. The primary outcome was a composite of cardiovascular death, nonfatal MI, or nonfatal stroke. Propensity
score matching identified 3599 pairs of patients with and without beta blocker use. Aspirin and statin use (each) was approximately 75 percent.
After a median follow-up of 44 months, there was a trend toward a lower incidence of the primary outcome with beta blocker therapy (16.9
versus 18.6 percent, respectively; hazard ratio 0.90, 95% CI 0.79-1.03). However, little difference was seen in the event rates in the beta
blocker and no beta blocker groups as early as two years.
A 2013 observational study evaluated outcomes in 5628 patients with ST-elevation MI (STEMI) treated with primary percutaneous coronary
intervention. During a median follow-up of nearly four years, mortality rates did not differ between patients with and without beta blocker
therapy (5.2 versus 6.2 percent) [27]. The absence of a significant difference persisted after multivariate and propensity score matching.
However, subgroup analyses revealed that beta blocker treatment was associated with a significantly lower mortality for only high-risk patients,
such as those with heart failure.
The role of long-term beta blocker therapy in patients with significant left ventricular systolic dysfunction is discussed separately. (See
"Rationale for and clinical trials of beta blockers in heart failure due to systolic dysfunction", section on 'Degree and duration of beta blockade'
and "Use of beta blockers and ivabradine in heart failure with reduced ejection fraction", section on 'Dosing'.)
Choice of drug For long-term administration, we believe that the benefit from beta blockers (table 2) is a class effect and that agents
without intrinsic sympathomimetic activity (ISA), such as pindolol, are preferred [39-41]. 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 [24].
We start with a beta-1-selective agent in most patients. Usual initial doses are metoprolol tartrate (immediate release preparation) 50 to 100
mg twice daily or metoprolol succinate (extended release preparation) 50 or 100 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.
Patients with heart failure and systolic left ventricular dysfunction should be treated long-term with carvedilol, extended-release preparation
metoprolol, or bisoprolol. (See "Overview of the therapy of heart failure with reduced ejection fraction", section on 'Beta blocker'.)
Heart rate goal We suggest reducing the heart rate below 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 [42]. This hypothesis was confirmed in a 2007 meta-regression analysis of 17 trials including nearly 31,000 MI patients
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who were placed on either a beta blocker (14 trials) or a rate slowing calcium channel blocker (three trials) [43]. 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 [39,40].
Patients with active bronchospasm, severe bradycardia, or heart block greater than first degree (unless the patient has a permanent
pacemaker).
Patients with myocardial infarction (MI) precipitated by cocaine use; there is a risk of precipitating coronary artery spasm [44]. (See
"Evaluation and management of the cardiovascular complications of cocaine abuse", section on 'Reperfusion and revascularization'.)
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 "Use
of beta blockers and ivabradine in heart failure with reduced ejection fraction", section on 'Initiation of therapy'.)
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 [22,45-52].
COPD/asthma Beta blockers are safe and effective in MI patients with mild to moderate pulmonary disease (table 3) 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 [48]. 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) [22].
In a cohort study of 1063 patients with mild or moderate COPD (table 3) who sustained a first MI, mortality was lower in those who
started or were previously taking a beta blocker (adjusted hazard ratios 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 [53].
LV dysfunction/heart failure The benefit of beta blockers in post-MI patients in the trials described above were performed before the
availability of angiotensin converting enzyme (ACE) inhibitors and generally did not assess patients with asymptomatic LV dysfunction or heart
failure [14,16,17]. They were also performed before the 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 "Use of beta blockers and ivabradine in heart
failure with reduced ejection fraction".)
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 "Treatment of acute myocardial
infarction in 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 [54-56]. The use of beta blockers in
patients with peripheral artery disease, including abdominal aortic aneurysm, is discussed elsewhere. (See "Management of claudication".)
Patients treated with antiarrhythmic drugs Beta blockers are effective in patients treated with antiarrhythmic drugs (figure 3 and
figure 4) [11,37,57]. This was illustrated in a pooled analysis of patients in the CAMIAT and EMIAT trials of amiodarone in acute MI [57]. 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) [57]. Antiarrhythmic drugs other than
amiodarone have not been similarly studied. (See "Role of antiarrhythmic drugs for ventricular arrhythmias in patients with a prior myocardial
infarction" and "Prophylaxis against ventricular arrhythmias during and after acute myocardial infarction".)
RECOMMENDATIONS OF OTHERS Our approach to the long-term use of beta blockers in patients with acute myocardial infarction (MI) is
similar to that made in the 2011 guideline on secondary prevention published by the American Heart Association/American College of
Cardiology [58]. The 2011 European Society of Cardiology guideline for the management of acute coronary syndromes in patients presenting
without persistent ST-segment elevation does not make a recommendation for or against indefinite beta blocker use [59].
SUMMARY AND RECOMMENDATIONS
In the broad range of patients with ST elevation and non-ST elevation myocardial infarction (MI), including those who have or have not
received revascularization, beta blockers reduce short-term complications and improve long-term survival. For all patients who have
sustained an acute MI, we recommend treatment with oral beta blockers (Grade 1A). (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. (See 'Primary PCI' above.)
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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 to get the heart rate below 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), MI precipitated by cocaine use, 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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myocardial infarction. Results of the Thrombolysis in Myocardial Infarction (TIMI) II-B Study. Circulation 1991; 83:422.
30. Comparison of invasive and conservative strategies after treatment with intravenous tissue plasminogen activator in acute myocardial
infarction. Results of the thrombolysis in myocardial infarction (TIMI) phase II trial. The TIMI Study Group. N Engl J Med 1989; 320:618.
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randomised placebo-controlled trial. Lancet 2005; 366:1622.
32. Barron HV, Rundle AC, Gore JM, et al. Intracranial hemorrhage rates and effect of immediate beta-blocker use in patients with acute
myocardial infarction treated with tissue plasminogen activator. Participants in the National Registry of Myocardial Infarction-2. Am J
Cardiol 2000; 85:294.
33. Faxon DP. Beta-blocker therapy and primary angioplasty: what is the controversy? J Am Coll Cardiol 2004; 43:1788.
34. Ibanez B, Macaya C, Snchez-Brunete V, et al. Effect of early metoprolol on infarct size in ST-segment-elevation myocardial infarction
patients undergoing primary percutaneous coronary intervention: the Effect of Metoprolol in Cardioprotection During an Acute Myocardial
Infarction (METOCARD-CNIC) trial. Circulation 2013; 128:1495.
35. Pizarro G, Fernndez-Friera L, Fuster V, et al. Long-term benefit of early pre-reperfusion metoprolol administration in patients with acute
myocardial infarction: results from the METOCARD-CNIC trial (Effect of Metoprolol in Cardioprotection During an Acute Myocardial
Infarction). J Am Coll Cardiol 2014; 63:2356.
36. Halkin A, Grines CL, Cox DA, et al. Impact of intravenous beta-blockade before primary angioplasty on survival in patients undergoing
mechanical reperfusion therapy for acute myocardial infarction. J Am Coll Cardiol 2004; 43:1780.
37. Kennedy HL, Brooks MM, Barker AH, et al. Beta-blocker therapy in the Cardiac Arrhythmia Suppression Trial. CAST Investigators. Am J
Cardiol 1994; 74:674.
38. Bangalore S, Steg G, Deedwania P, et al. -Blocker use and clinical outcomes in stable outpatients with and without coronary artery
disease. JAMA 2012; 308:1340.
39. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial
infarction. www.acc.org/qualityandscience/clinical/statements.htm (Accessed on August 24, 2006).
40. www.acc.org/qualityandscience/clinical/statements.htm (Accessed on September 18, 2007).
www.acc.org/qualityandscience/clinical/statements.htm (Accessed on September 18, 2007).
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their first myocardial infarction and persistent electrocardiographic ST-segment depression. Am Heart J 1998; 135:261.
42. Kjekshus JK. Importance of heart rate in determining beta-blocker efficacy in acute and long-term acute myocardial infarction
intervention trials. Am J Cardiol 1986; 57:43F.
43. Cucherat M. Quantitative relationship between resting heart rate reduction and magnitude of clinical benefits in post-myocardial
infarction: a meta-regression of randomized clinical trials. Eur Heart J 2007; 28:3012.
44. Kloner RA, Hale S. Unraveling the complex effects of cocaine on the heart. Circulation 1993; 87:1046.
45. Spargias KS, Hall AS, Greenwood DC, Ball SG. beta blocker treatment and other prognostic variables in patients with clinical evidence
of heart failure after acute myocardial infarction: evidence from the AIRE study. Heart 1999; 81:25.
46. Dargie HJ. Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN
randomised trial. Lancet 2001; 357:1385.
47. Lichstein E, Hager WD, Gregory JJ, et al. Relation between beta-adrenergic blocker use, various correlates of left ventricular function
and the chance of developing congestive heart failure. The Multicenter Diltiazem Post-Infarction Research Group. J Am Coll Cardiol
1990; 16:1327.
48. Chen J, Radford MJ, Wang Y, et al. Effectiveness of beta-blocker therapy after acute myocardial infarction in elderly patients with chronic
obstructive pulmonary disease or asthma. J Am Coll Cardiol 2001; 37:1950.
49. Vantrimpont P, Rouleau JL, Wun CC, et al. Additive beneficial effects of beta-blockers to angiotensin-converting enzyme inhibitors in the
Survival and Ventricular Enlargement (SAVE) Study. SAVE Investigators. J Am Coll Cardiol 1997; 29:229.
50. Exner DV, Dries DL, Waclawiw MA, et al. Beta-adrenergic blocking agent use and mortality in patients with asymptomatic and
symptomatic left ventricular systolic dysfunction: a post hoc analysis of the Studies of Left Ventricular Dysfunction. J Am Coll Cardiol
1999; 33:916.
51. Gundersen T, Kjekshus J. Timolol treatment after myocardial infarction in diabetic patients. Diabetes Care 1983; 6:285.
52. Malmberg K, Herlitz J, Hjalmarson A, Rydn L. Effects of metoprolol on mortality and late infarction in diabetics with suspected acute
myocardial infarction. Retrospective data from two large studies. Eur Heart J 1989; 10:423.
53. Quint JK, Herrett E, Bhaskaran K, et al. Effect of blockers on mortality after myocardial infarction in adults with COPD: population
based cohort study of UK electronic healthcare records. BMJ 2013; 347:f6650.
54. Califf RM, Lokhnygina Y, Velazquez EJ, et al. Usefulness of beta blockers in high-risk patients after myocardial infarction in conjunction
with captopril and/or valsartan (from the VALsartan In Acute Myocardial Infarction [VALIANT] trial). Am J Cardiol 2009; 104:151.
55. Radack K, Deck C. Beta-adrenergic blocker therapy does not worsen intermittent claudication in subjects with peripheral arterial disease.
A meta-analysis of randomized controlled trials. Arch Intern Med 1991; 151:1769.
56. Solomon SA, Ramsay LE, Yeo WW, et al. beta blockade and intermittent claudication: placebo controlled trial of atenolol and nifedipine
and their combination. BMJ 1991; 303:1100.
57. Boutitie F, Boissel JP, Connolly SJ, et al. Amiodarone interaction with beta-blockers: analysis of the merged EMIAT (European
Myocardial Infarct Amiodarone Trial) and CAMIAT (Canadian Amiodarone Myocardial Infarction Trial) databases. The EMIAT and
CAMIAT Investigators. Circulation 1999; 99:2268.
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and other Atherosclerotic Vascular Disease: 2011 update: a guideline from the American Heart Association and American College of
Cardiology Foundation. Circulation 2011; 124:2458.
59. Hamm CW, Bassand JP, Agewall S, et al. ESC Guidelines for the management of acute coronary syndromes in patients presenting
without persistent ST-segment elevation: The Task Force for the management of acute coronary syndromes (ACS) in patients presenting
without persistent ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2011; 32:2999.
Topic 96 Version 24.0
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Page 7 of 16
GRAPHICS
Benefit of propranolol after myocardial infarction
Results of the Beta Blocker Heart Attack Trial which randomized 3837
patients with an acute myocardial infarction to propranolol or placebo. At an
average follow-up of 25 months, propranolol significantly reduced total,
cardiovascular, and sudden death mortality and reduced the incidence of
nonfatal infarction and all coronary events. Benefit occurred in all patient
groups, but was more marked in those with heart failure (HF).
Data from Chadda K, Goldstein S, Byington R, et al. Circulation 1986; 73:503.
Graphic 80761 Version 2.0
04/10/2015
Page 8 of 16
Killip classification of acute myocardial infarction

Class I
No evidence of heart failure
Class
II
Findings consistent with mild to moderate heart failure (S3 gallop, lung rales less than one-half way up the
posterior lung fields, or jugular venous distension)
Class
III
Overt pulmonary edema
Class
IV
Cardiogenic shock
04/10/2015
Page 9 of 16
Beta blocker properties

Drug
Acebutolol
Alpha
blockade
Beta-1
selectivity
No
Yes
ISA
Yes
MSA
Lipophilicity
Yes
Low
Usual
dose*
100 to 400 mg
twice per day
Half life,
hours
3 to 4
Elimination
Hepatic
(primary)
Renal
(secondary)
Atenolol
No
Yes
No
No
Low
50 to 200 mg
once daily
6 to 9
Renal
Betaxolol
No
Yes
No
Yes
Low
10 to 20 mg
once daily
14 to 22
Hepatic
(primary)
Renal
(secondary)
Bisoprolol
No
Yes
No
No
Moderate
2.5 to 20 mg
once daily
9 to 12
Renal and
hepatic
Carteolol
No
No
Yes
No
Low
2.5 to 5 mg
Renal
3.125 to 25
mg twice per
day
7 to 10
Biliary
(primary)
IV only 250 to
500
micrograms/kg
over one
minute then
25 to 50
micrograms/kg
per minute as
IV infusion;
titrate
incrementally
up to
9 minutes
Blood
esterases
3 to 4
Hepatic
3 to 4
(7 to 9 hours
in poor
metabolizers)
Hepatic via
CYP2D6
(polymorphic)
Orally 50 to
400 mg once
Apparent
half-life
Hepatic via
CYP2D6
daily
prolonged by
continuous
osmotic
release over
(polymorphic)
once daily
Carvedilol
Esmolol
Yes
No
No
Yes
No
No
Yes
No
High
Low
Hepatic
(secondary)
maximum of
300
microgram/kg
per minute
Labetalol
Metoprolol
tartrate
Yes
No
No
Yes
Yes
(Beta 2 )
Low
No
Low
Moderate
IV 20 mg
Orally 100-400
mg two or
three times
per day
Moderate
IV 1.25 to 5
mg
Orally 25 to
100 mg two or
three times
per day
Metoprolol
succinate
No
Yes
No
Low
Moderate
(extended
release)
~20 hours
Nadolol
No
No
No
No
Low
40 to 160 mg
once daily
20 to 24
Renal
Nebivolol
No
Yes
No
No
High
5 to 40 mg
once daily
10 to 12
(19 to 32
Hepatic
poor
metabolizers)
Oxprenolol
No
No
Yes
Yes
Moderate
40 to 80 mg
three times
per day
1.5
Hepatic
04/10/2015
Penbutolol
No
No
Yes
No
High
Page 10 of 16
10 to 40 mg
Hepatic
3 to 4
Hepatic
(primary)
once daily
Pindolol
No
No
Yes
Low
Moderate
5 to 30 mg
twice per day
Renal
(secondary)
Propranolol
No
No
No
Yes
High
IV 1 to 5
mg
3 to 4
Hepatic
Orally 10 to 80
mg two to four
times daily
Sotalol
No
No
No
No
Low
80 to 160 mg
twice per day
12
Renal
Timolol
No
No
No
No
Moderate
10 to 30 mg
twice per day
4 to 5
Hepatic
(primary)
Renal
(secondary)
ISA: intrinsic sympathomimetic activity; MSA: membrane stabilizing activity; IV: intravenous.
* Range of usual, oral, anti-hypertensive dose, unless "IV" noted.
Duration of hypotensive effect, in general, is longer than may be predicted by serum half-life.
Usual initial IV dose. Subsequent dosing generally needed. See drug monograph for detail.
Not available in US.
Sotalol has independent class III antiarrhythmic activity.
Prepared with data from:
1. Frishman WH, Alwarshetty M. -Adrenergic blockers in systemic hypertension pharmacokinetic considerations related to
current guidelines. Clin Pharmacokinet 2002; 41:505.
2. Brubacher JR. -Adrenergic Antagonists. In: Goldfrank's Toxicologic Emergencies, 9th ed, Nelson LS (Ed), McGraw-Hill, New
York 2010.
04/10/2015
Page 11 of 16
Severity of airflow limitation in COPD (based on postbronchodilator FEV 1 )

In patients with FEV 1 /FVC <0.7:
GOLD 1
Mild
FEV 1 80 percent predicted
GOLD 2
Moderate
50 percent FEV 1 <80 percent
GOLD 3
Severe
30 percent FEV 1 <50 percent

predicted
GOLD 4
Very severe
FEV 1 <30 percent predicted
predicted
FEV 1 : forced expiratory volume in one second; FVC: forced vital capacity; respiratory failure: arterial partial pressure of oxygen
(PaO 2 ) less than 60 mmHg (8 kPa) with or without arterial partial pressure of CO 2 (PaCO 2 ) greater than 50 mmHg (6.7 kPa) while
breathing ambient air at sea level.
From the Global Strategy for the Diagnosis, Management and Prevention of COPD 2013, Global Initiative for Chronic Obstructive Lung
Disease (GOLD), www.goldcopd.org.
04/10/2015
Page 12 of 16
Beta blocker after MI is effective in patients with

chronic lung disease
In an analysis of 201,752 patients with an acute myocardial infarction

(MI), those with chronic obstructive pulmonary disease (COPD) who
received a beta blocker had a significant increase in survival at two years
compared to patients with COPD who did not receive this therapy (83.2
versus 72.2 percent).
Data from Gottlieb SS, McCarter RJ, Vogel RA. N Engl J Med 1998; 339:489.
04/10/2015
Page 13 of 16
Beta blockers reduce mortality in high-risk patients after MI
The Cardiac Arrhythmia Suppression Trial (CAST) randomized 1735 postmyocardial

infarction (MI) patients with a left ventricular ejection fraction 40 percent and
ventricular arrhythmia to an antiarrhythmic drug (encainide, flecainide, or moricizine)
or placebo. Patients who were receiving concomitant beta blocker therapy had a lower
incidence of all-cause mortality, arrhythmic death, or cardiac arrest compared to
those not receiving beta blockers.
Data from Kennedy HL, Brooks MM, Barker AH, et al, for the CAST Invetigators, Am J
Cardiol 1994; 74:674.
04/10/2015
Page 14 of 16
Possible interaction between beta blockers and

amiodarone after acute MI
An intention to treat analysis of the two-year total cardiac mortality in

1486 patients with a recent acute myocardial infarction (MI) and a left
ventricular ejection fraction below 40 percent in the EMIAT trial. Those
receiving a beta blocker with amiodarone had a trend toward a better
outcome compared to patients receiving amiodarone alone (P = 0.06).
No effect of concomitant therapy with digoxin or ACE inhibitors was
noted.
Data from Kennedy HL. Am J Cardiol 1997; 80:1208.
04/10/2015
Page 15 of 16
Beta blocker plus amiodarone improves survival after a

myocardial infarction
A pooled analysis of patients in the EMIAT and CAMIAT trials shows that allcause mortality after a myocardial infarction is lower with a combination of
amiodarone and a beta blocker compared with beta blocker alone or no beta
blocker with or without amiodarone.
Data from Boutitie F, Boissel JP, Connolly SJ, et al. Circulation 1999; 99:2268.
04/10/2015
Page 16 of 16
Benefit of beta blocker plus amiodarone after

myocardial infarction
A pooled analysis of patients in the EMIAT and CAMIAT trials shows that
all-cause mortality, arrhythmic death, rescucitated cardiac arrest, and
non arrhythmic cardiac death were reduced in patients taking beta
blocker; the decrease was most prominent in those treated with the
combination of beta blocker and amiodarone.
Pl: placebo; Am: Amiodarone.
Data from Boutite F, Boissel JP, Connolly SJ, et al, and the EMIAT and
CAMIAT Investigators. Circulation 1999; 99:2268.
Disclosures
Disclosures: Robert S Rosenson, MD Grant/Research/Clinical Trial Support: Amgen [Lipids (Evolocumab)]; Sanofi [Lipids (Alirocumab)]; Astra Zeneca [Thrombosis
(Ticagrelor)]. Consultant/Advisory Boards: Aegerion [Lipids (Lomitapide)]; Amgen [Lipids (Evolocumab)]; Astra Zeneca [Lipids (Epanova)]; Genzyme [Lipids (Mipomersen)];
Sanofi [Lipids (Alirocumab)]; GlaxoSmithKline [COPD (Relovir)] Guy S Reeder, MD Nothing to disclose. Harold L Kennedy, MD, MPH Nothing to disclose. Christopher P
Cannon, MD Grant/Research Support: Accumetrics (Platelets and ACS [Verify Now platelet test]); Arisaph (Lipids); AstraZeneca (ACS, lipids, and GI [Ticagrelor,
Rosuvastatin, PPI]); Boehringer-Ingelheim (AF [Dabigatran]); CSL Behring (Lipids); Essentialis (Lipids); GlaxoSmithKline (Lipids and DM); Janssen (AF and DM [Rivaroxaban
and Cangliflozen); Merck (Lipids [Ezetimibe]); Regeneron (Lipids); Sanofi (Lipids and ACS [clopidogrel]); Takeda (DM [Pioglitazone]). Consultant/Advisory Boards: BristolMyers Squibb (AF [Apixaban]); Lipimedix (Lipids); Pfizer (AF, DM, and Lipids [Apixaban, Etrugliflozin, Atorvastatin]); Kowa (lipids). Gordon M Saperia, MD, FACC Nothing to
disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and
through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate
standards of evidence.
Conflict of interest policy
04/10/2015

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Acute myocardial infarction: Role of beta blocker therapy

Official reprint from UpToDate

Acute myocardial infarction: Role of beta blocker therapy

Acute myocardial infarction: Role of beta blocker therapy

Acute myocardial infarction: Role of beta blocker therapy

Acute myocardial infarction: Role of beta blocker therapy

Acute myocardial infarction: Role of beta blocker therapy

Acute myocardial infarction: Role of beta blocker therapy

Acute myocardial infarction: Role of beta blocker therapy

Acute myocardial infarction: Role of beta blocker therapy

Killip classification of acute myocardial infarction

No evidence of heart failure

Overt pulmonary edema

Graphic 65592 Version 5.0

Acute myocardial infarction: Role of beta blocker therapy

Beta blocker properties

Acute myocardial infarction: Role of beta blocker therapy

Acute myocardial infarction: Role of beta blocker therapy

Severity of airflow limitation in COPD (based on postbronchodilator FEV 1 )

FEV 1 80 percent predicted

50 percent FEV 1 <80 percent

30 percent FEV 1 <50 percent

FEV 1 <30 percent predicted

Acute myocardial infarction: Role of beta blocker therapy

Beta blocker after MI is effective in patients with

In an analysis of 201,752 patients with an acute myocardial infarction

Acute myocardial infarction: Role of beta blocker therapy

Beta blockers reduce mortality in high-risk patients after MI

The Cardiac Arrhythmia Suppression Trial (CAST) randomized 1735 postmyocardial

Acute myocardial infarction: Role of beta blocker therapy

Possible interaction between beta blockers and

An intention to treat analysis of the two-year total cardiac mortality in

Acute myocardial infarction: Role of beta blocker therapy

Beta blocker plus amiodarone improves survival after a

Acute myocardial infarction: Role of beta blocker therapy

Benefit of beta blocker plus amiodarone after

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