Decreases death after myocardial infarction and are under-prescribed in elderly patients.
Class II agents are beta blockers which inhibit SA and AV node depolarization and slow heart rate.
They also decrease cardiac oxygen demand and can prevent cardiac remodeling.
Are the drugs of choice for the treatment of hypertension in patients with coronary artery disease and angina.
Pharmacodynamic consequences of beta1 -receptor blockade include decreases in (1) resting and exercise heart rate, (2) cardiac output, and (3) systolic and diastolic blood pressure.
Beta blockers have a negative chronotropic effect that decreases the heart rate at rest and after exercise, a negative inotropic effect that decreases cardiac output, reduction of sympathetic outflow from the central nervous system (CNS), and suppression of renin release from the kidneys.
Reduce ischemia and angina because of their negative inotropic and chronotropic actions.
Decreases heart rate and increases diastolic filling time for coronary perfusion and the negative inotropic and chronotropic actions reduce myocardial oxygen demands.
Beta blockers reduce all-clause mortality in patients with AMI with high heart rate, but not those with low heart rates (Park Jj).
The efficacy of beta blockers in patients with heart failure and reduced ejection fraction is well documented.
After myocardial infarction, long-term beta blocker therapy, reduce mortality by approximately 20%: however these results mainly involve patients with large myocardial infarction and left ventricular systolic dysfunction.
These studies pre-date advancements with percutaneous coronary interventions, antithrombotic agents, high intensity statins, renin-angiotensin- aldosterone system antagonists.
In the era of modern reperfusion strategies, beta blockers did not significantly reduce mortality.
Not all beta blockers are the same, some are cardio selective (affecting only beta 1 receptors) while others are non-selective, affecting beta 1 and 2 receptors.
Cardio selective, B1 selective, agents without intrinsic sympathomimetic activity, such as metaprolol or bisoprolol are recommended for treating patients with coronary artery disease, hypertension and angina.
Beta blockers that target the beta-1 receptor are called cardio selective because beta-1 is responsible for increasing heart rate; hence a beta blocker will slow the heart rate.
No specific beta-blocker chosen after myocardial infarction is preferable to another in reducing mortality.
Diminishes sympathetic nervous system activity, has antiarrhythmic properties, decreases heart rate, decreases systolic blood pressure and decreases myocardial credit contractility.
In patients with heart failure with reduced ejection fraction, they offer a substantial reduction in adverse events and justify the theory of protection against excessive neurohumoral activation.
Among survivors with acute myocardial infarction without heart failure or left ventricular systolic dysfunction, use is associated with a reduced five-year all cause mortality in patients who have high heart rates but not in those with low heart rate ( Park J)
The heart rate lowering effect of beta blockers is attributed to the beneficial properties, among others.
Use reduces myocardial oxygen consumption, myocardial ischemia, infarction and death.
Beta blockers provide no outcome benefit in stable coronary artery disease patients without prior myocardial infarction and may be less effective as an antihypertensive agent and have pseudo antihypertensive effect.
Can reduce total mortality of patients with congestive heart failure and ischemic coronary artery syndromes by 30-40% (Goldstein S.).
Treatment with beta blockers is the standard of care for patients with coronary artery disease, especially if they have had a myocardial infarction.
Beta blockade recommended for many cardiovascular conditions including: stable ischemic heart disease, unstable angina, ST elevation myocardial infarction in hemodynamically stable patients, non-STEMI, heart failure, secondary prevention and risk reduction.
In a study of 17,035 patients with myocardial infarction, only 45% of patients adhered to beta blocker use at one year after MI (Kramer JL et al).
With ST elevation myocardial infarction oral administration of beta blockers is associated with decreased risk of cardiogenic shock, ventricular arrhythmias, and acute heart failure (Grace).
In the above study the Global Registry of Acute Coronary Events investigators found early receipt of any form of beta blockers was associated with an increase in hospital mortality.
In an observational study of patients with known prior myocardial infarction, known coronary artery disease without myocardial infarction, or those with coronary artery disease risk factors only: the use of beta blockers was not associated with a lower risk of composite cardiovascular events(Bangalore S et al).
In the above study 44,708 patients with data from the REACH registry were used.
A meta-analysis showed that beta blockers resulted in a 23% reduction in death after myocardial infarction, with a mean follow-up of 1.4 years.
Most studies demonstrating improvement of survival with beta blockers after MI were performed in the era before modern reperfusion or medical therapy was routine.
Added to patients with CHF result in a 41% reduction in hospital admissions.
Long-term treatment in heart failure with carvedilol produces greater effects on left ventricular fraction then metoprolol.
Less effective in African-Americans for treatment of hypertension.
Use of beta blockers decreases the risk of death among surgery patients.
Beta adrenergic blockers reduce portal pressure by reducing portal venous inflow by decreasing in cardiac output and splanchnic blood flow.
Nonselective beta-blockers prevent esophageal variceal bleeding.
Do not prevent variceal formation in patients with cirrhosis and portal hypertension.
Use is frequently withheld in patients with chronic obstructive pulmonary disease because of the potential to provoke bronchospasm and-induced respiratory insufficiency.
Only one third of patients with COPD receive beta blockers after an acute coronary event (Chen J).
Evidence exists and that treatment with beta blockers, particularly those that are cardioselective, is safe in patient’s with congestive heart failure and COPD (Salpeter S).
Metoprolol is associated with the significant twofold increase risk of exacerbations of COPD, but without increase in mortality.
Bisoprolol in COPD does not reduce the risk of exacerbations in COPD.
The use of preoperative beta blockade in postoperative coronary artery bypass grafting outcomes reveals no mortality advantage and paradoxically increases incidence of atrial fibrillation (Brinkman et al).
Should not be abruptly discontinued in patients with coronary artery disease, as sere exacerbation of angina, myocardial infarction, and ventricular arrhythmias have been reported following the abrupt discontinuation of therapy with beta blockers.
Should be tapered over 1 to 2 weeks when possible.
If the angina worsens or acute coronary insufficiency develops, the drug should be restarted promptly, at least temporarily.
In general, patients with bronchospastic diseases should not receive beta blockers.
Because beta blocker withdrawal has been associated with an increased risk of MI and chest pain, patients already on beta blockers should generally continue treatment throughout the perioperative period.
Should be avoided, as other beta blockers, in patients with bronchospasm.
Use of BB should be continued perioperatively, and patients should be monitored closely when anesthetic agents which depress myocardial function are used.
The withdrawal of beta blocker agents prior to major surgery may impair the heart’s ability to respond to reflex adrenergic stimuli and increase the risks of general anesthesia and surgical procedures.
Its beta-blocking effects can be reversed by beta agonists, such as dobutamine or isoproterenol.
Early perioperative beta blocker exposure is associated with a reduction in 30 day all cause mortality and cardiac morbidity in patients undergoing noncardiac surgery (London MJ et al).
In a review of 36 trials ofnoncardiac surgery there was no association between beta blockers and all cause mortality or strokes (Blessberger HK et al).
In the above studies there was significant reduction in acute myocardial infarctions and supraventricular tachycardias for beta blocker use in noncardiac surgery, while there was increased episodes of hypotension and bradycardia.
In the above studies there was no association between beta blockers ventricular arrhythmias, congestive heart failure or length of stay.
Use in patients with heart failure or a recent MI lowers the risk of major adverse cardiovascular events and all-cause mortality within 30 days after non cardiac surgery (Andersson C et al).
In the above study no benefit was seen in patients treated with BB with stable heart disease.
It is proposed the beta blockers may prevent untoward events in the perioperative setting in high risk patients by protecting against catecholamine surges.
Randomized controlled clinical trials of perioperative beta blockers have yielded conflicting results.
In a review a 53 trials revealed no association between beta blocker use and all cause mortality, or with the incidence of acute myocardial infarction, cerebrovascular events, hypotension, bradycardia or congestive heart failure (Blessberger HK et al).
In the above study there was a decreased incidence of supraventricular tachycardias and ventricular arrhythmias with the use of beta blockers in cardiac surgery.
Guidelines for cardiac surgery, it is recommended beta blocker therapy in patients with ejection fraction greater than 30% undergoing coronary artery bypass grafting to improve survival and prevent postoperative atrial fibrillation.
Guidelines for noncardiac surgery support the use of beta blockers in patients already receiving long-term treatment, and the initiation should be considered in individuals with more than 3 cardiovascular risk factors or evidence of ischemia on preoperative testing.
Initiation of beta blockers for patients with cardiovascular risk factors should be started in advance of surgery, about 2-7 days, and dose tried titration based on heart rate may be beneficial.
Use in patients with heart failure or a recent MI lowers the risk of major adverse cardiovascular events and all-cause mortality within 30 days after non cardiac surgery (Andersson C et al).
Among patients with acute myocardial infarction, who underwent early coronary angiography, and had a preserved left ventricular ejection fraction of 50% or greater, long term beta blocker treatment did not lead to a lower risk of composite primary and point of death from any cause or new myocardial infarction than no beta blocker use (REDUCE-AMI Investigators).
In the above study no benefit was seen in patients treated with BB with stable heart disease
May mask some of the manifestations of hypoglycemia, particularly tachycardia.
May blunt perioperative inflammatory response and use can increase the threshold for ischemic induced ventricular arrhythmias.
Beta blockers may mask clinical signs of hyperthyroidism, such as tachycardia.
Abrupt withdrawal of beta blockers in these patients may be followed by an exacerbation of symptoms or may precipitate a thyroid storm.
Can precipitate or aggravate symptoms of arterial insufficiency in patients with peripheral vascular disease.
In noncardiac surgery preoperative beta blockade is used to titrate heart rate and blood pressure, and is recommended for patients with known coronary disease, inducible ischemia, and multiple cardiac risk factors for patients who undergo high-risk procedures.
lnterruption of long-term beta blocker treatment in patients with the history of MI was not shown to be non-inferior to a strategy of beta blocker continuation with respect to outcome death, non-fatal myocardial infarction, non-fatal, stroke or hospitalization for cardiovascular reasons, nor did it seem to improve the patients quality of life.