β-adrenergic receptor (AR) antagonists (beta blockers or β-blockers) are a class of cardiovascular drugs that inhibit adrenergic receptors.1 Adrenergic receptors are G-protein coupled transmembrane proteins that are activated by catecholamines, specifically noradrenaline and adrenaline. ARs are divided into 3 families, β1, β2, and β3 ARs. Due to the differential affinities, ligand activation of β-ARs can vary. β-adrenergic signaling can elicit different responses in various organs and tissues including the heart, lungs, gastrointestinal tract, adipocytes, kidney glomerular cells, and peripheral nerve cells.
β-ARs are expressed on cardiomyocytes. β1-AR is the most abundant receptor subtype expressed in the heart with four times more expression than β2, while β3-AR is the least expressed.2 In cardiomyocytes, β1-ARs are coupled to G-proteins.1 They have stimulatory effects on the heart, increasing cardiac contractility, rate of myocardial relaxation, and chronotropy.
β2-ARs are associated with activating and inhibitory G-proteins, and although they primarily stimulate activating G-proteins, they can also have inhibitory effects on the heart. β3-ARs are coupled to inhibitory G-proteins and have negative effects on heart inotropy.1 They can also activate nitric oxide synthase (NOS), guanylate cyclase (GC), and the production of cGMP.
Beta Blockers Mechanism of Action
Three generations of β-AR antagonists currently exist.1 They differ based on their selectivity which allows them to elicit different responses. The first generation of beta blockers are nonselective antagonists of β1 and β2 receptors. The second generation of beta blocker shows dose-dependent cardioselectivity for β1 receptors over β2 receptors. The third generation of beta blockers inhibits β1 receptors on cardiomyocytes, and function as cardiovascular vasodilators by blocking α1-adrenoreceptor activity and activation of β3-ARs.
Beta blocker activity can decrease heart rate, heart strength, cardiac output, activity of renin-angiotensin system, and blood pressure.1 Due to its vasodilating properties, third generation β-blockers decrease peripheral vascular resistance. Through activation of NOS and GC, third generation beta blockers exhibit angiogenic, antioxidant, antifibrotic, and anti-apoptotic properties, which reduces cardiac remodeling, and endothelial and cardiac dysfunction.
Pharmacokinetics and Pharmacodynamics of Beta Blockers
Sotalol and propranolol are first-generation beta blockers, and propranolol is the first of its class used in clinical practice.1 Second generation beta blockers include atenolol and metoprolol, and labetalol. Carvedilol, and nebivolol are third generation β-blockers.1 β-blocker can be lipophilic (propranolol, metoprolol, third generation) or hydrophilic (atenolol).1 They show a range of values in serum availability and half-life. They are often metabolized by the liver or can be cleared without biotransformation (atenolol).1
Beta blocker inhibitory activity has been demonstrated by: (1) reduction in resting and exercise heart rate and cardiac output, (2) reduction of systolic and diastolic blood pressure, (3) decreased atrioventricular nodal conduction and increased atrioventricular nodal refractoriness, (4) inhibition of isoproterenol induced tachycardia, (5) reduction in reflex orthostatic tachycardia.3–9
Precautions and Warnings
- β-adrenergic inhibition may lead to more severe cardiac failure due to lowered myocardial contractility
- In patients with aortic or mitral valve disease, or compromised left ventricular function, continued β-adrenergic depression may lead to cardiac failure
- Abrupt therapy interruption in patients with coronary artery disease, worsening of angina pectoris, and in some cases myocardial infarction and death can happen
- Beta blocker treatment can worsen symptoms of arterial insufficiency in patients with peripheral or mesenteric vascular disease due to reduced cardiac output
- β-blockers should be avoided in patients with bronchospastic disease
- β-blockers should not be routinely discontinued prior to major surgery. However, there is an increased risk of general anesthesia and surgical procedure due to the impaired heart response to adrenergic stimuli
- β-blockers may mask hypoglycemia and should be used with caution in diabetic patients
- β-blockers may mask some sign of hyperthyroidism. Abrupt withdrawal may lead to thyroid storm
- Patients with a history of severe anaphylactic reaction may be more reactive to repeated challenge and unresponsive to the usual dose of epinephrine while taking β-blockers
- β-blockers should be used with caution in patients with impaired liver function
- Prinzmetal’s variant angina
- β−blocker withdrawal syndrome: condition of adrenergic hypersensitivity that can arise after abrupt discontinuation of the therapy. Symptoms include elevated blood pressure and high heart rate. In patients with stable angina, abrupt discontinuation of medicine can lead to unstable angina and myocardial infarction (MI). If discontinuation is needed, beta blocker tapering is required to prevent adverse cardiac effects of adrenergic hypersensitivity3-10
Beta Blockers Indications
- Ventricular arrhythmia
- Delay in recurrence of atrial fibrillation/atrial flutter
- Angina pectoris due to coronary atherosclerosis
- Acute myocardial infarction
- Heart failure
- Left ventricular dysfunction following myocardial infarction3-9
Side Effects of Beta Blockers
- Cardiovascular (chest pain, edema, hypotension, bradycardia, heart failure, and syncope)
- Central nervous system (depression, dizziness, fatigue, headache, insomnia, abnormal dreams, anxiety, impotence, and paraesthesia)
- Dermatological (rash, pruritus)
- Gastrointestinal problems (constipation, diarrhea, dyspepsia, flatulence, nausea, vomiting, and abdominal pain)
- Metabolic (hyperglycemia, weight gain, increased blood urea nitrogen, and nonprotein nitrogen, hypercholesterolemia, and peripheral edema)
- Genitourinary (micturition, dysuria, and nocturia)
- Musculoskeletal (arthralgia, myalgia, back pain, and joint pain)
- Respiratory (cough, dyspnea, rhinitis, pharyngitis, and wheezing)
- Special senses (abnormal vision, conjunctivitis, and dry eye)
- Liver and biliary system (increased bilirubin and alkaline phosphatase)3-9
Beta Blockers Contraindications
- Persistent severe bradycardia
- Second- and third-degree heart block
- Overt cardiac failure
- Cardiogenic shock
- Sick sinus syndrome (except when permanent pacemaker present)
- Severe hepatic impairment
- Bronchospastic conditions
- Severe hypersensitivity3-9
Drug Interactions with Beta Blockers
- Other β-blocking drugs
- Catecholamine-depleting drugs (reserpine and guanethidine)
- Calcium antagonist (verapamil and diltiazem)
- Digitalis glycosides
- CYP2D6 inhibitors
Primary Beta Blockers Indications
Beta Blockers for Angina
Angina: Presentation and Diagnosis
Patients with angina present with retrosternal chest pain, sensation of pressure, tightness or discomfort in chest, and pain in the shoulders, arms, neck, back, upper abdomen, or jaw.11 Symptoms of angina may include dyspnea, nausea, and lightheadedness.
Angina can be stable or unstable. Unstable angina is one of the conditions of acute coronary syndrome, that also includes ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI).19 Stable angina happens in response to physical and emotional stress, whereas unstable angina occurs without physical or minimal exertion.19 Symptoms of stable angina generally dissipate with the use of nitroglycerin.11
Angina: Diagnostic Workup
Diagnostic workup for angina includes physical exam and assessment of medical history. A physical exam can differentiate angina from other causes of chest pain, like aortic stenosis, hypertrophic cardiomyopathy, or pulmonary hypertension. A crescendo-decrescendo systolic murmur is indicative of aortic stenosis and hypertrophic cardiomyopathy, and they can be distinguished with Valsalva maneuver, squatting, and hand grip. Loud and widely dispersed P2 component of the second heart sound or a right ventricular heave can indicate pulmonary hypertension.
Electrocardiogram (ECG) should be performed to screen for evidence of prior myocardial infarction (MI) or left ventricular hypertrophy. Functional stress testing to provoke ischemia in combination with ECG is the primary diagnostic tool for stable angina. Testing used to diagnose stable angina includes Coronary computed tomographic angiography (CCTA), which is able to detect nonobstructive plaque that may be missed by stress testing. It has recently become one of the first-line tests used to diagnose angina11
Angina: Differential Diagnosis
- Cardiovascular conditions (unstable angina, NSTEMI, STEMI, myocarditis, and pericarditis)
- Gastrointestinal conditions (esophageal spasm, and gastroesophageal reflux)
- Pulmonary conditions (asthma, chronic obstructive pulmonary disease (COPD), and pulmonary embolism)
- Musculoskeletal conditions (costochondritis and injury)12
Beta Blockers for Angina: Indication Management by Drug-Class Use
Beta blockers are used as first-line antianginal drugs for therapy and to manage symptoms unless contraindication or intolerance is present.11 The selection of an appropriate therapeutic drug to treat angina is guided by a patient’s comorbidities.13 Therefore, the combination of a beta blocker and calcium channel blocker is the primary combination for the treatment of angina in patients with prior MI and left ventricular dysfunction.13
However, in patients with stable coronary disease without prior MI or decreased left ventricular function, who have undergone percutaneous coronary intervention, long term use of beta blockers does not associate with reduction of future cardiovascular events.14,15
Prevention of Recurrent Myocardial Infarction (RMI)
Recurrent myocardial infarction (RMI) is one of the most concerning of the adverse cardiovascular events in survivors of acute myocardial infarction (AMI).16 Approximately, 10% of the all MI patients are at risk of developing a RMI within the year of AMI.17
Prevention of RMI: Presentation and Diagnosis
Chest pain that occurs at rest or with minimal exertion for more than 10 minutes is the most common symptom of MI.18 Pain frequently starts in the retrosternal area and radiates into the left arm, neck, and jaw. Chest pain can be accompanied by palpitation, nausea, syncope, dyspnea, and excessive sweating.18,20
MI can be divided into ST-elevated (STEMI) and non-ST-elevated (NSTEMI) MI based on ST segment elevation. STEMI is diagnosed based on ECG findings of ST elevation.19 NSTEMI is diagnosed based on elevated cardiac biomarkers in the absence of ST elevation.21 Cardiac troponins are the most sensitive and specific biomarkers of NSTEMI. They become elevated within a few hours upon the onset of symptoms and can be elevated for several days or even longer depending on the size of the infarction.21
Prevention of RMI: Diagnostic Workup
Diagnostic workup includes physical examination that can alternatively diagnose chest pain, some of which can be life threatening.21 A 12-lead ECG should be done and interpreted within 10 minutes of arrival to the emergency room. If initial ECG is not diagnostic, serial ECG should be performed.
Biomarkers of myocardial necrosis (serial cardiac troponin I or T) should be measured.21 A troponin value above the 99th percentile of the upper reference level is the appropriate cutoff point for the diagnosis of myocardial necrosis.20 Additional diagnostic workup may include imaging using x-ray, computed tomography (CT), and transthoracic echocardiogram.
Prevention of RMI: Differential Diagnosis
Imbalance in myocardial oxygen consumption and demand, is a hallmark of MI caused by coronary artery obstruction can happened as a result of other conditions including:
- Excessive oxygen demand in the presence of stable flow-limited lesion
- Acute coronary insufficiency due to vasospastic angina (prinzmetal), coronary embolism, and coronary arteritis
- Non-coronary causes (hypotension, severe anemia, hypertension, tachycardia, hypertrophic cardiomyopathy, and severe aortic stenosis)
- Nonischemic myocardial injury (myocarditis, cardiac contusion, and cardiotoxic drugs)
- Stress cardiomyopathy
- Pulmonary embolism
- Severe heart failure
- Nonischemic cardiovascular causes of chest pain (aortic dissection, expanding aortic aneurysm, pericarditis, and pulmonary embolism)
- Noncardiovascular causes of chest, back, and upper abdominal pain (pneumonia, pneumothorax, gastroesophageal reflux, esophageal spasm, peptic ulcer, pancreatitis, biliary disease, costochondritis, cervical radiculopathy, psychiatric disorders, sickle cell crisis, and herpes zoster) 21
Prevention of RMI: Indication Management by Drug-Class Use
According to the American Heart Association (AHA)/ American College of Cardiology (ACC) guidelines21, oral beta blocker therapy should be initiated in the first 24 hours following MI if the patients don’t have signs of heart failure, evidence of low-output state, increased risk for cardiogenic shock, and other contraindication to β−blocker therapy (class of recommendation (CoR) I, level of evidence (LoE) A).
The 2014 AHA/ACC guidelines also state that continuous use of beta blockers is reasonable in patients with normal left ventricular function and without angina after initial MI (CoR IIa, LoE C).21 The 2013 AHA/ACC and 2017 ESC guidelines recommend long term use of beta blockers in patients after STEMI with preserved left ventricular ejection function (LVEF) and no angina (Class I for ACC/AHA; class IIA for ESC).22,23
However, most of the studies of the long term benefits of beta blockers were conducted before the widespread use of percutaneous coronary intervention and use of antiplatelets and statins; therefore, the long-term benefits of beta blockers for the prevention of recurrent MI and other cardiovascular events are not fully established.23 Holt et al. found no association between long-term beta blocker therapy and reduction of cardiovascular death, recurrent MI, or a composite outcome of cardiovascular events.24
Beta Blockers for Hypertension
Hypertension is the leading cause of the death worldwide, with 10.4 million deaths per year attributed to elevated blood pressure. 25
Hypertension: Presentation and Diagnosis
The following guidelines are used to diagnose hypertension:
- Office blood pressure measurement:
- Grade I 140-159 mmHg systolic and 90-99 mmHg diastolic
- Grade II ≥ 160 mmHg systolic ≥ 100 mmHg diastolic
- Ambulatory blood pressure measurement:
- 24-hour average ≥ 130 mmHg systolic and ≥ 80 mmHg diastolic
- Awake average ≥ 135 mmHg systolic and ≥ 85 mmHg diastolic
- Asleep average ≥ 120 mmHg systolic and ≥ 70 mmHg diastolic
- Home blood pressure measurement ≥ 135 mmHg (systolic) and ≥ 85 mmHg diastolic25
Blood pressure measurement in the office is the most common method of diagnosing hypertension. The diagnosis should be made based on 2 to 3 office visits spaced 1 to 4 weeks apart. Hypertension can be diagnosed based on a single visit if the measured blood pressure is ≥ 180 mmHg and other signs of cardiovascular disease are present.
Patients with hypertension are often asymptomatic or they can present with chest pain, dyspnea, palpitations, claudication, peripheral edema, headaches, blurred vision, nocturia, hematuria, and vertigo. Signs of secondary hypertension may be present like muscle weakness, cramps, arrhythmias, flash pulmonary edema, sweating, snoring, daytime sleepiness, or symptoms of thyroid disease.
Hypertension: Diagnostic Workup
Diagnostic workup includes blood pressure measurement in both arms, preferably simultaneously in a comfortable environment. Measurements should be taken 3 times at 1 minute intervals. Physical exams can assist with confirmation of diagnosis and identification of hypertension-mediated organ damage or secondary hypertension.
Medical history including a history of cardiovascular disease, family history of hypertension, assessment of overall cardiovascular risk scored based on BP levels, and additional risk factors according to the ESC/ESH guidelines.26 Laboratory tests include sodium, potassium, serum creatinine, and estimated filtration rate, and if available lipid profile, fasting glucose, urine test, and 12-lead ECG.
Hypertension: Differential Diagnosis
- Secondary hypertension
- Coarctation of the aorta
- Renal artery stenosis
- Chronic kidney disease
- Aortic valve disease27
Beta Blockers for Hypertension: Indication Management by Drug-Class Use
Beta blockers are one of the five major drug classes recommended for the treatment of hypertension.25 When compared to placebo, beta blockers significantly reduce the risk of stroke, heart failure, and major cardiovascular events in patients with hypertension.28 Beta blockers are equally as effective as other blood pressure-lowering drug classes in preventing cardiovascular events in hypertensive patients, with the exception of stroke.26
Beta blockers are associated with an increased risk of diabetes in predisposed patients.26 β-blockers are the treatment of choice in hypertensive patients with symptomatic angina, post-MI, HFrEF, need for the heart rate control, or as an alternative to angiotensin-converting enzyme or ACE inhibitors (ACEi) and angiotensin II receptor blockers in younger hypertensive women.26
In the case of uncomplicated hypertension, hypertension with chronic kidney disease, beta blockers can be added if hypertension proved to be resistant to treatment combination consisting of ACEi or angiotensin II receptor blockers with calcium channel blockers and diuretic.26
The vasodilating β-blocker, labetalol, is considered the first-line of treatment in hypertensive emergencies, including malignant hypertension, hypertensive encephalopathy, acute coronary event, eclampsia, and severe pre-eclampsia.26 Beta blockers with the exception of metoprolol should be used as blood pressure controlling medicine in hypertensive psychiatric patients with drug-induced tachycardia.25
Beta Blockers for Heart Failure
Heart failure is a complex clinical syndrome with symptoms resulting from deficits in ventricular blood pumping. The ACC/AHA classify development and progression of heart failure into four categories29:
Stage A – At risk for heart failure (asymptomatic and without structural heart disease, but with risk-increasing disease present, like hypertension, cardiovascular disease, diabetes, obesity, exposure to cardiotoxic agent, genetic marker of cardiomyopathy, and familiar myopathy)
Stage B – Pre-heart failure (asymptomatic with structural heart disease, evidence of filling pressure, increased natriuretic peptide, and persistent elevated levels of cardiac troponin in the absence of competing diagnosis)
Stage C – Symptomatic heart failure
Stage D – Advanced heart failure that interferes with daily activities and requires hospitalization
Another important classification of heart failure is based on the LVEF. LVEF classification is important because of its prognostic values in response to treatment.29 Most clinical trials select patients based on their LVEF values. According to the ACC/AHA, heart failure is classified as:29
- Heart failure with reduced LVEF if LVEF value is less or equal 40% (HFrEF)
- Heart failure with improved LVEF if previous LVEF less or equal 40% and the follow-up value more than 40% (HFimpEF)
- Heart failure with preserved LVEF if LVEF value is equal or more than 50 % (HFpEF)
- Heart failure with mid-range LVEF if LVEF values are between 40 and 50%
Heart Failure: Presentation and Diagnosis
Symptoms of heart failure include:30
- Dyspnea – exertional dyspnea, orthopnea (dyspnea that develops in recumbent position, and it is relieved with head elevation), paroxysmal nocturnal dyspnea (dyspnea that develops during the night after several hours of sleep and it requires longer positional relief), and dyspnea at rest
- Ankle swelling
- Chest pain
- Nocturia and oliguria
- Cerebral symptoms -confusion, memory problems, anxiety, insomnia, and headaches
Diagnosis of heart failure requires 2 major criteria, or 1 major and 2 minor criteria.31 Major criteria include:
- Paroxysmal nocturnal dyspnea
- Neck vein distention
- Acute pulmonary edema
- S3 gallop
- Increased central venous pressure
- Hepatojugular reflux
- Weight loss of more than 4.5 kg in 5 days in response to treatment
Minor criteria include:
- Bilateral ankle edema
- Nocturnal cough
- Exertional dyspnea
- Pleural effusion
- Decrease in vital capacity by 1/3 from maximum recorded
Heart Failure: Diagnostic Workup
Diagnostic workup for heart failure includes a physical exam and medical history. A critical component of a physical exam is to look for signs of clinical congestion that are the result of elevated cardiac filling pressure. Clinical congestion can be assessed by jugular venous distention, orthopnea, a square-wave response to the Valsalva maneuver, and leg edema.32
Laboratory testing includes CBC, electrolytes, complete metabolic profile, TSH levels, and urine analysis. Per the recommendation of the AHA/ACC (COR = 1 and LOE = A), specific laboratory tests that measure B-type natriuretic peptide (BNP) and N-terminal natriuretic peptide (NT-proBNP) are recommended to support or exclude the diagnosis of heart failure in symptomatic patients, to risk stratify patients with previous diagnosis of heart failure, or to determine the prognosis in patients hospitalized with heart failure. An ECG is a part of the routine evaluation of patients with suspected heart failure.33
A chest X-ray is also used in patients with suspected heart failure to evaluate heart size and pulmonary congestion, and to detect other possible cardiac or pulmonary causes contributing to patient symptoms. A transthoracic echocardiogram is an integral part of the diagnostic workup. LVEF values from the transthoracic echocardiogram are essential for the classification of heart failure and in determining the appropriate therapy.
Additional imaging techniques can be used such as CMR, SPECT or radionuclide ventriculography, PET, cardiac CT, or ICA.29 Genetic testing may be used if genetic causes of cardiomyopathy are suspected.
Heart Failure: Differential Diagnosis
- Acute renal failure
- Acute respiratory distress syndrome (ARDS)
- Pulmonary fibrosis
- Nephrotic syndrome
- Pulmonary embolism34
Beta Blockers for Heart Failure: Indication Management by Drug-class Use
For patients in stage B (pre-heart failure) with LVEF less than or equal 40 %, beta blockers should be used to prevent symptomatic heart failure. For these patients in stage B with LVEF less than or equal 40 %, and a recent or remote history of MI or acute coronary syndrome, beta blockers are categorized as a Class I recommendation per the AHA/ACC guidelines, and should be used to reduce mortality.35,36 This treatment can improve LVEF, lessen the symptoms of heart failure, and improve clinical status.
Even if symptoms do not improve, long-term treatment should be maintained to reduce the risk of major cardiovascular events. Three β-blockers are recommended bisoprolol, sustained-release metoprolol, and carvedilol.
Beta Blockers for Arrhythmia
Arrhythmia is a condition of irregular heartbeat that includes changes in the rate and the heartbeat rhythm.37 Broadly, arrhythmias include tachycardias (increased heartbeat) and bradycardia (slower heartbeat).37 Based on its site of origin, tachycardias are divided into two main categories, supraventricular tachycardias (SVT), and ventricular tachycardias (VT), characterized by the narrow and wide QRS complex on ECG, respectively.
Occasionally, SVTs can present with wide QRS, as in case of SVT with bundle-branch block and SVT with AV conduction through an accessory pathway.37
SVTs include a wide range of arrhythmias originating in the atrium of the atrioventricular node that can be divided into two groups based on the rhythm pattern.38,39:
1. Regular SVTs:
- Atrial flutter
- Atrioventricular recurrent tachycardia
- Atrioventricular recurrent tachycardia
- Atrial tachycardia
- Sinus tachycardia
2. Irregular SVTs:
- Atrial fibrillation
- Atrial tachycardia with variable block
- Atrial flutter with variable block
- Multifocal atrial tachycardia
- Frequent premature atrial bloc
SVT: Presentation and Diagnosis
SVTs can be symptomatic or asymptomatic (identified by surface ECG). ECG documentation is required for the diagnosis of SVT.38,40 Patients with symptomatic SVTs present with palpitations, dyspnea, fatigue, chest pain or tightness, poor effort tolerance, dizziness, syncope, and troubled sleeping. In the case of hemodynamically unstable atrial fibrillation, the following conditions may be observed: syncope, symptomatic hypotension, acute heart failure, pulmonary edema, myocardial ischemia, and cardiogenic shock.40
Atrial fibrillation is a supraventricular tachyarrhythmia with uncoordinated atrial electrical activation and consequently ineffective atrial contraction.40 It is the most common type of cardiac arrhythmia.41 Atrial fibrillation is diagnosed based on irregular R-R intervals in the absence of p-waves and irregular atrial activation on a 12-lead ECG recording or a single-lead ECG tracing of > 30 seconds.40
SVT: Diagnostic Workup
Diagnostic workup for all SVT patients should include a physical exam, complete medical history and concurrent conditions, 12-lead ECG to establish diagnosis and asses ventricular rate, and the identification of ischemia, structural defects, and conductivity problems. Complete blood work (full blood count, electrolytes, thyroid, and kidney function) and transthoracic echocardiogram should be part of diagnostic workup.
Selected atrial fibrillation patients should be evaluated for the presence of pulmonary embolisms and examined by transesophageal echocardiogram to evaluate for atrial thrombus.40
SVT: Differential Diagnosis
- Atrioventricular nodal reentry tachycardia
- Multifocal atrial tachycardia
- Paroxysmal supraventricular tachycardia
- Wolff-Parkinson-White Syndrome
- Regular tachycardia:
- No Visible P waves AVNRT
- Visible P waves:
- Atrial rate greater than ventricular rate = Atrial flutter or Atrial tachycardia
- Atrial rate not greater than ventricular rate:
- Long RP (RP longer than PR) = Atrial tachycardia, PJRT, Atypical AVNT
- Short RP interval – Less than 70 ms = AVNRT
- Short RP interval – More than 70 ms = AVRT, AVNRT, AT
- Atrial fibrillation, AT/flutter with variable AT conductivity, MAT37
Beta Blockers for SVT: Indication Management by Drug-Class Use
In patients with atrial fibrillation with minimal symptoms, rate control is the initial treatment strategy and beta blockers are one class of drugs that can be used to achieve an adequate heart rate. β-blockers are preferred for the management of atrial fibrillation in patients with a history of heart failure with reduced ejection fraction (HFrEF) and acceptable with in patients with heart failure with preserved ejection fraction (HFpEF).41 β-blockers are used as synergistic reagents in the rhythm control strategy for atrial fibrillation or AFIB management.41
The beta blockers currently used in clinical practice include metoprolol, carvedilol, and esmolol. Adverse effects include hypotension, bradycardia, masking of hypoglycemia in diabetic patients, and worsening symptoms in patients with asthma or chronic obstructive pulmonary disease (COPD).41 In the patients with reactive airways disease, atrial fibrillation rate control therapy should be initiated with β-1 receptor selective β-blocker to minimize the risk of bronchospasm.41
Contraindications include second or third degree heart block.41 In patients with hemodynamically stable regular SVTs, β-blockers are considered a reasonable choice if vagal maneuvers and adenosine administration fails to terminate SVTs. In patients with Wolff Parkinson White syndrome or new pre-excitation pattern on ECG, AV-nodal blockers, including β-blockers should be avoided because of their potential to cause life-threatening ventricular arrhythmia.38,43
Narrow Beta Blockers Indications
Beside the treatment for cardiovascular conditions, beta blockers are used in treatment of hyperthyroidism, essential tremor, portal hypertension, glaucoma and migraine.44 Although not approved by FDA, beta blockers are also used by some individuals for management of anxiety due to its strong anxiolytic properties.44
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Ivana Celic, PhD, is a biomedical scientist and freelance medical and scientific writer. Her research interests include genome plasticity, cancer, aging, neurodegenerative disease, and infertility. She actively participates in laboratory research, scientific writing, and presentations.