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Atrial Fibrillation

Disease Details

Family Health Simplified

Description
Atrial fibrillation is an irregular and often rapid heart rate that can increase the risk of strokes, heart failure, and other heart-related complications.
Type
Atrial fibrillation (AF) is a type of cardiac arrhythmia characterized by an irregular and often rapid heart rate. The genetic transmission of atrial fibrillation can be complex and is not always inherited in a straightforward manner. While there are familial forms of AF suggesting a genetic component, the inheritance pattern is often multifactorial, involving multiple genes and environmental factors. In some cases, specific genetic mutations may follow an autosomal dominant pattern of inheritance.
Signs And Symptoms
AF is usually accompanied by symptoms related to a rapid heart rate. Rapid and irregular heart rates may be perceived as the sensation of the heart beating too fast, irregularly, or skipping beats (palpitations) or exercise intolerance and occasionally may produce anginal chest pain (if the high heart rate causes the heart's demand for oxygen to increase beyond the supply of available oxygen). Other possible symptoms include congestive heart failure symptoms such as fatigue, shortness of breath, or swelling. Loss of consciousness can also occur on atrial fibrillations due to lack of oxygen and blood to the brain. The abnormal heart rhythm (arrhythmia) is sometimes only identified with the onset of a stroke or a transient ischemic attack (TIA). It is not uncommon for a person to first become aware of AF from a routine physical examination or electrocardiogram, as it often does not cause symptoms.Since most cases of AF are secondary to other medical problems, the presence of chest pain or angina, signs and symptoms of hyperthyroidism (an overactive thyroid gland) such as weight loss and diarrhea, and symptoms suggestive of lung disease can indicate an underlying cause. A history of stroke or TIA, as well as high blood pressure, diabetes, heart failure, or rheumatic fever, may indicate whether someone with AF is at a higher risk of complications.
Prognosis
Atrial fibrillation can progress from infrequent occurrences to more frequent occurrences, ultimately becoming permanent. But the majority of cases do not progress, especially among patients with a healthy lifestyle.
Atrial fibrillation increases the risk of heart failure by 11 per 1000, kidney problems by 6 per 1000, death by 4 per 1000, stroke by 3 per 1000, and coronary heart disease by 1 per 1000. Women have a worse outcome overall than men. Evidence increasingly suggests that atrial fibrillation is independently associated with a higher risk of developing dementia.
Onset
Atrial fibrillation (AFib) can have a variable onset. It may begin suddenly, with episodes that may stop on their own, or it may be persistent and require treatment to restore and maintain a normal heart rhythm. Some individuals experience paroxysmal AFib, where the irregular heartbeats come and go. The onset can be influenced by several factors, including age, underlying heart disease, high blood pressure, and lifestyle factors such as alcohol consumption and stress.
Prevalence
The prevalence of atrial fibrillation (AF) increases with age. In the general population, it affects approximately 1-2% of people. Among those over 80 years old, the prevalence can be as high as 10-15%.
Epidemiology
Atrial fibrillation is the most common arrhythmia and affects more than 33 million people worldwide. In Europe and North America, as of 2014, it affects about 2% to 3% of the population. This is an increase from 0.4 to 1% of the population around 2005. In the developing world, rates are about 0.6% for males and 0.4% for females. The number of people diagnosed with AF has increased due to better detection of silent AF and increasing age and conditions that predispose to it.It also accounts for one-third of hospital admissions for cardiac rhythm disturbances, and the rate of admissions for AF has risen in recent years. AF is the cause for 20% to 30% of all ischemic strokes. After a transient ischemic attack or stroke, about 11% are found to have a new diagnosis of atrial fibrillation. 3% to 11% of patients with AF have structurally normal hearts. Approximately 2.2 million individuals in the United States and 4.5 million in the European Union have AF.The number of new cases each year of AF increases with age. In people older than 80 years, it affects about 8%. In contrast, in younger people the prevalence is estimated to be 0.05% and is associated with congenital heart disease or structural heart disease in this demographic. As of 2001, it was anticipated that in developed countries, the number of people with atrial fibrillation was likely to increase during the following 50 years, due to the growing proportion of elderly people.
Intractability
Atrial fibrillation (AFib) is not considered intractable. It can often be managed with a combination of lifestyle changes, medications, and procedures. Treatment options include:

1. **Medications**: Anticoagulants, rate control drugs, and rhythm control drugs.
2. **Procedures**: Electrical cardioversion, catheter ablation, and surgical interventions.
3. **Lifestyle Changes**: Diet, exercise, and avoiding triggers.

While AFib can be a chronic condition, many patients achieve good control of symptoms and prevent complications with appropriate treatment.
Disease Severity
Atrial fibrillation (AF) severity can vary widely among individuals. It ranges from occasional, mild symptoms to persistent, severe manifestations that significantly impact quality of life. Some individuals may experience no symptoms, while others might suffer from palpitations, shortness of breath, chest pain, dizziness, or fatigue. The severity is often classified based on the frequency and duration of AF episodes, as well as the degree of symptoms and impact on daily activities. It's important for individuals with AF to be closely monitored by healthcare professionals to manage the condition and reduce the risk of complications such as stroke or heart failure.
Healthcare Professionals
Disease Ontology ID - DOID:0060224
Pathophysiology
The normal electrical conduction system of the heart allows electrical impulses generated by the heart's own pacemaker (the sinoatrial node) to spread to and stimulate the muscular layer of the heart (myocardium) in both the atria and the ventricles. When the myocardium is stimulated it contracts, and if this occurs in an orderly manner allows blood to be pumped to the body. In AF, the normal regular electrical impulses generated by the sinoatrial node are overwhelmed by disorganized electrical waves, usually originating from the roots of the pulmonary veins. These disorganized waves conduct intermittently through the atrioventricular node, leading to irregular activation of the ventricles that generate the heartbeat.
Carrier Status
Atrial fibrillation (AF) does not have a "carrier status" because it is a condition rather than a directly inherited genetic disorder. AF is characterized by irregular and often rapid heart rhythm, which can lead to blood clots, stroke, heart failure, and other heart-related complications. The development of AF can be influenced by genetic factors, but it typically results from a combination of genetic predisposition, age, lifestyle factors, and underlying health conditions.
Mechanism
Atrial fibrillation (AF) is a common cardiac arrhythmia characterized by rapid and irregular beating of the atria. Here's an overview of its mechanisms and molecular mechanisms:

### Mechanism:
1. **Electrical Disturbances**: AF is primarily caused by abnormal electrical impulses in the atria. These impulses may originate from ectopic foci, often located in the pulmonary veins, leading to chaotic electrical activity.
2. **Structural Changes**: Structural remodeling of the atrial tissue, including fibrosis, dilation, and changes in the atrial myocardium, can disrupt the normal propagation of electrical signals.
3. **Functional Remodeling**: Changes in ion channel function and expression, as well as alterations in calcium handling, contribute to the disturbed electrical activity.

### Molecular Mechanisms:
1. **Ion Channel Dysfunction**: Abnormalities in atrial ion channels, such as those governing sodium (Na+), potassium (K+), and calcium (Ca2+) currents, play a crucial role. For instance:
- Reduced inward rectifier potassium current (IK1) and transient outward potassium current (Ito) can prolong action potential duration.
- Increased late sodium current (INa) can enhance cellular excitability.
2. **Calcium Signaling**: Dysregulation of calcium handling proteins, such as the ryanodine receptor (RyR2) and sarcoplasmic reticulum Ca2+-ATPase (SERCA2), can lead to intracellular calcium overload, contributing to triggered activity and arrhythmogenesis.
3. **Fibrosis**: Molecular pathways involving transforming growth factor-beta (TGF-β) and connective tissue growth factor (CTGF) can promote atrial fibrosis, creating a substrate for re-entry circuits and sustaining AF.
4. **Genetic Factors**: Mutations in genes encoding ion channels (e.g., KCNQ1, KCNE2), gap junction proteins (e.g., connexin 40), and other structural proteins (e.g., titin) are linked to familial forms of AF.

These interconnected mechanisms and molecular pathways disrupt the normal rhythm of the heart, causing atrial fibrillation and contributing to its persistence and recurrence.
Treatment
Treatment of atrial fibrillation (AFib) typically involves a combination of strategies aimed at controlling the heart's rhythm and rate, preventing blood clots, and addressing any underlying conditions. Key treatment options include:

1. **Medications**:
- **Rate control**: Beta-blockers, calcium channel blockers, and digoxin to control heart rate.
- **Rhythm control**: Anti-arrhythmic medications such as amiodarone, sotalol, or flecainide to maintain normal heart rhythm.
- **Anticoagulants**: Warfarin, dabigatran, rivaroxaban, or apixaban to reduce the risk of stroke by preventing blood clots.

2. **Cardioversion**:
- **Electrical cardioversion**: A procedure where an electric shock is delivered to the heart to restore a normal rhythm.
- **Pharmacologic cardioversion**: Using medications to achieve the same goal.

3. **Catheter Ablation**:
- A minimally invasive procedure where areas of the heart causing abnormal rhythms are targeted and destroyed using radiofrequency energy or cryotherapy.

4. **Surgical Procedures**:
- **Maze procedure**: Creating a pattern of scar tissue in the atria to disrupt the pathways of abnormal electrical signals.

5. **Lifestyle Changes**:
- Managing underlying conditions such as hypertension, diabetes, and sleep apnea.
- Avoiding alcohol, excessive caffeine, and other triggers.

Treatment plans are individualized based on the severity of the condition, the presence of other health issues, and patient-specific factors.
Compassionate Use Treatment
In cases of atrial fibrillation (AFib), compassionate use or experimental treatments may be considered when standard treatments are not effective or suitable. These include:

1. **Left Atrial Appendage Occlusion Devices**: Devices such as the WATCHMAN are designed to reduce stroke risk in patients who cannot take long-term anticoagulants. These devices are sometimes considered experimental or off-label in certain situations.

2. **Gene Therapy**: Experimental approaches are being investigated to directly target genetic factors that contribute to AFib.

3. **New Anticoagulants**: Investigational oral anticoagulants or next-generation anticoagulants may be used under compassionate use protocols when traditional drugs like warfarin or DOACs (Direct Oral Anticoagulants) are not suitable.

4. **Stem Cell Therapy**: Research is ongoing into the use of stem cell therapy to repair damaged heart tissue and potentially correct the electrical dysfunction that causes AFib.

5. **Novel Ablation Techniques**: Experimental methods, such as the use of pulsed electric fields (PEF) for ablation, are being studied as less invasive or more effective alternatives to traditional ablation procedures.

These treatments are usually reserved for individuals who have not responded adequately to conventional therapies and are offered under specific regulatory and ethical guidelines.
Lifestyle Recommendations
For atrial fibrillation, lifestyle recommendations include:

1. **Regular Exercise:** Engage in moderate physical activity to improve cardiovascular health.
2. **Healthy Diet:** Adopt a heart-healthy diet rich in fruits, vegetables, whole grains, and lean proteins. Reduce salt, sugar, and unhealthy fats.
3. **Weight Management:** Maintain a healthy weight to reduce the risk of atrial fibrillation.
4. **Limit Alcohol Intake:** Excessive alcohol can trigger atrial fibrillation episodes.
5. **Avoid Stimulants:** Limit caffeine and avoid stimulants that may exacerbate symptoms.
6. **Quit Smoking:** Smoking increases the risk of heart disease and atrial fibrillation.
7. **Stress Management:** Implement stress-reducing techniques such as yoga, meditation, or deep breathing exercises.
8. **Monitor Other Health Conditions:** Manage underlying conditions like hypertension, diabetes, or sleep apnea, which can contribute to atrial fibrillation.
9. **Routine Medical Check-ups:** Regular follow-ups with your healthcare provider to monitor and manage your condition effectively.

Making these lifestyle changes can help manage atrial fibrillation symptoms and reduce the risk of complications.
Medication
Several medications are associated with an increased risk of developing atrial fibrillation. Few studies have examined this phenomenon, and the exact incidence of medication-induced atrial fibrillation is unknown. Medications that are commonly associated with an increased risk of developing atrial fibrillation include dobutamine and the chemotherapy agent cisplatin. Agents associated with a moderately increased risk include nonsteroidal anti-inflammatory drugs (e.g., ibuprofen), bisphosphonates, and other chemotherapeutic agents such as melphalan, interleukin 2, and anthracyclines. Other medications that rarely increase the risk of developing atrial fibrillation include adenosine, aminophylline, corticosteroids, ivabradine, ondansetron, and antipsychotics. This form of atrial fibrillation occurs in people of all ages but is most common in the elderly, in those with other atrial fibrillation risk factors, and after heart surgery.
Repurposable Drugs
Repurposable drugs for atrial fibrillation (AF) can include medications originally designed for other conditions but found to be effective for AF management. These may include:

1. **Amiodarone**: Originally an antiarrhythmic for ventricular arrhythmias, it is also effective for AF.
2. **Dronedarone**: A derivative of amiodarone, used for maintaining sinus rhythm in AF patients.
3. **Flecainide**: An antiarrhythmic initially for other types of arrhythmias, now used for AF.
4. **Sotalol**: Initially a treatment for ventricular arrhythmias, now used to manage AF due to its beta-blocking and antiarrhythmic properties.
5. **Beta-blockers (e.g., Metoprolol, Carvedilol)**: Originally for hypertension and coronary artery disease, now also used to control ventricular rate in AF.
6. **Calcium channel blockers (e.g., Diltiazem, Verapamil)**: Initially for hypertension and angina, these can help control heart rate in AF.

Repurposing these drugs can provide effective management for atrial fibrillation, often using known safety profiles and mechanisms of action.
Metabolites
Atrial fibrillation (AF) can influence and be influenced by various metabolic processes. Some metabolites of interest in the context of atrial fibrillation include:

1. **Lactate**: Elevated levels can indicate poor oxygenation and metabolic stress.
2. **Glucose**: Dysregulation in glucose metabolism can be a risk factor for AF.
3. **Free Fatty Acids**: Elevated levels may be indicative of metabolic syndrome, which is associated with AF.
4. **Amino Acids**: Certain amino acids, like branched-chain amino acids, might be altered in AF patients.
5. **C-reactive protein (CRP)**: Although not a metabolite, CRP is an inflammatory marker often elevated in AF patients, indicating a role of inflammation in disease pathology.

Further research is ongoing to fully understand the complex metabolic interactions in atrial fibrillation.
Nutraceuticals
Nutraceuticals such as omega-3 fatty acids, Coenzyme Q10, and certain antioxidants have been studied for their potential roles in managing atrial fibrillation (AF), although their effectiveness and safety are still under research. Always consult a healthcare provider before starting any nutraceutical regimen for AF.
Peptides
Atrial fibrillation (AF) is an irregular and often rapid heart rate that can lead to blood clots, stroke, heart failure, and other heart-related complications. While peptides are not typically the first line of treatment for AF, certain peptide-based medications and natriuretic peptides (like BNP and NT-proBNP) are used as biomarkers to assess the severity and risk stratification in AF patients.

BNP (B-type natriuretic peptide) and NT-proBNP (N-terminal pro b-type natriuretic peptide) levels are often elevated in patients with AF and can be used to evaluate the extent of heart strain and guide treatment decisions. Elevated levels are associated with worse prognosis and can guide the need for more aggressive interventions.

Research into peptide-based therapies for AF is ongoing, exploring their potential in regulating heart rhythm and reducing cardiac stress. However, the main strategies currently involve rate or rhythm control with medications, catheter ablation, and anticoagulation to prevent stroke.