Tests used to Diagnose Afib

Written by WebMD Editorial Contributors

• Doctor Exam
• Does AFib Show Up on an Electrocardiogram (EKG)?
• Holter Monitor
• Event Monitor
• Mobile Cardiac Telemetry (MCT)
• Stress Test
• Echocardiogram
• Blood Tests
• Portable Electrocardiogram
• Fitness Trackers
• Electrophysiology Study
• More

Atrial fibrillation, or AFib, may or may not cause symptoms. Your doctor could find it during a regular physical. Or you might make an appointment after you notice signs like a fluttering heartbeat or fatigue.

If your doctor thinks you have it, the first thing they’ll do is listen to your heart. They may be able to hear your irregular heartbeat with a stethoscope. If not, they may ask for tests to confirm the diagnosis, find out what’s causing it, and figure out the best way to treat it.

Sometimes your primary care or family doctor is the one who diagnoses AFib. But your doctor may refer you to a:

• Cardiologist, a doctor who specializes in heart diseases and conditions
• Electrophysiologist, a doctor who specializes in arrhythmias

When you make an appointment with your doctor or the specialist to see if you might have atrial fibrillation, ask if you need to do anything to prepare. You may need to follow a special diet before blood tests, for example.

To make the most of your time with the doctor, be ready to describe your symptoms and when they happen. Make a list of medications you take, including supplements and over-the-counter medicines. And be prepared with information about your health history and that of close family members.

Take note of any questions you have for your doctor, such as:

• What could be causing my symptoms?
• What kind of tests will I need?
• What are the recommended treatments for my condition? Are there any effective alternatives?
• Do I need to make changes to my lifestyle?

During your exam, the doctor will ask detailed questions about your:

• Symptoms
• Health habits
• Health problems
• Family medical history

During the physical exam, they are likely to:

• Listen to your heartbeat’s rate and rhythm
• Take your pulse and blood pressure
• Listen to your lungs

Yes. This simple, painless test is the most helpful to diagnose AFib. It records your heart’s electrical activity. It can show the:

• Speed of your heartbeat
• Rhythm of your heartbeat
• Strength and timing of electrical signals passing through your heart

A doctor or technician places small patches, called electrodes, on different areas of your body, including several on your chest. These pick-up signals that make wave patterns on the EKG results. It gives your doctor a picture of your heart’s overall electrical activity.

But because the test is a quick snapshot, a standard EKG won’t always catch AFib. Sometimes you’ll need a portable heart rhythm monitor to keep tabs on your ticker over a longer time.

You keep this device with you for 24 to 48 hours while it continuously records your heart’s electrical activity. The extra time gives a better chance of picking up an abnormal heart rhythm, what doctors call an arrhythmia.

Just as with a regular EKG, you’ll have small electrodes attached to your chest. Wires connect these electrodes to a small recorder you can clip onto a belt, keep in a pocket, or hang around your neck.

Then you just go about doing what you usually do. Your doctor will check the recorded results later.

This works like a Holter monitor, but it records your heart’s activity only at certain times, usually for a 30-day period. It might automatically start recording when it senses something is off. Or you might have to push a button when you feel:

• Dizzy
• Weak
• Lightheaded
• A racing or fluttering heart

You may need to wear it for a month or so — as long as it takes to catch and record the trouble.

You might hear this called mobile cardiac monitoring. You wear this small device 24/7, and it monitors your heart as you go about your daily life. Most send a Bluetooth signal to a data center, which analyzes the info and gives your doctor a report.

It’s just what it sounds like: A test that puts extra stress on your heart to see how it responds to working hard and beating fast. You’ll be hooked up to an EKG during the test, and the technician will watch your heart rate and blood pressure, too.

Exercise is an easy way to get your heart pumping. You might ride a stationary bicycle, or walk or run on a treadmill. That’s why this is sometimes called a treadmill test.

If your body can’t handle intense activity, you can take a special medicine that makes your heart beat faster instead.

This test uses sound waves and a computer to create a moving picture of your heart. An echo gives your doctor information about:

• The size and shape of your heart
• How well the heart muscle and valves are working
• Where the heart muscle isn’t contracting the right way

Transthoracic echocardiogram (TTE). This imaging test gives your doctor a picture of your heart. The doctor uses a device called an ultrasound transducer to give off and read sound waves that bounce off the walls and valves in your heart. A computer uses the data to create a video of your heart. Your doctor can see the size of your heart, how well it’s working, how well your heart valves are working, and if you have any blood clots.

Transesophageal echocardiogram (TEE). This imaging test gives the doctor a picture of your heart. They’ll place a probe down your esophagus (the tube that connects your mouth to your stomach). It goes right behind your heart. Once the probe is in place, it works the same way as a TTE.

These can point your doctor to what might be causing your AFib. Blood tests may check for infection, thyroid and kidney problems, signs of a heart attack, and more.

You might hear this called a handheld EKG. Or it could look like a wristwatch. It has electrodes on the back that take your pulse at your chest or your wrist. You can get one from a discount store, drugstore, or online. The doctor may suggest you do it so you can take a quick reading when you feel something. It’ll store your EKG data in its memory for your doctor to read.

Popular smartwatches outfitted with special sensors called photoplethysmographic sensors (or PPGs) can detect AFib.

An electrophysiology study (EPS) can help your doctor understand what’s causing your abnormal heartbeat and figure out the best way to treat it.

In this operation, your cardiologist inserts a thin, flexible electrode into a blood vessel leading to your heart, usually in your neck or groin. They then use an imaging system to guide the electrode to your heart. Once there, the electrode can measure your heart’s electrical signals.

Your doctor will give you a numbing medication before the surgery to keep you from feeling pain. You might also get a sedative to help relax you. The procedure may take 1-4 hours, and you’ll rest in a recovery room for 4-6 hours after that.

Top Picks

Tests used to Diagnose Afib

Written by WebMD Editorial Contributors

• Doctor Exam
• Does AFib Show Up on an Electrocardiogram (EKG)?
• Holter Monitor
• Event Monitor
• Mobile Cardiac Telemetry (MCT)
• Stress Test
• Echocardiogram
• Blood Tests
• Portable Electrocardiogram
• Fitness Trackers
• Electrophysiology Study
• More

Atrial fibrillation, or AFib, may or may not cause symptoms. Your doctor could find it during a regular physical. Or you might make an appointment after you notice signs like a fluttering heartbeat or fatigue.

If your doctor thinks you have it, the first thing they’ll do is listen to your heart. They may be able to hear your irregular heartbeat with a stethoscope. If not, they may ask for tests to confirm the diagnosis, find out what’s causing it, and figure out the best way to treat it.

Sometimes your primary care or family doctor is the one who diagnoses AFib. But your doctor may refer you to a:

• Cardiologist, a doctor who specializes in heart diseases and conditions
• Electrophysiologist, a doctor who specializes in arrhythmias

When you make an appointment with your doctor or the specialist to see if you might have atrial fibrillation, ask if you need to do anything to prepare. You may need to follow a special diet before blood tests, for example.

To make the most of your time with the doctor, be ready to describe your symptoms and when they happen. Make a list of medications you take, including supplements and over-the-counter medicines. And be prepared with information about your health history and that of close family members.

Take note of any questions you have for your doctor, such as:

• What could be causing my symptoms?
• What kind of tests will I need?
• What are the recommended treatments for my condition? Are there any effective alternatives?
• Do I need to make changes to my lifestyle?

During your exam, the doctor will ask detailed questions about your:

• Symptoms
• Health habits
• Health problems
• Family medical history

During the physical exam, they are likely to:

• Listen to your heartbeat’s rate and rhythm
• Take your pulse and blood pressure
• Listen to your lungs

Yes. This simple, painless test is the most helpful to diagnose AFib. It records your heart’s electrical activity. It can show the:

• Speed of your heartbeat
• Rhythm of your heartbeat
• Strength and timing of electrical signals passing through your heart

A doctor or technician places small patches, called electrodes, on different areas of your body, including several on your chest. These pick-up signals that make wave patterns on the EKG results. It gives your doctor a picture of your heart’s overall electrical activity.

But because the test is a quick snapshot, a standard EKG won’t always catch AFib. Sometimes you’ll need a portable heart rhythm monitor to keep tabs on your ticker over a longer time.

You keep this device with you for 24 to 48 hours while it continuously records your heart’s electrical activity. The extra time gives a better chance of picking up an abnormal heart rhythm, what doctors call an arrhythmia.

Just as with a regular EKG, you’ll have small electrodes attached to your chest. Wires connect these electrodes to a small recorder you can clip onto a belt, keep in a pocket, or hang around your neck.

Then you just go about doing what you usually do. Your doctor will check the recorded results later.

This works like a Holter monitor, but it records your heart’s activity only at certain times, usually for a 30-day period. It might automatically start recording when it senses something is off. Or you might have to push a button when you feel:

• Dizzy
• Weak
• Lightheaded
• A racing or fluttering heart

You may need to wear it for a month or so — as long as it takes to catch and record the trouble.

You might hear this called mobile cardiac monitoring. You wear this small device 24/7, and it monitors your heart as you go about your daily life. Most send a Bluetooth signal to a data center, which analyzes the info and gives your doctor a report.

It’s just what it sounds like: A test that puts extra stress on your heart to see how it responds to working hard and beating fast. You’ll be hooked up to an EKG during the test, and the technician will watch your heart rate and blood pressure, too.

Exercise is an easy way to get your heart pumping. You might ride a stationary bicycle, or walk or run on a treadmill. That’s why this is sometimes called a treadmill test.

If your body can’t handle intense activity, you can take a special medicine that makes your heart beat faster instead.

This test uses sound waves and a computer to create a moving picture of your heart. An echo gives your doctor information about:

• The size and shape of your heart
• How well the heart muscle and valves are working
• Where the heart muscle isn’t contracting the right way

Transthoracic echocardiogram (TTE). This imaging test gives your doctor a picture of your heart. The doctor uses a device called an ultrasound transducer to give off and read sound waves that bounce off the walls and valves in your heart. A computer uses the data to create a video of your heart. Your doctor can see the size of your heart, how well it’s working, how well your heart valves are working, and if you have any blood clots.

Transesophageal echocardiogram (TEE). This imaging test gives the doctor a picture of your heart. They’ll place a probe down your esophagus (the tube that connects your mouth to your stomach). It goes right behind your heart. Once the probe is in place, it works the same way as a TTE.

These can point your doctor to what might be causing your AFib. Blood tests may check for infection, thyroid and kidney problems, signs of a heart attack, and more.

You might hear this called a handheld EKG. Or it could look like a wristwatch. It has electrodes on the back that take your pulse at your chest or your wrist. You can get one from a discount store, drugstore, or online. The doctor may suggest you do it so you can take a quick reading when you feel something. It’ll store your EKG data in its memory for your doctor to read.

Popular smartwatches outfitted with special sensors called photoplethysmographic sensors (or PPGs) can detect AFib.

An electrophysiology study (EPS) can help your doctor understand what’s causing your abnormal heartbeat and figure out the best way to treat it.

In this operation, your cardiologist inserts a thin, flexible electrode into a blood vessel leading to your heart, usually in your neck or groin. They then use an imaging system to guide the electrode to your heart. Once there, the electrode can measure your heart’s electrical signals.

Your doctor will give you a numbing medication before the surgery to keep you from feeling pain. You might also get a sedative to help relax you. The procedure may take 1-4 hours, and you’ll rest in a recovery room for 4-6 hours after that.

Top Picks

Diagnostics and treatment of atrial fibrillation (atrial fibrillation) in Krasnoyarsk

Atrial fibrillation (AF), or atrial fibrillation (many doctors still call it that), is one of the most common arrhythmias.

It is more common in older people than in younger people. Let’s figure out together why it occurs – the causes of atrial fibrillation – and how it can be dangerous for a person.

In the human heart there are not only muscle cells (myocardium), which contract and ensure the work of the heart as a pump for pumping blood, but also special cells that generate electric current and conduct it to the myocardium. The so-called conduction system of the heart consists of these special cells, through which an electrical impulse propagates. In a healthy heart, an electrical impulse that stimulates the contraction of the heart occurs in the right atrium, in the sinus node. Therefore, a normal heart rhythm is called sinus. From the sinus node, the impulse propagates along the fibers of the conducting system in the atria, causing them to contract. Blood is pumped through the open mitral and tricuspid valves into the ventricles of the heart. Then the impulse enters the atrioventricular node (atrioventricular), which is a kind of checkpoint into the ventricles. Fibers come out of it, called the “legs of the bundle of His”. Moving along the bundle of His, the impulse leads to a contraction of the ventricles and the release of blood into the aorta and pulmonary artery.

In a healthy heart, the impulse is formed at regular intervals, from 60 to 90 times per minute. In different situations, the pulse rate of the same person is 60 (for example, in a state of rest and rest), and 90 (during physical exertion, excitement) beats per minute. By changing the pulse rate, a healthy heart adjusts to the body’s changing oxygen needs. The same happens with blood pressure, which can vary throughout the day from 100/70 to 140/90 mmHg Art. (fine).

What is atrial fibrillation?

When atrial fibrillation (atrial fibrillation) the electrical impulse moves through the atria chaotically, instead of “friendly” contraction of the atria, they tremble, “flicker”. Due to the fact that the muscle fibers of the atria contract at different times, there is no single contraction and ejection of blood into the ventricles. Since the atria begin to contract not only chaotically, but also very often, the atrioventricular node does not pass all the contractions to the ventricles, an equal period of time is not observed. Therefore, when you try to count the pulse, the intervals between beats will be different, and the pulse will be “uneven”. Also note that the pulse has become different in content – one contraction is stronger, and the other can barely be determined under the fingers. The reason for this phenomenon is the disorganized work of the heart. Part of the contractions of the ventricles occurs when they have had time to fill with blood, and part – with empty ventricles, “idling.”

Forms

Atrial fibrillation (atrial fibrillation) may be paroxysmal or chronic. If attacks of arrhythmia (paroxysms) do not last long (from a few minutes to 7 days) and the normal rhythm is restored spontaneously, this form of atrial fibrillation is called paroxysmal.

Can atrial fibrillation be a health hazard?

Atrial fibrillation (atrial fibrillation) in most cases does not directly threaten your life, as it happens with ventricular tachycardia, ventricular fibrillation. To a greater extent, atrial fibrillation affects the accelerated development of heart failure, reducing the quality of human life. However, in certain situations, patients with atrial fibrillation are at risk. The chaotic contraction of the muscle fibers of the atria leads to the fact that instead of a complete simultaneous emptying of blood from the atria into the ventricles, the blood begins to stagnate in the atria. Conditions arise for the formation of blood clots (thrombi), which sometimes move with the blood flow into the ventricles and further into the systemic circulation. Such traveling clots (emboli) can clog the vessels of the brain (causing a stroke), limbs, and internal organs. Complication can be fatal.

The most favorable conditions for the formation of blood clots are created in chronic (permanent) form of atrial fibrillation , or if paroxysm atrial fibrillation lasts more than 2 days. In addition, AF (atrial fibrillation) contributes to the onset and progression of heart failure and coronary insufficiency. In patients with cardiac arrhythmia, the quality of life is significantly reduced: a constant feeling of danger of arrhythmia at any time, complete dependence on the availability of medical care.

Symptoms of atrial fibrillation (atrial fibrillation)

Atrial fibrillation, or atrial fibrillation , manifests itself in different ways: ic). With paroxysmal form of fibrillation , attacks of different duration occur, from several minutes to 7 days. Such attacks stop spontaneously. With a stable form of atrial fibrillation , paroxysms do not go away on their own, last more than 7 days, the help of doctors is needed to restore sinus rhythm (medication or electrical impulse therapy). At permanent form of atrial fibrillation fails to restore sinus rhythm.

Most often, atrial fibrillation begins with a paroxysmal form, later the attacks become more frequent, longer, it is more and more difficult to restore sinus rhythm, and then it is not possible at all – atrial fibrillation passes into a permanent form . For any form of atrial fibrillation, drug treatment is required, which should be carried out under the supervision of a physician. Atrial fibrillation can be detected during a screening mass ECG study, for example, when recording a stationary ECG during a physical examination or accidentally, when recording an ECG over the phone at a sports center, pharmacy or laboratory. Sometimes paroxysm of atrial fibrillation may develop during exercise tests, such as bicycle ergometry (VEM). But most often paroxysms of atrial fibrillation (atrial fibrillation) can be registered during long hours of ECG recording on a special small portable monitor – Holter monitoring .

Causes of atrial fibrillation (atrial fibrillation)

Causes that lead to atrial fibrillation (atrial fibrillation) may be different. Atrial fibrillation can be an independent disease (idiopathic form), but more often atrial fibrillation occurs in people suffering from cardiovascular diseases: valvular heart disease, coronary heart disease, hypertension, cardiomyopathy, pericarditis and myocarditis, heart surgery. Also at risk of getting atrial fibrillation are people suffering from thyroid pathology (hyperthyroidism – thyrotoxicosis, or “toxic goiter”). Sometimes rhythm disturbance is the first manifestation of thyroid disease, so at the first paroxysm of atrial fibrillation doctors always examine her.

The following video (in English) describes atrial fibrillation in great detail and clearly:

Alcohol abuse is also a common cause of atrial fibrillation . Frequent alcohol intake disrupts the level and balance of electrolytes in the blood (potassium, sodium and magnesium ions are very important for the work of any muscles, but primarily for the heart) and has a direct toxic effect on the heart, leading to the expansion of the atria and ventricles, reducing contractile function. Perhaps the appearance of atrial fibrillation in patients with chronic lung diseases, against the background of general severe diseases, pathology of the gastrointestinal tract (reflux esophagitis, hiatal hernia) is also one of the causes of atrial fibrillation, or atrial fibrillation.

Atrial fibrillation: what to do, how to treat?

Diagnosis of atrial fibrillation (atrial fibrillation) is based on an electrocardiogram (ECG) recording. Sometimes atrial fibrillation is asymptomatic and is detected by chance, for example, when an ECG is recorded with prof. examination or during inpatient treatment for another disease. However, most often the patient goes to the doctor with complaints of interruptions in the work of the heart, attacks of rapid, irregular heartbeat, which may be accompanied by weakness, shortness of breath, sweating, dizziness, a feeling of “internal trembling”, pain in the heart area and a decrease in blood pressure. When an attack occurs suddenly, you should definitely consult a doctor or call an ambulance team. It is very important that the ECG recording be made exactly at the time of the attack – the doctor will be able to accurately determine the nature of the arrhythmia, make a diagnosis and prescribe the correct treatment.

If attacks occur frequently enough, but they cannot be “caught” on a conventional ECG, the patient is referred for 24-hour ECG monitoring (Holter, Holter monitoring). Within 24 hours (or more, depending on the device), the patient’s ECG is recorded and recorded electronically with a special palm-sized device that the patient carries with him. The record is processed on a computer, and if during the examination the patient had attacks of arrhythmia, they will be recorded and documented. The doctor will receive all the necessary information.

It may happen that no seizure occurs during Holter monitoring. A second study will be required, and so on until the arrhythmia is “caught”. If seizures are rare, this is very difficult to do. In such cases, the doctor may recommend a test to provoke the onset of an attack – transesophageal atrial stimulation (TEAS). When performing PPSP, a thin electrode is inserted through the patient’s nose into the esophagus, which is installed at the level of the atria and, using a special device, allows electrical impulses to be applied to the heart. If a paroxysm of AF occurs, an ECG is recorded, then sinus rhythm is restored. CHPSP is carried out only in a hospital, in special departments specializing in the treatment of cardiac arrhythmias.

Atrial fibrillation paroxysm – what to do?

If you experienced an attack of uneven heart palpitations for the first time, you should immediately consult a doctor or call an ambulance team. Even if you feel good. Remember – it is very important to fix the attack on the ECG. The attack may end on its own after a while, but it is necessary to restore the correct rhythm within the first two days. The more time passes from the onset of the paroxysm, the more difficult it is for the heart to restore normal functioning and the higher the risk of blood clots in the chambers of the heart. If more than two days have passed since the onset of the attack or you do not know exactly the time of its occurrence, it is necessary to restore the heart rhythm only under the supervision of a doctor after examining the heart chambers on echocardiography, echocardiography (to exclude already formed blood clots) and special preparation with blood thinners (to prevent thrombosis).

If paroxysms of atrial fibrillation (atrial fibrillation) occur frequently, it is necessary to develop a plan of action with your doctor during an attack. With good tolerability of arrhythmia and with short (no more than 24 hours) attacks of arrhythmia, which often end on their own, you can not take special actions. It is necessary to continue taking the drugs recommended by the doctor without changing the dose. Your doctor may recommend a single dose of an antiarrhythmic drug in addition to basic therapy, or a temporary increase in the dose of medications already taken, when an attack occurs. If during the paroxysm of atrial fibrillation the state of health worsens significantly, or the arrhythmia lasts more than a day, a visit to the doctor is mandatory.

Which is “better” – seizures or persistent atrial fibrillation (atrial fibrillation)?

For a long time, doctors believed that the only optimal result of treatment was the restoration of proper, sinus rhythm. And now, in most cases, the doctor will advise you by all means to restore and maintain sinus rhythm. However, not in all cases. Studies have shown that if it is impossible to effectively maintain the restored sinus rhythm (when the heart constantly “breaks” into atrial fibrillation), permanent atrial fibrillation (atrial fibrillation) with medically controlled heart rate of about 60 beats per minute is safer than frequent paroxysms of atrial fibrillation (especially protracted, requiring the introduction of high doses of antiarrhythmic drugs or electrical impulse therapy).

The physician decides whether to restore sinus rhythm or maintain permanent atrial fibrillation. In each case, such a decision is individual and depends on the cause of the development of arrhythmia, the disease against which it arose, on its tolerance and the effectiveness of the treatment of atrial fibrillation to maintain the correct rhythm.

An attack that lasts more than two days should be treated only under medical supervision, after special training. If sinus rhythm is successfully restored, your doctor will adjust your ongoing antiarrhythmic therapy and recommend taking blood thinners for at least a month after cardioversion.

Treatment of atrial fibrillation (atrial fibrillation)

There are several ways to treat atrial fibrillation (atrial fibrillation) – restore sinus rhythm. This is the intake of antiarrhythmic drugs inside, the introduction of antiarrhythmic drugs intravenously and cardioversion (electropulse therapy, EIT). If the doctor restores the rhythm in the clinic or at the patient’s home, most often they start with intravenous drugs, then taking pills. The procedure is carried out under ECG control, the doctor observes the patient for 1-2 hours. If the restoration of sinus rhythm has not occurred, the patient is hospitalized in a hospital. In the hospital, drugs can also be administered intravenously, but if the time is limited (the duration of the attack approaches the end of the second day) or the patient does not tolerate the paroxysm (a decrease in blood pressure is observed, etc. ), EIT is more often used.

Cardioversion is performed under intravenous anesthesia, so the electrical shock is painless for the patient. The success of rhythm recovery depends on many factors: the duration of the attack, the size of the heart cavities (in particular, the left atrium), sufficient saturation of the body with an antiarrhythmic drug), etc. EIT efficiency approaches 90-95%.

If the paroxysm of atrial fibrillation lasts more than two days, it is possible to restore the rhythm only after special training. The main stages are taking blood-thinning drugs under the control of a special analysis (INR) and transesophageal echocardiography (TEE) before EIT to exclude blood clots in the heart cavities.

Attacks of atrial fibrillation – how to prevent?

In order for the paroxysms of atrial fibrillation not to resume, the patient must constantly take an antiarrhythmic drug. For the purpose of prevention. To date, there are many antiarrhythmics, the choice of the drug should be made by the doctor. A patient with atrial fibrillation needs to be monitored by a cardiologist, during which regular examinations are carried out (for example, echocardiography once a year, or daily Holter monitoring, if necessary, to assess the effectiveness of treatment), treatment correction. The selection of drug therapy is always, for any disease, a very painstaking task that requires literacy and perseverance on the part of the doctor and understanding and diligence on the part of the patient. Individual can be not only the effectiveness, but also the tolerability of treatment.

Failure of medical therapy for atrial fibrillation may be an indication for surgical treatment. In the left atrium (near the confluence of the pulmonary veins) there are zones in which electrical impulses are formed that can trigger atrial fibrillation. The increased electrical activity of these zones can be detected using a special electrophysiological examination (EPS). A special catheter is inserted into the cavity of the heart, the information obtained allows you to make an electrical “map” and determine the trigger (“starting”) areas. The study is performed under local anesthesia and is quite safe for the patient. After determining the “starting” areas, an operation is performed – radiofrequency ablation of trigger zones (RFA). The catheter, using high-frequency current, destroys these areas and disrupts the triggering of the arrhythmia. In four cases out of five, atrial fibrillation no longer resumes. In an animated form, the RFA process of trigger zones in atrial fibrillation is presented in the video.

Atrial fibrillation became permanent

In a certain proportion of patients suffering from attacks of atrial fibrillation, sooner or later there comes a time when it is no longer possible to restore sinus rhythm. Atrial fibrillation becomes permanent. As a rule, this happens in patients with significantly enlarged left atrium (4. 5 cm or more). Such an enlarged atrium is simply not able to maintain sinus rhythm. With a permanent form, the patient also needs medical supervision.

The goals of treatment are to keep the heart rate within 60-70 beats per minute at rest, prevent the formation of blood clots in the heart cavities and reduce the risk of thromboembolic complications.

Heart rate control is carried out with beta-blockers, digoxin or calcium antagonists (verapamil group), selecting an individual dose of the drug according to the principle “the higher the dose, the lower the heart rate.” At the optimal dose, the titration is completed and the patient receives it daily. The effectiveness of heart rate control can be assessed using 24-hour Holter ECG monitoring. If a decrease in the frequency of the rhythm cannot be achieved with pills, doctors resort to surgical methods. The arrhythmologist surgeon isolates the atria from the ventricles and implants a pacemaker that is programmed for a certain number of heartbeats at rest and adapts to stress.

To prevent thrombus formation, drugs are used that “thinn” the blood, that is, slow down the processes of blood clotting. For this purpose, aspirin and anticoagulants (most often warfarin) are used. To date, the approach to the tactics of anticoagulant therapy is determined on the basis of an assessment of the risk of thromboembolic complications and the risk of bleeding while taking these drugs, and is approved in the National Russian recommendations of the All-Russian State Audit Committee.

Many patients are afraid to start taking medications because complications such as bleeding are listed in the instructions. You should know that before prescribing anticoagulants, the doctor always weighs the benefits and risks of treatment with the drug, and prescribes only when he is completely sure that the benefits greatly outweigh the risks. Strict adherence to the recommendations and regular monitoring of blood tests (international normalized ratio (INR) for patients receiving warfarin) plus your awareness of the main mechanisms of action of the drug and the tactics of your actions at the first signs of bleeding make such treatment completely predictable and as safe as possible.

Relatively recently, endovascular occlusion of the left atrial appendage began to be performed in Russia to prevent the development of stroke in patients with chronic atrial fibrillation. The operation is an alternative to the use of anticoagulants in patients for whom these drugs are contraindicated, or for those who are indicated for the use of warfarin, but for one reason or another they do not receive it. Over 90% of thrombi that cause cardioembolic strokes in non-valvular atrial fibrillation form in the “ear” (natural appendage) of the left atrium, due to a decrease in blood flow velocity. This operation is performed in an X-ray operating room under dual control – transesophageal echocardiography and fluoroscopy.

Preliminary analysis of computed tomography data. For access, a puncture and catheterization of the femoral vein is performed. Through the conductor, the instruments are passed into the right atrium, after positioning, the interatrial septum is punctured, and through this puncture the conductor enters the left atrium. Then the implantation site is selected and the size of the occluder is selected. The occluder is installed at the mouth of the left atrial appendage, stopping the blood flow in it and, thus, the appearance of blood clots in this anatomical formation is excluded. In Krasnoyarsk, such operations are performed at the Regional Clinical Hospital.

Cardiologists of the “Center of Modern Cardiology” have not only all modern functional and laboratory methods for diagnosing diseases that cause atrial fibrillation , but also vast experience in diagnosing and treating various forms of atrial fibrillation .

About atrial fibrillation – read also AFIB Matters (in Russian)

A rare form of systemic amyloidosis with kidney damage – Afib amyloidosis | Batyushin

Introduction

Amyloidosis refers to the category of systemic diseases caused by the accumulation of amyloid proteins in a single organ or tissue or systems of organs and tissues of hereditary or acquired origin. There are more than thirty amyloid proteins that can cause the development of this pathological process in a wide range of acquired and hereditary diseases (Table 1) [1].

Table 1

Amloyldose options

9019 4

Systemic and/or local

9019 4

C

901 93

9022 4

902 24

The most common forms of systemic amyloidosis are AA-amyloidosis, which develops as a result of chronic infectious and non-infectious immunoinflammatory diseases, as well as AL-amyloidosis, which develops as a result of hyperproduction of light chains of immunoglobulins. Renal amyloidosis develops in approximately 50-65% of cases as part of systemic amyloidosis, however, amyloid nephropathy is an infrequent finding in clinical practice during puncture nephrobiopsy. This is due to the rare use of nephrobiopsy as a diagnostic method for amyloidosis. According to a number of studies, it occurs in approximately 4.5% of all biopsies and ranks 7th in terms of frequency of detection [2]. At the same time, at the age of over 60 years, amyloid nephropathy is detected in 3.5% of cases, while at the age of less than 60 years – only in 0.5% of cases [3]. Even less common is amyloid kidney damage in other types of amyloidosis (on-AA and non-AL).

A rare form of amyloidosis is AFib amyloidosis, which refers to hereditary forms of amyloidosis with systemic manifestations, but predominantly affecting the kidneys [4]. Despite the rarity of occurrence (about 1.3% of the total number of verified forms of amyloidosis), it belongs to the category of the most common hereditary forms of amyloidosis in European countries [5]. AFib amyloidosis was first described by Benson et al. in a Peruvian-Mexican family in 1993 [6].

Fibrinogen is a 340 kDa plasma protein synthesized by the liver and plays an important role in the coagulation cascade. Fibrinogen consists of two identical heterotrimers, each of which consists of three polypeptide chains called Aα, Bβ and γ-chain [7]. These polypeptide chains are encoded respectively by genes FGA, FGB and FGG . Mutation of the Aα chain of wild-type fibrinogen does not usually result in amyloid deposition. AFib amyloidosis is an autosomal dominant inherited systemic amyloidosis. To date, 17 amyloidogenic mutations have been described, including 7 missense mutations (c.1627G > A, c.1633G > A, c.1634A > T, c.1670C > A, c.1676A > T, c.1712C > A, c.1718G > T), 8 deletion mutations (c.1611delA, c.1619_1622delTTGT, c.1620delT, c.1622delT, c.1624_1627delAGTG, c.1629delG, c.1632delT, c.1673delA) and 2 insertion-deletion mutations (c.1606_1620del 1619_1620insCA, c. 1720_1721delGGinsTT) [8]. The most common variant in Europe is c.1634A>T (E526V). The kidney is the predominant organ involved in AFib amyloidosis, which is manifested by proteinuria, edema, hypertension, and azotemia. On average, the disease manifests itself clinically at the age of 40–60 years [9].

Description of a clinical case

Patient R., 48 years old, was admitted to the nephrology bed of the urology department of Rostov-on-Don with complaints of increased blood pressure (BP) up to 170/100 mm Hg . Art., unexpressed swelling of the face, lower extremities, headache. From the anamnesis, it is known that for the first time elevated blood pressure figures were detected during examination before vaccination in October 2021. During the laboratory and instrumental examination at the outpatient stage at the place of residence, lipid metabolism disorders and multiple chondrodegenerative changes in the spine were revealed. Antihypertensive (losartan 100 mg) and lipid-lowering therapy (atorvastatin 10 mg) was prescribed, blood pressure monitoring was recommended. However, the patient did not comply with the recommendations. In April 2022, a repeated examination revealed proteinuria up to 3.71 g/l, azotemia with a creatinine level of 110 µmol/l, hyperuricemia (450 µmol/l), hyperkalemia, hypercholesterolemia up to 10 mmol/l , hypertriglyceridemia up to 5.17 mmol/l. In May 2022, the patient was hospitalized in the therapeutic department of the State Budgetary Healthcare Institution of the Republic of Belarus named after I. ON THE. Semashko” in Simferopol with complaints of increased blood pressure, heaviness in the occipital region, dizziness, weakness, fatigue. Laboratory studies revealed proteinuria up to 2.0 g/l, cylindruria, azotemia persisted (creatitinine levels 110–100 µmol/l, GFR 53–64 ml/min), hyperuricemia increased (490 µmol/l), hypercholesterolemia up to 7.9 mmol/l, hypoalbuminemia (28 g/l), hypoproteinemia (50 g/l) appeared. The patient was treated, but the complaints persisted. Clinically noted periodically headaches, accompanied by an increase in blood pressure to 150/100 mm Hg. Art. During echocardioscopy, an increase in myocardial mass was noted (the mass index of the left ventricular myocardium was 114 g/m ² ), which was probably due to arterial hypertension. During the ultrasound examination of the abdominal cavity, hepatomegaly was noted, which is probably due to the involvement of the liver in the systemic process. When monitoring laboratory parameters in dynamics, an increase in proteinuria was noted, hypercholesterolemia persists. Due to the lack of effect from therapy, he came to Rostov-on-Don for a consultation with a nephrologist at the CB RZD-Medicine. During a conversation with the patient, it turned out that he was from Palestine, the family history was burdened on the maternal side (hypercholesterolemia and myocardial infarction). Daily proteinuria reached 9 at the time of examination..45 g / day. Electrophoresis of protein fractions of blood and urine with immunofixation was performed on an outpatient basis, according to which no M-gradient was detected in the blood, there was no Bence-Jones protein in the urine, and there was no pathological content of immunoglobulins.

In order to clarify the diagnosis, a puncture nephrobiopsy was performed on October 18, 2022. Light-optically, 8 out of 12 glomeruli were sclerosed. The surviving glomeruli are sharply hypertrophied, in the thickened basement membranes there are deposits of homogeneous, weakly eosinophilic, GHS-positive material, giving a weak positive Congo red color for amyloid. Tubulo-interstitium atrophy (about 25% of the area) with replacement by fibrous tissue and moderate lymphohistiocytic infiltrates, proteinaceous and vacuolar dystrophy of tubulocytes, numerous proteinaceous cylinders were revealed. Immunohistochemical examination does not reveal A-type amyloid. Immunofluorescent examination of the biopsy specimen revealed a weak luminescence of IgG, IgA, complement C3, lambda in the glomeruli intramembranously, in the walls of the vessels of the interstitium and cylinders. Electron microscopy made it possible to see dilated basement membranes in the glomerulus, accumulations of fibrils in separate areas similar to amyloid fibrils, and weakly granular deposits. Individual deposits have a high electron density (Fig. 1). Based on the data of a comprehensive pathomorphological study and laboratory parameters, it was concluded that the patient had amyloidosis of non-AA, non-AL type. The patient underwent mass spectrometry of blood and urine in order to identify a certain type of protein.

Figure 1. Homogeneous deposit of increased electron density (left), deposit with low granularity (right).

The rheumatoid factor was within the normal range (5.11 IU/ml, the norm is 0.00–14.00), the free kappa-chains of immunoglobulins in the blood were 14.42 μg/ml (the norm is 3.25–15, 81), free lambda chains — 17.13 µg/ml (norm — 3.23–28.05), kappa/lamda content index of immunoglobulin light chains — 0.34 (norm — 0.30–1.90). In the daily analysis of urine, proteinuria was represented mainly by albumin (60.32%), Bence-Jones protein was not detected. Figures 2 and 3 show the mass spectrograms of the blood and urine of patient R.

Figure 2. Fragment of the mass spectrogram of a biosample (blood serum) Fragment of the mass spectrogram of a biosample (urine)

Tables 2 and 3 present the spectrum of proteins, detected in pathological concentrations in the blood and urine of patient R. Myosin X and annexin found in the blood at elevated concentrations are usually evidence of invasion of amyloid masses into body tissues, and the soluble form of the endothelin receptor, platelet glycoprotein H-complement factor, fibrillin, antitrypsin and perrilin are witnesses of dysregulation of the coagulation and vascular-platelet components of hemostasis, often observed in various systemic processes. The identification of apolipoprotein AIV as a component of the amyloid protein complex is also understandable and has been described, among other things, in AFib amyloidosis [4]. The most interesting finding was the detection of high concentrations of fibrinogen alpha chains, which, in our opinion, is the main component of the amyloid complex.

Table 2

Spectrum of detected proteins in blood serum

1

900 02 When analyzing the results of mass spectrometry of urine, increased concentrations of the Aα chain of fibrinogen were also recorded, as well as components indicating the activation of the complement system and inflammation.

Table 3

Spectrum of detected peptides and proteins in urine0189

Protein name

Molecular

mass, Yes

pI

probability