Pericarditis is an inflammation of the lining of the heart which has a variety of different causes including viruses. Chronic pericarditis may lead to atrial fibrillation (AF) which is a rapid beating of the upper chambers of the heart. Pericarditis can usually be treated with medications but occasionally will reuire surgery to "strip" the heart of the thickened lining. The best test to evaluate the need for this is an echocardiogram. Depending on the results of the echocardiogram additional testing such as a transesophageal echocardiogram (TEE) or right heart cath may be needed.
AF is generally treated with medications. There are many different types of medications of which sotalol is one of them. Often we will use flecanide or propafenone in a young person with AF. There are some new ablation techniques that can cure AF and these may be an option for you at some point. I have attached some more info on pericarditis and AF. If you would like a second opinion at the Cleveland Clinic I would recommend Dr. Bill Stewart or Dr. Brian Griffin.
Acute pericarditis classically presents with progressive, often severe, chest pain over hours. This mechanical pain is typically postural, being worse on lying supine and relieved by sitting forward. It is often pleuritic and aggravated by coughing and swallowing. The pain may radiate to the neck, and less frequently to the arms and back, making differentiation from coronary ischemic pain more difficult. There is often a low-grade fever associated with viral and idiopathic pericarditis, while purulent pericarditis is associated with very high fevers and systemic sepsis.
The presence of a pericardial rub is pathognomonic for pericarditis, though its absence does not exclude the syndrome. This "to and fro" rasping sound has a timing consistent with the cardiac cycle. It is best appreciated with the diaphragm of the stethoscope applied to the lower left sternal edge and is creaking in nature-like leather on leather. The sound classically has a triple cadence, with components related to (a) atrial systole, (b) ventricular systole and (c) ventricular diastole. In one-third of cases, the rub is biphasic, while in 10% it is monophasic. The intensity of the sound can be attenuated by subcutaneous tissue thickness and hyperinflated lung volume. Further, the development of a pericardial effusion as part of the inflammatory syndrome can lead to waxing and waning of the rub over days, though a loud pericardial rub can still be heard occasionally in the presence of a significant effusion. The sound should be differentiated from a pleural rub, which, while similar in character, is timed with the respiratory cycle; subcutaneous emphysema, which may be an associate in post surgical or traumatic cases; and loud intracardiac murmurs such as ventricular septal defect.
The electrocardiogram represents the most useful diagnostic test in acute pericarditis . Inflammation of the sub-epicardial myocardium is thought to be the mechanism producing ST- and T-wave changes, while inflammation of the atrium is thought to cause the PR-segment changes. In contrast to the regional ST changes of myocardial ischemia, pericarditis produces widespread ECG changes in limb and precordial leads. Four phases of ECG abnormalities have been recognized: Stage 1, with ST elevation and upright T waves, is present in 90% of cases. Over days the ST changes resolve and the ECG may look normal (Stage II). There may be further evolution to T-wave inversion (Stage III) and finally to normal (Stage IV).
The ECG abnormalities should be differentiated most importantly from acute myocardial ischemia. The ST changes are more widespread in pericarditis, lack Q-waves and have a typical "saddle-shaped" or concave appearance. The other important differential diagnosis of these ECG changes is the "early repolarization" pattern. While difficult without clinical correlation, differentiation can be made by the presence of PR segment elevation (especially aVR) and ST elevation in V6, which is uncommon in the early repolarization syndrome. Most patients with acute pericarditis remain in sinus rhythm.
Chest radiography contributes relatively little to the diagnosis of acute pericarditis. The presence of cardiomegaly may be seen in the minority of cases where a significant pericardial effusion has accumulated. Laboratory analysis of blood often shows a modest leukocytosis and raised sedimentation rate. Radionuclide scanning with In-111385, Ga-67386,387 has been reported to be useful in identifying the pericardium as the source of an inflammatory syndrome of unknown diagnosis in some patients. MRI, with Gd-DTPA enhancement, has identified specific regions of the pericardium involved in the inflammatory process.
The following diagnostic algorithm has been proposed. All patients should have a complete history and physical examination, electrocardiography, and chest radiography. Diagnosis specific testing should include tuberculin skin testing, rheumatoid factor and antinuclear antibody, viral studies from pharyngeal, and fecal swabs. In more complex cases (i.e., symptoms and signs lasting longer than 1 week, clinical evidence of tamponade, or purulent pericarditis), echocardiography, sputum/gastric aspirate for tubercle bacillus examination, and blood cultures are indicated. Pericardiocentesis (either percutaneous or surgical) is indicated for clinical tamponade, evidence for purulent pericarditis, high suspicion of tumor, or illness lasting longer than 1 week.
A disorder of heart rate and rhythm in which the upper heart chambers (atria) are stimulated to contract in a very rapid and/or disorganized manner; this usually also affects contraction of the ventricles.
Causes, incidence, and risk factors:
Arrhythmias are caused by a disruption of the normal functioning of the electrical conduction system of the heart. Normally, the atria and ventricles contract in a coordinated manner. In atrial fibrillation and flutter, the atria are stimulated to contract very quickly. This results in ineffective and uncoordinated contraction of the atria.
The impulses may be transmitted to the ventricles in an irregular fashion, or only some of the impulses may be transmitted. This causes the ventricles to beat more rapidly than normal, resulting in a rapid or irregular pulse. The ventricles may fail to pump enough blood to meet the needs of the body.
Causes of atrial fibrillation and flutter include dysfunction of the sinus node (the "natural pacemaker" of the heart) and a number of heart and lung disorders including coronary artery disease, rheumatic heart disease, mitral valve disorders, pericarditis, and others. Hyperthyroidism, hypertension, and other diseases can cause arrhythmias, as can recent heavy alcohol use (binge drinking). Some cases have no identifiable cause. Atrial flutter is most often associated with a heart attack (myocardial infarction) or surgery on the heart.
Atrial fibrillation or flutter affects about 5 out of 1000 people. It can affect either sex. Atrial fibrillation is very common in the elderly, but it can occur in persons of any age.
Follow the health care provider's recommendations for the treatment of underlying disorders. Avoid binge drinking.
sensation of feeling heart beat (palpitations)
pulse may feel rapid, racing, pounding, fluttering,
pulse may feel regular or irregular
shortness of breath
breathing difficulty, lying down
sensation of tightness in the chest
Note: Symptoms may begin and/or stop suddenly.
Signs and tests:
Listening with a stethoscope (auscultation) of the heart shows a rapid or irregular rhythm. The pulse may feel rapid or irregular. The normal heart rate is 60 to 100, but in atrial fibrillation/flutter
the heart rate may be 100 to 175. Blood pressure may be normal or low.
An ECG shows atrial fibrillation or atrial flutter. Continuous ambulatory cardiac monitoring--Holter monitor (24 hour test)-- may be necessary because the condition is often sporadic (sudden beginning and ending of episodes of the arrhythmia).
Tests to determine the cause may include:
a coronary angiography (rarely)
an exercise treadmill ECG
Treatment varies depending on the cause of the atrial fibrillation or flutter. Medication may include digitalis or other medications that slow the heart beat or that slow conduction of the impulse
to the ventricles.
Electrical cardioversion may be required to convert the arrhythmia to normal (sinus) rhythm.
There is not a consensus on the best long term management of atrial fibrillation but many doctors feel it is important to try everything, including cardioversion (shock) to try to get the heart back into regular rhythm. The risks of staying in afib are stroke (if not on anticoagulation) and decreased heart heart function (tachycardia induced cardiomyopathy). Not all afib can be maintained in regular rhythm and those patients must live with the afib and take chronic anticoagulation (blood thinners).
The disorder is usually controllable with treatment. Atrial fibrillation may become a chronic condition. Atrial flutter is usually a short-term problem.
incomplete emptying of the atria which can reduce the amount of blood the heart can pump
emboli to the brain (stroke) or elsewhere--rare
Calling your health care provider:
Call your health care provider if symptoms indicate atrial
fibrillation or flutter may be present.
Q: Are there other safe drugs I could take at home to avoid cardioversion?
A: There are many different drugs that are used in the attempt to keep the heart in sinus rhythm (SR) but as with any medication they all have various side-effects. You doctor can work with you on finding the best drug for your case.
Q: What are the side effects to Toprol.
A: Toprol XL is a long acting version of metoprolol. This drug is a beta-blocker. Potential side-effects of beta-blockers include fatigue, problems with diabetic control, and impotence.
Q: It seems that the better physical shape I stay in the less I have a problem with A.F. Could exercise have an impact?
A: There is no known effect of exercise on atrial fibrillation (AF).
Q: Is a pacemaker an alternative?
A: In some people who are unable to be controlled with drugs the electrical connection between the atria (upper heart chambers) and ventricles (lower heart chambers) is electrically severed and a pacemaker is placed to control the ventricles. The atria remain in fibrillation but the side effect of the rapid heart rate is eliminated. Chronic anticoagulation is required, as there is a risk of blood clots forming in the atria.
Q: I have an uncle that was diagnosed with IHSS. Are IHSS and Mitral valve prolapse related problems?
The links below are good sources of information about atrial fibrillation.
You only have one heart, and one life of course, so follow through on this like your life depended on it,
because it does.
Bouts of pericarditis can lead to much worse conditions.
(Research constrictive pericarditis on this forum & you'll find our story.)
If my husband could go back & be where you are now....
he would seek out a cardiologist who specialized in diseases of the pericardium ASAP.
***@**** Good luck & God bless
Hi , I am 33 year old.. I have discovered that I have AFIB about 1 and a half year ago.. Since then I had 2 attacks of rapid heart beat.. The first one when I went into an emergency room. My hear rate went to 240 bits per minute.. Since then I am taking Betapace 80m a day with an aspirin. My new cardialogist wants me to take something more mild.. I had another attack about a week ago.. Where my pulse was fine but my heart was beatig fast.. Is betapace to strong of a drug?? and why?
Also is ablation a choice with my condition??
Your answers would be greatly appriciated..
does anybody know if A-fib is heriditary??
I had a pacemaker implanted 4/17/01. The atrial lead perforated and pericarditis w/effusion developed. Frequent atrial fibs also began. After 6 weeks I was put on prednisone. I was put on Betapace at low evels and the level increased to 280 mg at which point I didn't fibrillate. From 6/2 until 7/18 I had frequent painful pericarditis. On 7/18 the atrial lead was removed and a passive lead implanted in the atrial appendage. I am on 280 mg of Betapace and am beginning to decrease the prednisone along with the addition of colchicine. Am also on Toprol XL 25 mg. Even on this amount of medicine I have intermittent short bursts of fibrillation which stops spontaneously unlike previous fibs which required i.v. intervention.
Does anyone have experience with persistent pericarditis following pacemaker implantation?
I would appreciate any input? It has been nearly 4 months of pain and fibrillation. I am unable to do anything. I was a tennis player daily, an aerobics enthusist - now I am just miserable.