Posted By Gina Saikin on October 28, 1998 at 10:53:50:
In Reply to: Re: Pericarditis and atrial fibrulation posted by CCF CARDIO MD -CRC on October 26, 1998 at 12:41:29:
I am a 48 year old female with no history of heart problems. I had a mild
case of pericarditis apparently in April, with a diagnosis when a similar, more
painful case hit and a cardiologist heard a rub. I was treated with prednisone and
hospitalized. I had recurrent attacks in
June, July, August, all controlled out of hospital with naprosyn and pain
pills, with very little interest on the part of my physician who then expressed
doubt about the cardiologist's diagnosis since he had not heard the rub himself.
The echocardiograms done in May and June showed no significant fluid. None
were done on the recurrent episodes. In early October, I was once again
hospitalized, was only given demerol until I left the hospital and was given
indocin (?) until I saw my regular doctor who then had an echocardiogram done
which showed minimal fluid. He also heard the rub and now believes I have
recurrent pericarditis. After two weeks of bedrest and slow recuperation and
1 1/2 weeks of 30 mg of prednisone, I was hospitalized with atrial fibrulation.
I have been placed on digoxsin and my blood pressure runs around 105/75 with
dips to 94/64. I feel very confused, want to see a specialist and would like
more info about the connection between these conditions, diet, etc. My
own doctor was not on call during this hospitalization.
Any help appreciated
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.
I hope you find this information useful. Information provided in the heart forum is for general purposes only. Only your physician can provide specific diagnoses and therapies. Please feel free to write back with additional questions.
If you would like to make an appointment at the Cleveland Clinic Heart Center, please call 1-800-CCF-CARE or inquire online by using the Heart Center website at www.ccf.org/heartcenter. The Heart Center website contains a directory of the cardiology staff that can be used to select the physician best suited to address your cardiac problem.
A little over a year ago, I was diagnosed with a 'little fluid around my heart' (pericarditis, I later learned) and an MVP, apparently severe enough to have my cardiologist remind me vehemently to use antibiotics prophylatically. Now, chest pains have returned that mimic those last year...I went to the ER, at the behest of my family doc, who of course, ran all the standard cardiac tests, and found nothing at the time...they DID want to admit me, but - ahem - a little fast talking and proof of a negative nuclear scan this summer helped forstall that However, I did promise to get a follow-up echo - which I can't get for two more weeks. CAN one be more susceptible to pericarditis once one has had it? Chest hurts almost all of the time...I sit at a desk most of the day (computer tech). I've had a lot of bouts of palpitations (event monitoring last summer showed 'occasional pvc's' - apparently not of concern to the cardiologist) with this pain, and noticed while I was in ER being monitored that my pulse rate was barely 60 (60-62 average), and my bp slightly high (160/80-90). I am NOT an athlete (matter of fact, um...kinda the opposite - I lead a rather sedentary life - well, as sedentary as I can be as a single mom of a 16 year old ADHD ). Could any/all of these things put together be of concern?
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