TOC | Cardiology | Pericarditis
Acute
Pericarditis
Current Concepts and Practice
Contemporary understanding of acute pericarditis rests on 3 main considerations1: (1) pericarditis occurs in every category of disease, common and exotic (the spectrum is so broad that with every new case, the clinician should devise an appropriate differential diagnosis) (Box),2 (2) to avoid therapeutic mishaps, pericarditis must not be mistaken for other syndromes,3 and (3) the etiological and clinical spectra of acute pericarditis change frequently and some classic assumptions and descriptions, perpetuated in some publications, are outdated (Table 1).4-9 Except immunocompromised individuals, especially in patients with acquired immunodeficiency syndrome, there has been a sharp decline in infectious pericarditis.10 Tuberculous pericarditis has declined markedly in developed countries.11
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Pericarditis is common in many diseases like rheumatoid arthritis
and lupus in which it may or may not be apparent, or, as during
transmural myocardial infarction, usually concealed by other
signs and symptoms. When clinically recognizable, the presentation
remains classic: pain anywhere in the chest but mainly central
and usually pleuritic (ie, respirophasic and worse on
recumbency).1
However, pericarditic pain can have all the characteristics of
ischemic pain, including the same routes of
radiation.2(pp94-113)
A common clinical finding is pain occurring in or radiating to
one or both trapezius ridges (both phrenic nerves pass through the
anterior pericardium and innervate each trapezius
ridge1-2(pp94-113).
Patients who complain of shoulder or neck pain should be asked
to point to its location to identify any trapezius ridge
involvement.
Suspicion of acute pericarditis necessitates careful auscultation, particularly the left lower sternal edge and at the cardiac borders. A monophasic, diphasic, or triphasic pericardial rub is diagnostic of acute pericarditis.1, 12 Although rubs are virtually 100% specific, sensitivity depends on frequency of auscultation, because they tend to come and go over hours. Without a rub, it is difficult at the bedside to be certain about acute pericarditis.
Fortunately, in most cases of common etiologiesidiopathic, autoimmune, or viral (often clinically identical)the early electrocardiogram (ECG) remains classic (ie, near-ubiquitous ST segment [J point] elevations), usually with PR segment depressions in most leads and the reverse always in a VR and usually V1 (Figure 1). The PR segment deviations may precede ST elevation if the patient is observed soon after the onset of symptoms.2(pp40-54) Many patients have only PR segment depressions, often missed or misinterpreted as ST elevations. Historically,1, 13 the ECG findings in a patient with pericarditis progressed from ST elevations (stage 1) through descent of the J points (stage 2) followed by T wave inversion (stage 3) to stage 4 (restitution to the baseline ECG).6 Today, except for purulent pericarditis,1 stage 1 alone is frequently the only ECG finding if the patient is promptly treated, presumably due to effective nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin. Although the stage 1 ECG finding is quasi-diagnostic, 43% of patients with rubs presenting in the emergency department had an atypical ECG.13 A common but poorly understood mimic of the stage 1 ECG finding is early repolarization.
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In the absence of large controlled clinical trials, anecdotal therapeutic experience must be cited. Aspirin may be effective, but the widest contemporary experience is with ibuprofen1 and, because of the demonstrated effectiveness of colchicine (as monotherapy or combined therapy), the best combination may be ibuprofen, 800 mg every 8 hours, and colchicine, 0.6 mg twice daily.14 Colchicine also tends to prevent recurrent pericarditis. Ibuprofen has the advantage of relatively few adverse effects and the potential advantage of increasing coronary flow. In contrast, indomethacin usually controls pain but has a poor adverse effect profile and reduces coronary flow.15 (No trials of cyclooxygenase 2 inhibitors for pericarditis are available.) Although controlled trials are lacking, combined therapy usually suffices within 1 to 3 days. Combined therapy could be continued for 7 to 14 days followed by tapering for another 1 or 2 weeks because of the possibility of early recurrence. An oral corticosteroid should only be used if it is also indicated for an underlying disease or if the patient's syndrome is severe and resistant to NSAIDs.1 It appears that the early use of corticosteroids in most forms of pericarditis actually contributes to recurrence, frequently a stubborn, corticosteroid-dependent, and disabling syndrome.14 Most patients do not wish to be physically active during an acute attack, and physical activity could exacerbate accompanying superficial myocarditis; indeed, classic ST-T segment changes reflect myocarditis.1-2(pp40-54)
The most common confusing element in the diagnosis of acute
pericarditis is ECG misinterpretation, especially as acute
myocardial infarction. The differential diagnosis is summarized
in
Table
2. Computers are prone to diagnose infarction, usually
inferolateral, which is especially misleading in patients with
nonpleuritic chest pain. This has led to thrombolysis with no
coronary lesion, sometimes causing pericardial hemorrhage and
tamponade.16
For unknown reasons, this is uncommon with warfarin
anticoagulation. Differential diagnosis may become more difficult,
because serum enzyme and troponin levels usually
rise.1
These reflect the superficial myocarditis with creatine phosphokinase
of muscle band and troponin levels roughly paralleling the degree
of ST elevation. These levels are not yet investigated in
epistenocardiac pericarditispericarditis early in the course
of myocardial
infarction.17
In practice, confusion with pulmonary syndromes including pleurisy,
mainly because of respirophasic pain, is not often a problem.
Occasionally pulmonary embolism symptoms suggest pericardial disease,
rarely with a pulmonary Dressler syndrome (clinically dry or effusive
pericarditis following pulmonary
embolism).1-2(pp94-113)
The pain of dissecting aortic hematoma may not only simulate
pericarditis, but dissecting blood may enter the pericardium producing
rubs and suggestive ECG
abnormalities.2(pp94-113)
Echocardiography or computed tomography usually identifies the
aortic lesion.
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Pericardial
Effusion and Cardiac Tamponade
Any form of pericardial inflammation can induce pericardial effusion
and bleeding; therefore, an echocardiogram is recommended. Doppler
echocardiographic study either will show an effusion or can be
used as a baseline for any subsequent hemodynamic compromise (ie,
cardiac tamponade), usually signaled by increasing shortness of
breath that can mimic heart failure. The prime clinical sign of
tamponade is pulsus paradoxus (PP), an inspiratory fall in arterial
pressure of at least 10 mm
Hg.1,
18
The sensitivity and specificity of PP are difficult to determine:
4 authoritative studies between 1991 and 1999 give its prevalence
between 12% and
75%.17
The echocardiogram frequently shows diastolic chamber collapses
of the right atrium, right ventricle, or both, occasionally the
left atrium and rarely the left
ventricle.19
Right atrium and right ventricle collapses are sensitive and become
more specific if they last for at least a third of the cardiac
cycle.19
Combined right atrium and left atrium collapse is virtually
diagnostic of tamponade. However, hypovolemic patients can have
chamber collapses without tamponade, a particular problem in
patients with multiple trauma with chest and pericardial involvement
because bleeding elsewhere depletes blood
volume.1
In contrast, false negatives (no chamber collapses) occur with
increased stiffness of the right or left heart due to preexisting
hypertrophy and with significant valve disease, especially aortic
regurgitation.1,
19
These also tend to cancel PP. Doppler echocardiographic traces often
give a strong clue: greatly exaggerated respiratory variation of
all transvalvular flows; for the mitral valve, inspiratory reduction
of flow should be 25% or more of the expiratory level for maximum
specificity. Tamponading effusions must be removed by the most
expeditious means: paracentesis or surgical
drainage.1,
7
Once pain, fever, and evidence of tamponade are recognized and
managed, the question of etiology can be addressed. Overall,
the etiologic range is determined by 9 general categories
(Box).
Most cases continue to be idiopathic, presumably either viral
or autoimmune, and require no etiologically specific management.
Patients with human immunodeficiency virus may need antiretroviral
agents, especially because pericardial disease with acquired
immunodeficiency syndrome is a sign of a serious phase or a
superinfection requiring specific
antibiotics.1
The broad etiological spectrum of acute pericarditis requires
initial consideration of both common and unusual diseases that
could be responsible. Thus, diseases or conditions known to involve
the pericardium (eg, infections, vasculitides, neoplasia, and
chest trauma) always raise the possibility of acute pericarditis.
Examples of the many uncommon or rare causes include inflammatory
bowel disease,
thalassemia,
many drug reactions, pancreatitis, Gaucher disease, and even yellow
nail
syndrome.1-2(pp94-113)
Many others, often initially undiagnosed, may underlie a given
case because syndromes first presenting as acute pericarditis
necessarily masquerade as idiopathic pericarditis. This includes
a modern form of acute pericarditis following cardiac and
pericardial surgery, which is presumably
autoimune1:
the postpericardiotomy syndrome, appearing days, weeks, or months
postoperatively.1,
20
This and other iatrogenic
pericardiopathies3
are diseases of medical progress. Personal physicians evaluating
their postoperative patients most consider postpericardiotomy
syndrome in those presenting with a new, otherwise idiopathic,
acute pericarditis.
Acute pericarditis has a wide spectrum of etiologies, although
shifting with locally prevalent underlying diseases. Modern
advances have reduced the number of infectious cases and restricted
the ECG stage
sequence.2(pp40-54)
The NSAIDs, especially ibuprofen, recently with the addition of
colchicine, have been rapidly effective in most appropriately
diagnosed cases. However, misinterpretation as other disease,
especially acute myocardial infarction, pulmonary embolism, and
heart failure with tamponade, is common. Doppler echocardiographic
recording has largely solved the differential diagnosis of pericardial
effusion and aided the recognition of cardiac tamponade. Iatrogenic
pericarditis is a modern development following surgery and invasive
medical procedures. Finally, durable misconceptions
(Table
1) must be understood to avoid diagnostic and therapeutic
pitfalls.
Corresponding Author and Reprints: David H. Spodick, MD, DSc,
Cardiovascular Division, Worcester Medical Center, 20 Worcester
Center Blvd, Worcester, MA 01608 (e-mail:
david.spodick@tenethealth.com).
Financial Disclosure: Dr Spodick receives royalties from his book.2
Author Affiliation: University of Massachusetts Medical School, Cardiovascular Medicine Fellowship Program, Saint Vincent Hospital, Worcester.
1.
Spodick DH. Pericardial diseases. In: Braunwald E, Zipes DP, Libby P, eds.
Heart Disease. 6th ed. Philadelphia, Pa: WB Saunders & Co;
2001:823-1866.
2. Spodick DH. The Pericardium: A Comprehensive Textbook. New York, NY: Dekker; 1997.
3. Spodick DH, Bishop RL. Computer treason: intraobserver variability of an electrocardiographic computer system. Am J Cardiol. 1997;80:102-103. ISI | MEDLINE
4. Spodick DH. Frequency of arrhythmias in acute pericarditis determined by Holter monitoring. Am J Cardiol. 1984;53:842-845. ISI | MEDLINE
5. Merce J, Sagrista-Sauleda J, Permanyer-Miraldo G, et al. Correlation between clinical and Doppler echocardiographic findings in patients with moderate and large pericardial effusion: implications for the diagnosis of cardiac tamponade. Am Heart J. 1999;138:759-784. ISI | MEDLINE
6. Spodick DH. Diagnostic electrocardiographic sequences in acute pericarditis: significance of PR segment and PR vector changes. Circulation. 1973;48:575-580. ISI | MEDLINE
7. Reddy PS, Curtiss EI, Uretsky BF. Spectrum of hemodynamic changes in cardiac tamponade. Am J Cardiol. 1990;66:1487-1491. ISI | MEDLINE
8. Myers RB, Spodick DH. Constrictive pericarditis: clinical and pathophysiologic characteristics. Am Heart J. 1999;138:219-232. ISI | MEDLINE
9. Lieng LH, Oh JK, Seward JB, et al. Clinical profile of constrictive pericarditis in the modern era: a survey of 135 cases. J Am Coll Cardiol. 1996;27:32A-33A.
10. Zayas R, Anguita M, Torres F, et al. Incidence of specific etiology and role of methods for specific etiologic diagnosis of primary acute pericarditis. Am J Cardiol. 1995;75:378-382. CrossRef | ISI | MEDLINE
11. Fowler NO. Tuberculous pericarditis. JAMA. 1991;266:99-103. ABSTRACT
12. Maisch B. Pericardial diseases, with the focus on etiology, pathogenesis, pathophysiology, new diagnostic imaging methods, and treatment. Curr Opin Cardiol. 1994;9:379-388. ISI | MEDLINE
13. Bruce MA, Spodick DH. Atypical electrocardiogram in acute pericarditis: characteristics and prevalence. J Electrocardiol. 1980;13:61-66. ISI | MEDLINE
14. Permanyer-Miralda G, Sagrista-Sauleda J, Soler-Soler J. Primary acute pericardial disease: a prospective series of 231 consecutive patients. Am J Cardiol. 1985;56:623-630. ISI | MEDLINE
15. Friedman PL, Brown EJ Jr, Gunther S, et al. Coronary vasoconstrictor effect of indomethacin in patients with coronary-artery disease. N Engl J Med. 1981;305:1171-1175. ABSTRACT
16. Permanyer-Miralda G, Sagrista-Sauleda J, Shabetai R, et al. Pericarditis aguda: algunos aspectos del diagnostico etiologico del tratamiento. In: Soler-Soler J, Permanyer-Miralda G, Sagrista-Sauleda J, eds. Enfermedades del Pericardio. Barcelona, Spain: Edficiones Doyma; 1988:5-22.
17. Spodick DH, Roldan AC. The patient with pericardial disease. In: Roldan CA, Abrams J, eds. Evaluation for the Patient With Heart Disease: Integrating the Physical Exam and Echocardiography. Philadelphia, Pa: Williams & Wilkins; 2002:339-364.
18. Swami A, Spodick DH. Pulsus paradoxus in cardiac tamponade: a pathophysiologic continuum. Clin Cardiol. In press.
19. Reydel B, Spodick DH. Frequency and significance of chamber collapses during cardiac tamponade. Am Heart J. 1990;119:1160-1163. ISI | MEDLINE
20. Lee KS, Marwick T. Hemopericardium and cardiac tamponade associated with warfarin therapy. Cleve Clin J Med. 1993;60:336-338. ISI | MEDLINE
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