TOC | Cardiology | 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pericarditis change frequently and some classic assumptions and descriptions, perpetuated in some publications, are outdated (Table 1).4-9 Except immunocompromised individuals, especially in patients with acquired immunodeficiency syndrome, there has been a sharp decline in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
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.
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)
Confusion With Other Diseases
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.
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: email@example.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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