INTRODUCTION — The pericardium is a fibroelastic sac made up of visceral and parietal layers separated by a (potential) space, the pericardial cavity. In healthy individuals, the pericardial cavity contains 15 to 50 mL of an ultrafiltrate of plasma.
Diseases of the pericardium present clinically in one of several ways:
●Acute and recurrent pericarditis
●Pericardial effusion without major hemodynamic compromise
Acute pericarditis refers to inflammation of the pericardial sac. The term myopericarditis, or perimyocarditis, is used for cases of acute pericarditis that also demonstrate features consistent with myocardial inflammation. (See 'Diagnosis' below.)
The clinical presentation and diagnostic evaluation for acute pericarditis will be reviewed here. The etiology of pericarditis, treatment and prognosis of acute pericarditis, and other pericardial disease processes are discussed separately. (See "Etiology of pericardial disease" and "Acute pericarditis: Treatment and prognosis" and "Recurrent pericarditis" and "Myopericarditis" and "Cardiac tamponade" and "Constrictive pericarditis: Diagnostic evaluation" and "Pericardial effusion: Approach to diagnosis".)
EPIDEMIOLOGY — Acute pericarditis is the most common disorder involving the pericardium. Epidemiologic studies are largely lacking, and the exact incidence and prevalence of acute pericarditis are unknown. However, acute pericarditis is recorded in approximately 0.1 to 0.2 percent of hospitalized patients and 5 percent of patients admitted to the emergency department for nonischemic chest pain [1,2].
●In an observational study from an urban area in northern Italy, the incidence of acute pericarditis was 27.7 cases per 100,000 persons per year .
●In an observational study from Finland that included 670,409 cardiovascular admissions to 29 hospitals across the country over a 9.5-year period, the standardized incidence rate for pericarditis requiring hospitalization was 3.3 cases per 100,000 person-years .
Acute pericarditis is a common disorder in several clinical settings, where it may be either the first manifestation of an underlying systemic disease or represent an isolated process. In developed countries, most cases of acute pericarditis are considered of possible or confirmed viral origin, although the exact etiology of most cases remains undetermined following a traditional diagnostic approach . (See "Etiology of pericardial disease".)
Patients with human immunodeficiency virus (HIV) infection treated with antiretroviral therapy who develop acute pericarditis have an etiologic spectrum very similar to non-HIV-infected patients. However, HIV infection itself, along with tuberculosis, persist as major causes of acute pericarditis in developing countries or in patients without access to antiretroviral therapy. (See "Cardiac and vascular disease in patients with HIV", section on 'Pericardial disease'.)
CLINICAL FEATURES — Acute pericarditis can present with a variety of nonspecific signs and symptoms, depending on the underlying etiology. The major clinical manifestations of acute pericarditis include [2,4]:
●Chest pain – Typically sharp and pleuritic, improved by sitting up and leaning forward. (See 'Chest pain' below.)
●Pericardial friction rub – A superficial scratchy or squeaking sound best heard with the diaphragm of the stethoscope over the left sternal border. (See 'Pericardial friction rub' below.)
●Electrocardiogram (ECG) changes – New widespread ST elevation and PR depression. (See 'Electrocardiogram' below.)
●Pericardial effusion – A pericardial effusion is a common feature of pericarditis but is not required for diagnosis. (See 'Echocardiogram' below.)
Patients with an infectious etiology may present with signs and symptoms of systemic infection such as fever and leukocytosis. Viral etiologies in particular may be preceded by "flu-like" respiratory or gastrointestinal symptoms. Patients with a known autoimmune disorder or malignancy may present with signs or symptoms specific to their underlying disorder.
Chest pain — The vast majority of patients with acute pericarditis present with chest pain (>95 percent of cases) . The chest pain of pericarditis must always be distinguished from other common and/or life-threatening causes of chest pain (table 1) such as myocardial ischemia, pulmonary embolism, aortic dissection, gastroesophageal reflux disease, and musculoskeletal pain. (See "Evaluation of the adult with chest pain in the emergency department" and "Outpatient evaluation of the adult with chest pain".)
Chest pain that results from acute pericarditis is typically fairly sudden in onset and occurs over the anterior chest. Unlike pain due to myocardial ischemia, chest pain due to pericarditis is most often sharp and pleuritic in nature, with exacerbation by inspiration or coughing . One of the most distinctive features is the tendency for a decrease in intensity when the patient sits up and leans forward. This position (seated, leaning forward) tends to reduce pressure on the parietal pericardium, particularly with inspiration, and may also allow for splinting of the diaphragm. Radiation of chest pain to the trapezius ridge has also been considered to be fairly specific for pericarditis. In some patients, dull, oppressive pain may occur; in such cases, it is more difficult to distinguish pericarditis from other causes of chest pain.
Chest pain is likely to be present in cases of acute pericarditis caused by infection, but may be minimal or absent in patients with uremic pericarditis or pericarditis associated with a rheumatologic disorder (although in some patients, pleuritic chest pain and pericarditis can be the initial presentation of systemic lupus erythematosus). (See "Pericardial involvement in systemic autoimmune diseases".)
Pericardial friction rub — The presence of a pericardial friction rub on physical examination is highly specific for acute pericarditis (movie 1). Classically, pericardial friction rubs are triphasic, with a superficial scratchy or squeaking quality. Pericardial friction rubs are often intermittent, with an intensity that tends to wax and wane, and are best heard using the diaphragm of the stethoscope. (See "Auscultation of heart sounds", section on 'Pericardial friction rub and other adventitious sounds'.)
Pericardial friction rubs, which occur during maximal movement of the heart within its pericardial sac, are said to be generated by friction between the two inflamed layers of the pericardium. However, this commonly offered explanation for its mechanism may be an oversimplification, as patients with a pericardial effusion may also have an audible friction rub.
The classic pericardial friction rub consists of three phases, corresponding to movement of the heart during atrial systole, ventricular systole, and the rapid filling phase of early ventricular diastole. Patients in atrial fibrillation lack atrial systole, and therefore will have a two-phase rub. Additionally, for uncertain reasons, some rubs are present only during one (one component) or two phases (two components) of the cardiac cycle . In a review of auscultation and phonocardiography in 100 patients with a pericardial rub, the rub was triphasic in 52 percent of patients, biphasic in 33 percent, and monophasic in 15 percent .
Pericardial rubs may be localized or widespread, but are usually loudest over the left sternal border . The intensity of the rub frequently increases after application of firm pressure with the diaphragm, during suspended respiration, and with the patient leaning forward or resting on elbows and knees (picture 1). This last maneuver is designed to increase contact between visceral and parietal pericardium, but is seldom used in practice since it is cumbersome for the patient.
Friction rubs tend to vary in intensity and can come and go over a period of hours; therefore, the sensitivity for detection of a rub is variable and depends in large part on the frequency of auscultation. Pericardial rubs may be easier to hear in patients without a pericardial effusion, but this finding is not universal and is not well documented. In a report of 100 patients with acute pericarditis, a pericardial rub was present in 34 of 40 (85 percent) without an effusion . This prevalence is considerably higher than the 35 percent incidence of friction rubs reported in another series .
Breath-holds during auscultation permit distinction of a pericardial friction rub from a pleuropericardial or pleural rub. A pleuropericardial rub results from friction between the inflamed pleura and the parietal pericardium, while a pleural rub is the result of friction between the inflamed visceral and parietal pleura. As such, pleuropericardial and pleural rubs can be heard only during the inspiratory phase of respiration. (See "Auscultation of heart sounds", section on 'Pericardial friction rub and other adventitious sounds'.)
Electrocardiogram — The ECG in acute pericarditis may evolve through as many as four stages with highly variable temporal evolution of ECG changes. The four typical stages of ECG changes (figure 1) in patients with acute pericarditis include:
Typical ECG findings
●Stage 1, seen in the first hours to days, is characterized by widespread ST elevation (typically concave up) with reciprocal ST depression in leads aVR and V1 (waveform 1). There is also frequently an atrial current of injury, reflected by elevation of the PR segment in lead aVR and depression of the PR segment in other limb leads and in the left chest leads, primarily V5 and V6. Thus, the PR and ST segments typically change in opposite directions. PR segment deviation, which is highly specific, though less sensitive, is frequently overlooked.
The TP segment is recommended as the baseline for comparison when measuring both PR and ST segment changes in acute pericarditis.
●Stage 2, typically seen in the first week, is characterized by normalization of the ST and PR segments.
●Stage 3 is characterized by the development of diffuse T-wave inversions, generally after the ST segments have become isoelectric. It is typically seen in the subacute phase, and its duration is not well documented and likely highly variable.
●Stage 4 is represented by normalization of the ECG. It can occur directly from stage 1 in self-limited cases or with prompt response to medical therapy.
Atypical ECG findings — Pericarditis does not always result in the typical ECG changes described above. In many patients, the ECG returns to normal without going through the above stages if the disease responds well to treatment or spontaneously resolves. Moreover, some patients have no subepicardial inflammation, and the ECG remains normal, as discussed below.
Atypical ECG changes are seen in up to 40 percent of patients with acute pericarditis . Additionally, localized ST elevation and T-wave inversion occur before ST-segment normalization in a minority of patients with acute pericarditis without myocardial involvement. These changes can simulate ECG changes seen in patients with an acute coronary syndrome. (See 'Differentiation from acute myocardial infarction' below and "ECG tutorial: Myocardial ischemia and infarction" and "ECG tutorial: ST and T wave changes".)
Changes in the ECG in patients with acute pericarditis signify inflammation of the epicardium, since the parietal pericardium itself is electrically inert. However, some causes of pericarditis do not result in significant inflammation of the epicardium and, as such, may not alter the ECG. An illustration of this is uremic pericarditis, in which there is prominent fibrin deposition but little or no epicardial inflammation. As a result, the ECG often shows none of the changes associated with pericarditis .
The temporal evolution of ECG changes with acute pericarditis is highly variable from one patient to another. Treatment can accelerate or alter ECG progression. The duration of the ECG changes in pericarditis also depends upon its cause and the extent of associated myocardial damage .
Arrhythmias — Sustained arrhythmias are uncommon in acute pericarditis, except in the postthoracotomy setting. This was illustrated in a review of 100 consecutive patients in which only seven arrhythmias were identified; all were atrial and all occurred in patients with underlying heart disease . In a separate report comparing patients with myopericarditis and uncomplicated acute pericarditis, cardiac arrhythmias were more commonly present in patients with myopericarditis (odds ratio 17.6, 95% CI 5.7-54.1) . Thus, the presence of atrial or ventricular arrhythmias is suggestive of concomitant myocarditis or an unrelated cardiac disease.
Differentiation from acute myocardial infarction — While both acute pericarditis and acute myocardial infarction (MI) can present with chest pain and elevations in cardiac biomarkers, the ECG changes in acute pericarditis differ from those in acute ST-elevation MI (STEMI) in several ways (table 2) . These distinctions assume that the pericarditis does not occur during or soon after an acute MI. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction" and "Pericardial complications of myocardial infarction" and "ECG tutorial: ST and T wave changes" and "ECG tutorial: Myocardial ischemia and infarction".)
●Morphology – The ST-segment elevation in acute pericarditis begins at the J point, which represents the junction between the end of the QRS complex (termination of depolarization) and the beginning of the ST segment (onset of ventricular repolarization), rarely exceeds 5 mm, and usually retains its normal concavity (waveform 1). Although similar patterns can occur with STEMI (where ST-segment elevation also begins at the J point), the typical finding in a STEMI patient is convex (dome-shaped) ST elevation (a pattern not characteristic of acute pericarditis) that may be more than 5 mm in height (waveform 2).
●Distribution – ST-segment elevations in STEMI are characteristically limited to anatomical groupings of leads that correspond to the localized vascular area of the infarct (anteroseptal and anterior leads V1 to V4; lateral leads I, aVL, V5, and V6; inferior leads II, III, and aVF) (waveform 2). The pericardium envelops the heart, and, therefore, the ST changes are more generalized and typically present in most leads (waveform 1).
●Reciprocal changes – Acute STEMI is often associated with reciprocal ST-segment changes, which are not seen with pericarditis, except in leads aVR and V1.
●Concurrent ST and T-wave changes – ST-segment elevation and T-wave inversions do not generally occur simultaneously in pericarditis, while they commonly coexist in acute STEMI (waveform 2). Furthermore, the evolution of repolarization abnormalities often takes place more slowly and more asynchronously among affected leads in pericarditis than in STEMI.
●PR segment – PR elevation in aVR with PR depression in other leads due to a concomitant atrial current of injury is frequently seen in acute pericarditis but rarely seen in acute STEMI.
●Other – Hyperacute T waves (waveform 3), new pathologic Q waves, and QT prolongation are all rare in patients with acute pericarditis but are common in acute MI.
Differentiation from early repolarization variant — The early repolarization variant ECG pattern may be present in as many as 20 percent of healthy young adults and is often confused with acute pericarditis . Early repolarization variant is characterized by ST elevation of the J point at the beginning of the ST segment. As a result, there is elevation of the ST segment itself, which maintains its normal configuration (waveform 4). In early repolarization variant, ST elevation is most often present in the anterior and lateral chest leads (V3 to V6), although other leads can be involved. (See "Early repolarization".)
The following ECG features can be helpful in distinguishing acute pericarditis from early repolarization variant:
●ST elevations occur in both the limb and precordial leads in most cases of acute pericarditis (47 of 48 in one study), whereas approximately one-half of subjects with early repolarization variant have no ST deviations in the limb leads .
●PR deviation and evolution of the ST and T changes strongly favor pericarditis, as neither is seen in early repolarization variant.
●A ratio of ST elevation to T-wave amplitude in lead V6 greater than 0.24 favors the presence of acute pericarditis, as suggested by a small study ).
Patients with chronic kidney disease — Two forms of pericarditis have been described among patients with advanced chronic kidney disease: "uremic pericarditis," which generally refers to pericarditis beginning before dialysis or within eight weeks of dialysis initiation; and "dialysis-associated pericarditis," which refers to pericarditis typically arising any time after eight weeks of dialysis initiation. The clinical features of pericarditis in chronic kidney disease can have similarities to those observed with other causes, although classic ECG findings are less commonly seen in these patients.
●Uremic pericarditis results from inflammation of the visceral and parietal membranes of the pericardial sac. While the cause is uncertain, uremic toxins have been implicated due to the rapid resolution of symptoms that typically follows initiation of dialysis. With the exception of systemic immune disorders (such as lupus erythematosus or scleroderma), there is no relationship between uremic pericarditis and the underlying cause of kidney disease.
●Dialysis-associated pericarditis may have a more complex pathogenesis since it is less responsive to increasing the frequency or intensity of dialysis. Pericardial fluid among patients with dialysis-associated pericarditis is often serosanguinous due to heparin administration during dialysis and presence of uremic platelet dysfunction. It is also more likely to be associated with hemodynamic instability . The cause is not known, but repetitive anticoagulation, viral infection, and disordered calcium and phosphorous balance with hyperparathyroidism have been postulated to play a role in some patients.
Our approach to diagnostic testing — For a patient who presents with suspected acute pericarditis, we recommend the following evaluation, which is in general agreement with the recommendations of various professional societies [16,17]:
●History and physical examination – This evaluation should consider disorders that are known to involve the pericardium, such as prior malignancy, autoimmune disorders, uremia, recent MI, and prior cardiac surgery. The examination should pay particular attention to auscultation for a pericardial friction rub and the signs associated with cardiac tamponade.
●Initial testing in all suspected cases:
•An ECG. (See 'Electrocardiogram' above.)
•Chest radiography. (See 'Chest radiograph' below.)
•Echocardiography, with urgent echocardiography if cardiac tamponade is suspected. Even a small effusion can be helpful in confirming the diagnosis of pericarditis, although the absence of an effusion does not exclude the diagnosis . In addition, echocardiography can be particularly helpful if purulent pericarditis is suspected, if there is concern about myocarditis, or if there is radiographic evidence of cardiomegaly, particularly if this is a new finding. (See 'Echocardiogram' below.)
●Selected additional testing – Follow-up testing should be performed on a case-by-case basis and may include:
•Blood cultures if fever higher than 38°C (100.4°F), signs of sepsis, or a documented, concomitant bacterial infection (eg, pneumonia).
•Viral studies (eg, culture, polymerase chain reaction, viral serology, etc) are not routinely obtained (with the exception of serology for HIV and hepatitis C virus), since the yield is low and management is not altered for most patients .
•Antinuclear antibody (ANA) titer in selected cases (eg, young women, especially those in whom the history suggests a rheumatologic disorder). Rarely, acute pericarditis is the initial presentation of systemic lupus erythematosus (SLE). It is important to recognize that a positive ANA is a nonspecific test. A rheumatology consult should be sought in patients with pericarditis in whom a diagnosis of SLE is being entertained. (See "Non-coronary cardiac manifestations of systemic lupus erythematosus in adults".)
•Tuberculin skin test or an interferon-gamma release assay if not recently performed. The interferon-gamma release assay is most helpful in immunocompromised or HIV-positive patients and in regions where tuberculosis is endemic. However, the choice of testing varies by country and by level of suspicion. (See "Tuberculosis infection (latent tuberculosis) in adults: Approach to diagnosis (screening)", section on 'Diagnostic approach'.)
•Multimodality imaging is an integral part of modern management for pericarditis and pericardial diseases. Among multimodality imaging tests, echocardiography is recommended for all patients, followed by cardiovascular magnetic resonance (CMR) imaging with administration of gadolinium or computed tomography (CT) imaging for selected patients (eg, nondiagnostic echocardiography, concerns about constrictive pericarditis, complicated course, suspicion of specific etiology, etc) [16,19].
•Pericardiocentesis should be performed for therapeutic purposes in patients with cardiac tamponade, and should be considered for diagnostic purposes in patients suspected of having a malignant or bacterial etiology, or in patients with a symptomatic effusion refractory to medical therapy. (See "Pericardial effusion: Approach to diagnosis".)
Echocardiogram — Echocardiography is often normal in patients with the clinical syndrome of acute pericarditis unless there is an associated pericardial effusion. While the finding of a pericardial effusion in a patient with known or suspected pericarditis supports the diagnosis, the absence of a pericardial effusion or other echocardiographic abnormalities does not exclude it.
Large and/or hemodynamically significant pericardial effusions are rare as the initial presentation of acute pericarditis. In one series of 300 consecutive patients with acute pericarditis, pericardial effusion was present in 180 patients (60 percent). In most cases the effusion was small or moderate in size (79 and 10 percent, respectively) without hemodynamic consequences. Cardiac tamponade was present in only 5 percent of patients . (See "Echocardiographic evaluation of the pericardium" and "Pericardial effusion: Approach to diagnosis".)
Chest radiograph — Chest radiography is typically normal in patients with acute pericarditis. Although patients with a substantial pericardial effusion may exhibit an enlarged cardiac silhouette with clear lung fields (image 1), this finding is uncommon in acute pericarditis since at least 200 mL of pericardial fluid must accumulate before the cardiac silhouette enlarges [2,20]. However, acute pericarditis should be considered in the evaluation of a patient with new and otherwise unexplained cardiomegaly.
Cardiac biomarkers — Acute pericarditis may be associated with increases in serum biomarkers of myocardial injury such as cardiac troponin I or T. In one series of 118 consecutive cases with idiopathic acute pericarditis, an elevated level of cardiac troponin I was detected in 38 patients (32 percent) . Such patients should be considered to have myopericarditis.
Signs of inflammation — Since pericarditis is an inflammatory disease, laboratory signs of inflammation are common in patients with acute pericarditis. These include elevations in the white blood cell count, erythrocyte sedimentation rate, and serum C-reactive protein concentration. While elevation in these markers supports the diagnosis, they are neither sensitive nor specific for acute pericarditis. Additionally, in the hyperacute phase of pericarditis, these markers may remain normal, and increased levels may be found only on follow-up. However, markers of inflammation play a role in determining the optimal duration and approach to tapering of therapy. (See "Acute pericarditis: Treatment and prognosis".)
CMR and/or CT — Both CT and CMR can help to evaluate the thickness of the pericardium. CMR imaging is generally the preferred examination to depict the presence and intensity of pericardial and myocardial inflammation. CT is the preferred examination to study pericardial calcifications and concomitant pleuropulmonary diseases.
CMR provides useful assessment of pericardial inflammation (image 2) since the inflamed pericardium is bright and thickened on T2-weighted imaging (edema) and enhanced after contrast injection (late gadolinium enhancement). Concomitant myocarditis may also be depicted simultaneously during CMR. Evidence of pericardial inflammation by CT/CMR is a supportive finding for the diagnosis of pericarditis in doubtful cases (eg, atypical presentation, chest pain without C-reactive protein elevation or other objective evidence of disease) .
CT may be useful to confirm the diagnosis and to evaluate concomitant pleuropulmonary diseases and lymphadenopathies, thus suggesting a possible etiology of pericarditis (ie, tuberculosis, lung cancer) . Noncalcified pericardial thickening with pericardial effusion is suggestive of acute pericarditis. Moreover, with the administration of iodinated contrast media, enhancement of the thickened visceral and parietal surfaces of the pericardial sac confirms the presence of active inflammation. CT attenuation values can help in the differentiation of exudative fluid (20 to 60 Hounsfield units), as found with purulent pericarditis, and simple transudative fluid (<10 Hounsfield units).
In selected cases, 18F-fluorodeoxyglucose (FDG) positron emission tomography/CT may be helpful in identifying pericardial FDG uptake ("ring of fire") suggestive of inflammation or malignancy [18,22]. FDG uptakes are higher with tuberculous or malignant pericardial disease compared with idiopathic pericarditis .
Pericardiocentesis and pericardial biopsy — Studies in patients with acute pericarditis have reported a low yield for diagnostic pericardiocentesis and pericardial biopsy; however, some authors have advocated for a more extensive use of these techniques for diagnostic purposes. The majority of patients with uncomplicated acute pericarditis do not require invasive pericardial procedures. However, some high-risk patients may require pericardiocentesis for both therapeutic and diagnostic purposes (table 3). In addition, while pericardial biopsy is not required to make the diagnosis of acute pericarditis, it may rarely be necessary in an attempt to diagnose a specific etiology.
●Pericardiocentesis — In patients with a pericardial effusion, pericardiocentesis or surgical drainage can serve both diagnostic and therapeutic purposes. Among patients with acute pericarditis, decisions regarding drainage of a pericardial effusion are based on its echocardiographic characteristics (eg, size and composition) and clinical significance (eg, causing hemodynamic compromise).
•Patients with symptomatic effusions and evidence of cardiac tamponade should undergo prompt pericardial drainage. (See "Cardiac tamponade".)
•When a significant pericardial effusion is present, a diagnostic pericardiocentesis is indicated if a specific etiology is highly suspected and diagnosis cannot be reached by other means. The investigation is especially indicated when a neoplastic or bacterial etiology is suspected and a definite diagnosis can only be made by identification of the etiologic agent in the pericardial fluid. Fluid samples should be sent for cytology, tumor markers, Gram stain, bacterial cultures, and, if tuberculosis is suspected, polymerase chain reaction testing, adenosine deaminase, or gamma interferon levels. (See "Pericardial effusion: Approach to diagnosis" and "Pericardial disease associated with cancer: Clinical presentation and diagnosis".)
•Pericardiocentesis may also be performed for diagnostic and/or therapeutic purposes for large effusions refractory to medical treatment .
•Effusions that are small to moderate in size and do not cause hemodynamic compromise (ie, cardiac tamponade) generally do not require drainage, unless a sample of the effusion is necessary for diagnostic purposes. Moreover, pericardiocentesis performed percutaneously has a significantly higher complication rate if the effusion is not large.
A detailed discussion regarding the performance of pericardiocentesis and the treatment of pericardial effusions is presented separately. (See "Pericardial effusion: Approach to diagnosis".)
●Pericardial biopsy — Pericardial biopsy is generally performed as a part of a therapeutic procedure (surgical drainage) in patients with recurrent pericardial effusions and cardiac tamponade after prior pericardiocentesis (therapeutic biopsy), and as a diagnostic procedure in patients with an illness lasting more than three weeks despite treatment without a definite diagnosis. Technical advances in instrumentation with introduction of pericardioscopy, and in contemporary virology and molecular biology, have improved the diagnostic value of epicardial/pericardial biopsy. The diagnostic yield of pericardial biopsy is typically higher in patients with pericardial effusion with or without pericarditis than in those who present with apparent acute pericarditis without effusion. Polymerase chain reaction techniques may represent a useful adjunct to conventional laboratory studies in the investigation of pericardial samples, allowing the rapid identification of microorganisms otherwise not easily found [24,25]. Tissue samples should be sent for cytology, tumor markers, Gram stain, bacterial cultures, and, if tuberculosis is suspected, polymerase chain reaction testing. (See "Pericardial effusion: Approach to diagnosis", section on 'Pericardial fluid analysis and biopsy'.)
●Typical chest pain (sharp and pleuritic, improved by sitting up and leaning forward).
●Pericardial friction rub (a superficial scratchy or squeaking sound best heard with the diaphragm of the stethoscope over the left sternal border) (movie 1).
●Characteristic changes on the ECG (typically widespread ST-segment elevation) (waveform 1).
●New or worsening pericardial effusion.
These diagnostic criteria are consistent with the 2015 European Society of Cardiology guidelines on pericardial diseases . In atypical presentations, additional supporting findings include the evidence of systemic inflammation (eg, elevation of C-reactive protein) or pericardial inflammation on an imaging technique such as pericardial contrast-enhancement on computed tomography or pericardial edema and late gadolinium enhancement on cardiac magnetic resonance imaging [4,18]. (See 'CMR and/or CT' above.)
The diagnosis of acute pericarditis is usually suspected based on a history of characteristic pleuritic chest pain, and confirmed if a pericardial friction rub is present. Pericarditis should also be suspected in a patient with persistent fever and either a pericardial effusion or new unexplained cardiomegaly .
Myopericarditis or perimyocarditis — The term myopericarditis, or perimyocarditis, is used for cases of acute pericarditis that also demonstrate features consistent with myocardial inflammation. Because the same viruses that are responsible for acute pericarditis can also cause myocarditis, it is not uncommon to find some degree of myocardial involvement in patients with acute pericarditis. The terms "myopericarditis" and "perimyocarditis" are sometimes used interchangeably or they can be used to indicate the dominant site of involvement. Cases that involve the myocardium in which pericarditis is predominant (with normal ventricular function) are reported as myopericarditis; alternatively, the term perimyocarditis is sometimes used when myocardial involvement is most prominent (particularly if ventricular function is reduced). However, in clinical practice, myopericarditis is more common and this term is often used in both senses [26,27]. (See "Myopericarditis".)
ASSESSMENT OF RISK AND NEED FOR HOSPITALIZATION — High-risk patients with acute pericarditis should be admitted to the hospital in order to initiate appropriate therapy and expedite a thorough initial evaluation. Patients with high-risk features are at increased risk of short-term complications and have a higher likelihood of a specific disease etiology [5,28]. Conversely, patients with uncomplicated (ie, low-risk) acute pericarditis can usually be evaluated and sent home, with outpatient follow-up to assess the efficacy of treatment and complete the diagnostic evaluation [5,28].
Features of acute pericarditis associated with a higher risk or potential need for hospitalization include [5,28]:
●Fever (>38°C [100.4°F]).
●Subacute course over days to weeks (without acute onset of chest pain).
●Evidence suggesting cardiac tamponade (eg, hemodynamic compromise). (See "Cardiac tamponade".)
●A moderate to large pericardial effusion (ie, an end-diastolic echo-free space of more than 20 mm).
●Therapy with warfarin or non-vitamin K oral anticoagulants.
●Failure to show clinical improvement following seven days of appropriately dosed nonsteroidal antiinflammatory drug and colchicine therapy.
●Elevated cardiac troponin, which suggests myopericarditis/perimyocarditis. (See "Myopericarditis".)
Historically, many clinicians admitted all new cases of acute pericarditis to the hospital, but this is not necessary. In one report of 300 consecutive patients with acute pericarditis, 15 percent were deemed high risk at presentation and were hospitalized . In the remaining 85 percent of patients who were low risk, outpatient aspirin therapy was effective in 87 percent, and none of these patients had a serious complication (eg, cardiac tamponade) at a mean follow-up of 38 months.
Although chronic use of glucocorticoids should not be considered as a risk factor in a general population of patients with acute pericarditis, they were associated with an increased rate of complications in idiopathic or viral pericarditis . Glucocorticoid therapy given for the index attack may increase the chance of recurrence, possibly because of its deleterious effect on viral replication and clearance. (See "Recurrent pericarditis", section on 'Predictors of recurrence'.)
ESTABLISHING A DEFINITE ETIOLOGY — Because of the relatively benign course associated with the common causes of pericarditis, along with the relatively low yield of much of the diagnostic testing, it is not necessary to establish a definite etiology in all patients with acute pericarditis. Initial efforts should focus on excluding a significant pericardial effusion or cardiac tamponade, and the identification of patients in whom a more comprehensive evaluation should be performed to exclude causes that require specific therapy (eg, malignancy, tuberculosis, or purulent pericarditis) . In addition, among patients at high risk of coronary disease, MI must be ruled out by appropriate studies. (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department".)
The yield of the standard diagnostic evaluation to determine the etiology of acute pericarditis is relatively low. This was illustrated in three series that included a total of 784 unselected patients who underwent an extensive evaluation [7,28,29]. A specific diagnosis was established in only 130 patients (17 percent) (table 5). The most commonly confirmed diagnoses were:
●Neoplasia – 5 percent
●Tuberculosis – 4 percent
●Autoimmune etiologies – 5 percent
●Purulent pericarditis – 1 percent
In developed countries, unless there is an apparent medical or surgical condition known to be associated with pericarditis, most cases of acute pericarditis in immunocompetent patients are due to viral infection or are idiopathic (table 5) [5,28,30-32]. Acute viral or idiopathic pericarditis typically follow a brief and benign course after empiric treatment with antiinflammatory drugs. (See "Acute pericarditis: Treatment and prognosis".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Pericardial disease".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Pericarditis in adults (The Basics)")
●Beyond the Basics topic (see "Patient education: Pericarditis (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Epidemiology and etiology – Acute pericarditis (inflammation of the pericardial sac) is the most common disorder of the pericardium and is seen in approximately 0.1 percent of hospitalized patients and 5 percent of patients admitted to the emergency department for nonischemic chest pain. Cases are most commonly idiopathic (most probably viral in etiology). Other etiologies include bacterial infections, malignancy, and autoimmune disorders (table 5). The distribution of etiologies varies with geography and type of clinical setting (community hospital versus tertiary referral center). (See 'Epidemiology' above.)
●Clinical features – Acute pericarditis can present with a variety of nonspecific signs and symptoms, depending on the underlying etiology. Common clinical manifestations include chest pain (typically pleuritic), pericardial friction rub, characteristic ECG changes (diffuse ST elevation and PR depression), and pericardial effusion. Pericarditis should also be suspected in a patient with persistent fever and pericardial effusion or new unexplained cardiomegaly. (See 'Clinical features' above.)
●Diagnostic evaluation – For all patients with suspected acute pericarditis, the initial evaluation includes a comprehensive history and physical examination, selective blood work (assessing for markers of inflammation and myocardial damage), chest radiography, ECG, and echocardiography. Follow-up testing is performed in selected cases as needed and may include additional laboratory evaluation (eg, blood cultures, antinuclear antibody titer, HIV and hepatitis C virus serology) and additional cardiac imaging. (See 'Our approach to diagnostic testing' above.)
•Typical chest pain (sharp and pleuritic, improved by sitting up and leaning forward). (See 'Chest pain' above.)
•New or worsening pericardial effusion. (See 'Echocardiogram' above.)
●Indications for hospitalization – Patients with acute pericarditis with one or more high-risk features (including fever, subacute course, suspected cardiac tamponade, immunosuppression, acute trauma, treatment with oral anticoagulation, or elevated cardiac troponin) are at increased risk for complications and should generally be admitted to initiate appropriate therapy and to expedite a thorough initial evaluation. Conversely, patients with uncomplicated (ie, low-risk) acute pericarditis can usually be evaluated and sent home, with outpatient follow-up. (See 'Assessment of risk and need for hospitalization' above.)
●Role of testing to determine etiology – Given the relatively benign course associated with the common causes of pericarditis and the low yield of much diagnostic testing, it is not necessary to establish a definite etiology in all patients with acute pericarditis. Initial evaluation should focus on excluding a significant pericardial effusion or cardiac tamponade and identification of patients in whom a more comprehensive evaluation should be performed to exclude causes that require specific therapy (eg, malignancy, tuberculosis, or purulent pericarditis). (See 'Establishing a definite etiology' above.)
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