Acute pericarditis

Acute pericarditis is an acute inflammation of the visceral and parietal layers of the pericardium (with or without pericardial effusion) of various etiologies. Acute pericarditis can be an independent disease or a manifestation of a systemic disease.

ICD-10 code

• 130. Acute pericarditis.

Acute pericardial effusion included.

• 130.0. Acute nonspecific idiopathic pericarditis.
• 130.1. Infectious pericarditis.
• 130.8. Other forms of acute pericarditis.
• 130.9. Acute pericarditis, unspecified.

Epidemiology of acute pericarditis

The incidence of acute pericarditis is difficult to estimate because in many cases the disease is not diagnosed. The incidence of acute pericarditis among hospitalized patients is about 0.1%. The disease can occur at any age.

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Causes of acute pericarditis

About 90% of cases of isolated acute pericarditis are viral or of unknown etiology. Idiopathic acute pericarditis is diagnosed when a complete standard examination fails to identify a specific etiology. There is no clinical difference between idiopathic cases and viral pericarditis (probably most idiopathic cases are diagnosed viral infections).

The typical causes of acute pericarditis in the past (tuberculosis or bacterial infection) are now rare. Bacterial infections cause acute purulent pericarditis by direct extension of a pulmonary infection, with penetrating chest injuries, subphrenic abscess, or as a result of hematogenous infection with myocardial abscesses or infective endocarditis. Tuberculosis must be considered in cases of acute pericarditis without a rapid course, especially in groups of patients with a high risk of tuberculosis.

Acute pericarditis may occur in patients with myocardial infarction; it most commonly develops 1 to 3 days after transmural infarction (presumably due to the impact of necrotic myocardium on the adjacent pericardium); a second form of acute pericarditis associated with myocardial infarction, Dressler syndrome, typically occurs weeks to months after myocardial infarction. Acute pericarditis may develop after traumatic heart injury, surgical intervention on the pericardium, or after pulmonary infarction. Postcardiotomy syndrome, like Dressler syndrome, is presumably autoimmune in nature and occurs with signs of systemic inflammation, including fever and polyserositis. The incidence of pericarditis in myocardial infarction decreases after reperfusion treatment.

Acute pericarditis is also observed in patients with uremia requiring hemodialysis, rheumatic fever, SLE, rheumatoid arthritis and other rheumatic diseases. A high frequency of acute pericarditis is noted with irradiation of the chest and mediastinum.

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Pathogenesis of acute pericarditis

All symptoms of uncomplicated acute pericarditis are caused by inflammation of the pericardium. Increased vascular permeability during inflammation leads to exudation of liquid fractions of blood and fibrinogen into the pericardial cavity, which is deposited as fibrin and forms catarrhal and then fibrinous (dry) pericarditis. With extensive involvement of the pericardium in inflammation, exudation of liquid fractions of blood exceeds reabsorption, which leads to the formation of pericardial effusion (exudative pericarditis). Depending on the etiology of acute pericarditis, the effusion can be serous, serous-fibrinous, hemorrhagic, purulent, putrefactive. The volume of a large pericardial effusion can reach a liter or more (normally, the pericardial cavity contains 15-35 ml of serous fluid). Rapid accumulation of even a small amount of it can lead to increased pressure in the pericardial cavity. The resulting disturbance in filling the right cavities of the heart leads to a compensatory increase in systemic venous pressure. If the pressure in the pericardial cavity becomes equal to or higher than the filling pressure of the right cavities of the heart, cardiac tamponade develops with collapse of the right atrium and ventricle in diastole and a drop in cardiac output and systemic blood pressure. In approximately 15% of patients, acute pericarditis is combined with myocarditis.

Symptoms of acute pericarditis

The diagnosis of acute pericarditis is usually made in patients with a characteristic triad:

• auscultation of pericardial friction rub;
• chest pain;
• typical sequential ECG changes.

Further examination is aimed at assessing the presence of pericardial effusion and hemodynamic disturbances, as well as determining the cause of the disease.

Anamnesis and complaints of patients

Most patients with acute pericarditis (90%) experience chest pain:

• the pain is localized behind the sternum and spreads to the neck, left shoulder, arms, trapezius muscles; in children, pain in the epigastrium occurs;
• the onset of pain may be sudden, then the pain becomes constant (lasts for hours and days), often monotonous, may be sharp, dull, with a burning sensation or pressure;
• the intensity of pain can vary from mild to severe;
• the pain usually increases when inhaling, lying on your back, swallowing, or moving your body, and decreases when sitting upright or leaning forward;
• In some cases, heart pain may be absent, for example, this is often observed with pericarditis in patients with rheumatoid arthritis.

When studying the anamnesis of the disease in patients, a connection between the occurrence of heart pain and infection may be revealed; fever, weakness, myalgia may be observed in the prodromal period. Information about tuberculosis, autoimmune or tumor diseases in the past can help in diagnosing specific causes of acute pericarditis.

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Clinical symptoms that suggest pericardial effusion

Complaints of the patient.

• A feeling of pressure and discomfort in the chest.
• Heartbeat.
• Persistent dry "barking" cough, shortness of breath, hoarseness of voice.
• Hiccups, dysphagia.

Physical examination.

• Cardiovascular system
  • Expansion of cardiac dullness in all directions, change in the boundaries of the heart when changing position (in a standing position, the zone of dullness in the second and third intercostal spaces contracts, and in the lower sections it expands), unusual intensity of cardiac dullness, coincidence of the zone of absolute cardiac dullness with the zone of relative dullness in the lower sections.
  • The apical impulse is displaced upward and inward from the lower left border of cardiac dullness (Jardin's sign), the apical impulse is weakened.
  • Swelling of the jugular veins, increased central venous pressure.
  • Heart sounds are sharply weakened in the lower left sections of the cardiac dullness, but can be clearly heard inwards from the apical impulse.
  • If there is a pericardial friction rub, it is better heard in the supine position at the end of inspiration (Poten's symptom) or when the head is thrown back (Herx's symptom); with an increase in effusion, the rub may disappear.
  • Tachycardia (may be absent in hypothyroidism or uremia).
  • Acrocyanosis.
• Respiratory system
  • Evard's sign - dull percussion sound below the angle of the left scapula due to compression of the left lung by pericardial effusion, in this place the vocal fremitus is increased, breathing is weakened. When bending forward, the dullness under the scapula disappears, but unvoiced fine-bubble wheezing appears (Pen's sign).
• Digestive system
  • The abdomen does not participate in the act of breathing (Winter's sign) due to limited mobility of the diaphragm.
  • Small or slowly accumulating pericardial effusions may be asymptomatic. Large effusions occur in up to 5% of cases of acute pericarditis. Unrecognized pericardial effusions may lead to rapid, unexpected deterioration and death from cardiac tamponade.

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Complications of acute pericarditis

• cardiac tamponade;
• relapses of acute pericarditis occur in 15-32% of patients; more often in autoimmune pericarditis, some cases of relapse may be associated with reactivation of viral pericarditis or inadequate treatment during the first episode of acute pericarditis. Relapses are more common after treatment with glucocorticoids, pericardiotomy or creation of a pericardial window, less common after treatment with colchicine; relapses may recur spontaneously over several years or upon discontinuation of anti-inflammatory drugs;
• chronic constrictive pericarditis in outcome (less than 10%).

Idiopathic or viral acute pericarditis rarely progress to cardiac tamponade. Situations with a risk of cardiac tamponade include moderate or large fresh or increasing effusion, purulent acute pericarditis, tuberculous acute pericarditis, and hemorrhage into the pericardial cavity. The greatest risk of progression of pericardial effusion to tamponade is in patients with a recent large pericardial effusion with signs of diastolic collapse of the right heart. Although the probability of tamponade is low with small (according to transthoracic echocardiography) effusions, it can unexpectedly occur in cases of rapid fluid accumulation, such as in hemopericardium, or if there is actually a large but unusually located effusion that is not recognized by transthoracic echocardiography, as well as in some cases of a combination of a large pleural and small pericardial effusion. Therefore, tamponade should be suspected in patients with hemodynamic disturbances, regardless of the amount of pericardial fluid. Cardiac tamponade may occur suddenly or be observed for a long time. The clinical symptoms of cardiac tamponade depend on the degree of increase in pericardial pressure: with a slight increase in pressure (<10 mm Hg), tamponade is often asymptomatic, with a moderate and especially with a sharp increase in pressure (>15 and up to 20 mm Hg), a feeling of discomfort in the heart area and shortness of breath occur. Clinical and instrumental diagnostics of tamponade are presented below. If cardiac tamponade is suspected, urgent echocardiographic examination is indicated.

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Clinical symptoms suggestive of cardiac tamponade or its threat in acute pericarditis

Patient's complaints:

• the appearance of painful attacks of severe weakness with a weak, rapid pulse;
• the appearance of fainting, dizziness, fear of death;
• increased shortness of breath (due to hypovolemia of the pulmonary circulation).

Data from examination and physical research methods:

Cardiovascular system:

• swelling of the jugular veins (less noticeable in patients with hypovolemia); high central venous pressure (200-300 mm H2O) except in cases of low-pressure tamponade in patients with hypovolemia; a decrease in venous pressure during inspiration persists;
• arterial hypotension (may be absent, especially in patients with previously observed arterial hypertension);
• Beck's triad in pericardial tamponade: arterial hypotension, weakening of heart sounds, dilation of the jugular veins;
• paradoxical pulse: a decrease in systolic blood pressure by more than 10 mm Hg during inhalation;
• increasing tachycardia;
• weak peripheral pulse, weakening on inspiration;
• pronounced acrocyanosis.

Respiratory system:

• shortness of breath or rapid breathing without wheezing in the lungs.

Digestive system:

• enlargement and soreness of the liver;
• the appearance of ascites.

General inspection:

• the patient's position is sitting, leaning forward and resting his forehead on a pillow (Breitman's position), a deep bow position;
• pale skin, gray cyanosis, cold extremities;
• swelling of the face, shoulder and arm may appear, more on the left (compression of the innominate vein);
• increasing peripheral edema.

In the most severe cases, patients may lose consciousness and, with the exception of increased venous pressure, the clinical picture resembles hypovolemic shock. Unnoticed cardiac tamponade may debut with symptoms of complications associated with impaired blood circulation in organs - renal failure, shock liver, mesenteric ischemia. Cardiac tamponade in a patient with fever may be mistakenly assessed as septic shock.

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Technique for determining paradoxical pulse

The cuff is inflated to a pressure above systolic. As the air is slowly released, the intermittent first Korotkov sound is heard. By comparing it with the patient's breathing cycle, the point is determined at which the sound is heard during exhalation and disappears during inhalation. With a further decrease in pressure in the cuff, a point is reached at which the sound is heard throughout the breathing cycle. A difference in systolic pressure between these points of more than 10 mm Hg is defined as a positive paradoxical pulse. For quick clinical orientation, this sign can also be examined by simple palpation of the pulse on the radial artery, which significantly decreases or disappears during a normal shallow inspiration. Paradoxical pulse is not a pathognomonic symptom of cardiac tamponade and can also be observed in pulmonary embolism, subacute mitral regurgitation, right ventricular infarction, and bronchial asthma. On the other hand, paradoxical pulse is difficult to detect in patients with cardiac tamponade in severe shock, it may also be absent in cardiac tamponade in patients with concomitant pathological changes in the heart: aortic valve insufficiency, atrial septal defect, left ventricular hypertrophy or dilation,

Instrumental methods for diagnosing cardiac tamponade (Guidelines for the diagnosis and treatment of pericardial diseases of the European Society of Cardiology, 2004)

Research method	Results of the study in cardiac tamponade
ECG	May be normal or have non-specific changes (ST-T wave); electrical alteration (QRS voltage variability, less often T waves, caused by excessive cardiac mobility), bradycardia (in the late stage); electromechanical dissociation (in the atonal phase)
Chest X-ray	Enlarged cardiac shadow with normal pulmonary markings
EchoCG	Large "circular" pericardial effusion: late diastolic collapse of the right atrium (the most sensitive sign, observed in 100% of patients with cardiac tamponade), early diastolic collapse of the anterior free wall of the right ventricle; collapse of the right ventricle lasting more than a third of diastole (the most specific sign); collapse of the left atrial wall at the end of diastole and beginning of systole (observed in approximately 25% of patients with tamponade has high specificity); increased thickness of the left ventricular walls in diastole, "pseudohypertrophy"; dipatica of the inferior vena cava, decreased collapse of the inferior vena cava on inspiration (less than 50%); "swinging heart"
DEHOCG	Increased tricuspid flow and decreased mitral flow during inspiration (the opposite is true during expiration); in the systemic veins, systolic and diastolic flows are decreased during expiration and reverse flow is increased during atrial contraction
Color Doppler EchoCG	Significant mitral and tricuspid flow fluctuations associated with breathing
Cardiac catheterization	Confirmation of the diagnosis and quantitative assessment of hemodynamic disturbances; pressure in the right atrium is increased by 10-30 mm Hg (systolic X-sag is preserved and diastolic Y-sag of the right atrial pressure curve and systemic venous pressure is absent or decreased); pressure in the pericardial cavity is increased and almost equal to pressure in the right atrium (both pressures decrease during respiration): mean diastolic pressure in the right ventricle is increased and equal to pressure in the right atrium and pressure in the pericardial cavity (without "diastolic depression and plateau"); pulmonary artery diastolic pressure is slightly elevated and may correspond to the right ventricular pressure - pulmonary capillary wedge pressure is also elevated and is almost equal to the pericardial pressure and the right atrial pressure: left ventricular and aortic systolic pressure may be normal or decreased Confirmation that aspiration of pericardial effusion improves hemodynamics Identification of associated hemodynamic disturbances (left ventricular failure, constriction, pulmonary hypertension)
Angiography of the right and left ventricles	Atrial collapse and small hyperactive ventricular cavities
Computer tomography	Change in the configuration of the ventricles and atria (collapse of the atrium and ventricle)

Example of diagnosis formulation

Acute idiopathic pericarditis. HK0 (1 FC).

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Differential diagnosis of acute pericarditis

Differential diagnostics are performed with other diseases that are characterized by chest pain. First of all, life-threatening causes of pain and heart disease are excluded, such as myocardial infarction, aortic dissection, pulmonary embolism, angina. The differential diagnostic plan also includes pleurisy or pleuropneumonia, spontaneous pneumothorax, herpes zoster, esophagitis, esophagospasm, esophageal rupture, in some cases - acute gastritis and gastric ulcer, traumatic diaphragmatic hernia, Tietze syndrome and some other diseases that cause chest pain. Pericardial friction rub should be differentiated from pleural friction rub, the latter disappears when holding the breath, while pericardial friction rub persists when holding the breath.

Electrocardiogram changes in acute pericarditis are similar to those in myocardial infarction, early repolarization syndrome, and Brugada syndrome. However, in myocardial infarction, ST elevation is dome-shaped, changes are focal with reciprocal ST segment depression, and not diffuse as in acute pericarditis (in postinfarction pericarditis, ST segment elevation may also be localized); pathological Q and decreased R-wave voltage are characteristic, negative T appear before ST normalization, PR depression is atypical. In early repolarization syndrome, ST segment elevation is observed in fewer leads. PR segment depression and stage-specific ST-T changes are absent. In Brugada syndrome, ST segment elevation is limited to the right chest leads (VI-V3) against the background of QRS complex changes similar to right bundle branch block.

In case of pericardial effusion, differential diagnosis is carried out with effusions of non-inflammatory nature (in case of heart failure, nephrotic syndrome, hypothyroidism).

The clinical signs of cardiac tamponade are differentiated from other emergency conditions that cause arterial hypotension, shock, and increased systemic venous pressure, including cardiogenic shock in myocardial diseases, right ventricular myocardial infarction, acute right ventricular failure due to pulmonary embolism or other causes. When evaluating the results of an echocardiographic study in a patient with suspected cardiac tamponade, it should be borne in mind that diastolic collapse of the right atrium, characteristic of cardiac tamponade, may also be due to massive pleural effusion.

For the diagnosis of concomitant myocarditis in patients with acute pericarditis, the following signs are important:

• unexplained weakness and fatigue during physical exertion, palpitations,
• arrhythmias, especially ventricular;
• echocardiographic signs of myocardial dysfunction;
• ST segment elevation at the onset of the disease;
• elevated troponin I for more than 2 weeks, CPK and myoglobin.

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Diagnosis of acute pericarditis

The pathognomonic sign of acute pericarditis is pericardial friction rub, which is detected in 85% of patients with this disease:

• a scratching, scraping noise, like skin rubbing against skin;
• Typical noise (more than 50% of cases) has three phases:
  • 1st phase - pre-systolic murmur preceding the 1st tone, occurring during atrial systole;
  • 2~th phase - systolic murmur between the first and second sounds, occurring during ventricular systole and coinciding with the peak pulse in the carotid arteries;
  • 3rd phase - early diastolic murmur after the second tone (usually the weakest), reflects the rapid filling of the ventricles in early diastole;
• in case of tachycardia, atrial fibrillation or at the onset of the disease, the murmur may be biphasic systolic-diastolic or monophasic systolic;
• the noise is best heard above the left lower edge of the sternum within the limits of absolute cardiac dullness and is not conducted anywhere;
• the noise is variable over time, and is less audible at the onset of the disease. In order not to miss it, frequent repeated auscultation is necessary;
• may persist even when pericardial effusion appears.

Patients often have a low-grade fever; however, fever above 38 C with chills is unusual and may indicate the possibility of purulent bacterial acute pericarditis. Other signs of systemic or systemic disease may be present, depending on the etiology. The heart rhythm in acute pericarditis is usually regular, but tachycardia is common. Breathing may be shallow due to pain; dyspnea is possible.

In the presence of pericardial effusion, symptoms appear due to an increase in the volume of the pericardial sac, disruption of venous flow, and a decrease in cardiac output.

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Instrumental and laboratory diagnostics of acute pericarditis

ECG changes are the 3rd classic diagnostic sign of acute pericarditis (occurs in 90% of patients). Typical ECG changes consistently go through 4 stages.

• In the early stage of acute pericarditis, elevation of the ST segment with positive T waves in all leads except leads aVR and VI and deviations of the PR segment in the direction opposite to the P wave are typical. In some cases, depression of the PR segment is observed in the absence of ST segment elevation.
• After a few days, the ST segment and then the PR segment return to the isoline.
• T waves become progressively flattened and inverted in most leads.
• The ECG usually returns to baseline within 2 weeks.
• Typical ECG changes may be absent in patients with uremic pericarditis. Pericardial effusion is characterized by low ECG voltage and sinus tachycardia.

Transthoracic echocardiography is the standard for noninvasive diagnostics of pericardial effusion. It should be done in all patients with acute pericarditis or if this disease is suspected. Echocardiography in patients with acute pericarditis can detect pericardial effusion, a sign of which is an echo-free space between the visceral and parietal pericardium. Small effusions are represented by an echo-free space of less than 5 mm and are visible on the posterior surface of the heart. With moderate effusions, the thickness of the echo-free space is 5-10 mm. Large effusions are more than 1 cm thick and completely surround the heart. The presence of effusion confirms the diagnosis of acute pericarditis, but in most patients with dry acute pericarditis, the echocardiogram is normal. Echocardiography allows us to establish hemodynamic disturbances caused by the development of cardiac tamponade, thus characterizing the significance of the effusion, as well as to assess myocardial function, which is important for the diagnosis of concomitant myocarditis. Transesophageal echocardiography is useful for characterizing local effusions, pericardial thickening, and pericardial neoplastic lesions.

Chest X-ray is performed to evaluate the cardiac shadow, exclude changes in the lungs and mediastinum, which may indicate a specific etiology of pericarditis. In dry acute pericarditis, the cardiac shadow is unchanged. With significant pericardial effusion (more than 250 ml), an increase and change in the configuration of the cardiac shadow is observed ("flask shadow", spherical shape in acute large effusion, triangular shape in long-standing effusions), weakening of the pulsation of the cardiac shadow contour.

Laboratory blood tests (general analysis, biochemical analysis):

• Patients with acute pericarditis usually have signs of systemic inflammation, including leukocytosis, increased ESR, and elevated C-reactive protein levels;
• slightly elevated troponin I levels are observed in 27-50% of patients with viral or idiopathic pericarditis without other signs of myocardial damage. Troponin levels normalize within 1-2 weeks, a longer increase indicates myopericarditis, which worsens the prognosis; elevated CPK levels in acute pericarditis are observed less frequently;
• plasma creatinine and urea are sharply elevated in uremic acute pericarditis;
• HIV test.

Additional studies in acute pericarditis

Additional laboratory blood tests according to clinical indications:

• bacteriological examination (culture) of blood if purulent acute pericarditis is suspected;
• antistreptolysin-O titer in case of suspected rheumatic fever (in young patients);
• rheumatoid factor, antinuclear antibodies, antibodies to DNA, especially if the disease is prolonged or severe with systemic manifestations;
• assessment of styloid gland function in patients with large pericardial effusion (suspected hypothyroidism):
• Special studies for cardiotropic viruses are generally not indicated, since their results do not change treatment tactics.

Performing a tuberculin test, examining sputum for Mycobacterium tuberculosis if the disease lasts more than a week.

Pericardiocentesis is indicated in cardiac tamponade or suspected purulent, tuberculous or tumor exudative acute pericarditis. The clinical and diagnostic effectiveness of routine drainage of large pericardial effusion (more than 20 mm in diastole according to echocardiography) has not been proven. Pericardiocentesis is not indicated if the diagnosis can be established without this study or if the effusion in typical viral or idiopathic acute pericarditis is resolved due to anti-inflammatory treatment. Pericardiocentesis is contraindicated in case of suspected aortic dissection, uncorrected coagulopathy, anticoagulant treatment (if pericardiocentesis is planned for patients constantly receiving oral anticoagulants, INR should be reduced to <1.5), thrombocytopenia less than 50x10 ⁹ /l.

Analysis of pericardial fluid should include a study of the cellular composition (leukocytes, tumor cells), protein, LDH, adenosine deaminase (a marker of cell-mediated immune response to Mycobacterium tuberculosis, including activation of T-lymphocytes and macrophages), culture, direct examination and PCR diagnostics for Mycobacterium tuberculosis, special studies of pericardial fluid in accordance with clinical data (tumor markers if a malignant disease is suspected, PCR diagnostics for cardiotropic viruses if viral pericarditis is suspected, "milky" effusion is examined for triglycerides).

Computed tomography and magnetic resonance imaging can detect small and localized pericardial effusions that may be missed by echocardiography, characterize the composition of the pericardial fluid, and can be useful when other imaging studies are inconsistent.

If significant clinical activity persists for 3 weeks after initiation of treatment or cardiac tamponade recurs after pericardiocentesis with no established etiologic diagnosis, some authors recommend pericardioscopy, pericardial biopsy with histological and bacteriological examination.

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Indications for consultation with other specialists

In acute idiopathic cases, the patient is managed by a cardiologist or therapist.

In complicated or specific cases of acute pericarditis (tuberculous, purulent, uremic, tumor), a multidisciplinary approach is required, including consultations with a cardiac surgeon and specialists (infectious disease specialist, phthisiatrician, nephrologist, endocrinologist, oncologist).

Treatment of acute pericarditis

In idiopathic and viral pericarditis, treatment is aimed at reducing pericardial inflammation and pain relief. In specific cases of acute pericarditis of known etiology, etiotropic treatment is possible; if pericarditis is a manifestation of a systemic disease, treatment of this disease is carried out.

Indications for hospitalization

Most patients with viral or idiopathic acute pericarditis (70-85%) can be treated as outpatients, as the disease is usually benign, with symptoms lasting about 2 weeks and a good response to NSAIDs. If there is a small to moderate effusion, it resolves within a few weeks. Re-evaluation is not necessary unless symptoms recur or worsen.

To determine the indications for hospitalization, it is necessary to assess the presence of hemodynamic instability and the safety of outpatient treatment. The main indications for inpatient treatment are indicators of a poor prognosis:

• fever above 38°C;
• subacute course of the disease;
• immunosuppression;
• association of acute pericarditis with trauma;
• acute pericarditis in a patient taking oral anticoagulants;
• myopericarditis;
• large pericardial effusion;
• insufficient effect of NSAID treatment.

There are good practice recommendations for short-term hospitalization of all patients with acute pericarditis to assess risk factors, followed by discharge for outpatient treatment within 24–48 h for those patients who have no risk factors and whose pain has resolved rapidly with NSAIDs. Emergency hospitalization and intensive care unit treatment are necessary for pericardial effusion with cardiac tamponade. Hospitalization is also mandatory if additional invasive studies are needed to establish the etiology of the disease.

Non-drug treatment of acute pericarditis

Patients with acute pericarditis are advised to limit physical activity.

Drug treatment of acute pericarditis

The mainstay of treatment for acute pericarditis is the use of NSAIDs, which result in relief of chest pain in 85-90% of patients with idiopathic or viral acute pericarditis within a few days. According to the recommendations of the European Society of Cardiology (2004), ibuprofen is preferred (fewer side effects and no adverse effect on coronary blood flow) at a dose of 300-800 mg every 6-8 hours for several days or weeks until pain or effusion disappears. The preferred NSAID is acetylsalicylic acid (aspirin), 2-4 g/day for the treatment of patients with pericarditis after myocardial infarction (since there is experimental data that other NSAIDs can worsen the formation of a post-infarction scar). Parenteral administration of ketorolac (NSAID with pronounced analgesic effect) at 30 mg every 6 hours can be effective for pain relief in the first days of the disease. Sometimes, with intense pain, additional use of narcotic analgesics is necessary. There are also recommendations for prescribing a short course of treatment with prednisolone orally at a dose of 60-80 mg / day for 2 days with gradual complete withdrawal within a week. The effectiveness of adding statins to NSAIDs (rosuvastatin 10 mg / day) for a more rapid reduction in inflammation, noted in isolated studies, still needs to be confirmed and further assessed. When using NSAIDs, protection of the mucous membranes of the gastrointestinal tract should be provided (as a rule, inhibitors of H + and K + -ATPase are used to reduce gastric secretion). NSAIDs do not prevent heart failure, pericardial constriction or relapse of effusion in the future.

The results of the recently published randomized COPE study (Colchicine for Acute Pericarditis, 2005) allow for a broader recommendation for the routine use of colchicine in the treatment of acute pericarditis. Patients with acute pericarditis with recurrent or 14-day-long pain are given 1-2 mg of colchicine on the first day and then 0-5-1 mg/day in two doses (for at least 3 months), separately or in combination with NSAIDs. This treatment is well tolerated, reduces the likelihood of cardiac tamponade and the outcome of constrictive pericarditis, and is most effective for the prevention of relapses of acute pericarditis.

Acute pericarditis usually responds well to glucocorticoids, but there is evidence that patients who took them at the onset of the disease are more likely to experience relapses of acute pericarditis (presumably due to the experimentally confirmed likelihood of exacerbation of a viral infection). According to the randomized COPE study, the use of glucocorticoids is an independent risk factor for relapse of acute pericarditis, so their use can be considered only in patients with poor general condition who are resistant to NSAIDs and colchicine or in patients with autoimmune acute pericarditis. Before prescribing glucocorticoids, a thorough examination is necessary to clarify the etiology of acute pericarditis. Prednisolone is used orally at a dose of 1-1.5 mg / kg per day for at least a month, followed by a slow decrease in the dose before cancellation. Glucocorticoids should be canceled within 3 months, after which colchicine or ibuprofen is prescribed. There is evidence that intrapericardial administration of glucocorticoids is effective in autoreactive acute pericarditis and is not accompanied by an increased risk of relapse, but this limits the invasive nature of the method.

Features of treatment of acute pericarditis in the presence of pericardial effusion without the threat of tamponade:

• Specific treatment of pericardial effusion depends on the etiology;
• in idiopathic or viral acute pericarditis, anti-inflammatory treatment is usually effective;
• limitation of physical activity is indicated;
• it is necessary to avoid dehydration (erroneous prescription of diuretics can lead to the development of cardiac tamponade with “low venous pressure”);
• the use of beta-blockers, which suppress compensatory activation of the sympathetic system, and other drugs that slow the heart rate should be avoided;
• if the patient has previously received anticoagulants, it is advisable to temporarily discontinue them or replace indirect anticoagulants with heparins,

[ 40 ], [ 41 ], [ 42 ]

Treatment tactics for pericardial effusion with cardiac tamponade

• emergency pericardiocentesis or pericardial drainage (removal of even a small amount of fluid leads to significant relief of symptoms and improvement of hemodynamics;
• Removal of all effusion normalizes pericardial pressure, atrial and ventricular diastolic pressure, arterial pressure, and cardiac output, unless the patient has concomitant pericardial constriction or other heart disease). Pericardiocentesis is contraindicated in cardiac tamponade due to aortic dissection;
• replenishment of intravascular volume in preparation for pericardial drainage (small amounts of saline or colloidal solutions - 300-500 ml - can help improve hemodynamics, especially in hypovolemia; vasopressors dobutamine at a dose of 5-20 mcg/kg per minute, dopamine are less effective);
• lack of positive pressure ventilation - this reduces venous return and cardiac output and can cause a sudden drop in blood pressure;
• hemodynamic monitoring.

Echocardiographic signs of diastolic collapse of the right heart chambers in the absence of clinical signs of tamponade are not a mandatory basis for emergency pericardiocentesis. Such patients require careful clinical observation, since even a slight further increase in effusion can cause cardiac tamponade. In some patients, echocardiographic signs of compression of the right chambers may disappear within a few days, and pericardiocentesis can be avoided.

Surgical treatment of acute pericarditis

Pericardiocentesis is indicated in the following cases.

• cardiac tamponade;
• suspected purulent or neoplastic pericarditis;
• very large effusion with clinical manifestations, resistant to drug treatment for a week.

Drainage of the pericardium through an indwelling catheter (for several days) reduces the risk of recurrent tamponade if fluid accumulation continues. Surgical drainage of the pericardial cavity is preferred in cases of purulent pericarditis, recurrent effusions, or the need for pericardial biopsy. In a small number of patients with acute pericarditis with frequent and severe relapses despite medical treatment, surgical pericardiectomy may be necessary.

Approximate periods of incapacity for work

In uncomplicated idiopathic acute pericarditis, the period of disability is about 2-4 weeks.

[ 43 ], [ 44 ], [ 45 ]

Further management

After acute pericarditis, patients need to be monitored by a cardiologist for the purpose of timely diagnosis of relapse or the addition of constrictive pericarditis.

Treatment and prevention of relapses of acute pericarditis

Drug treatment - the results of the randomized study CORE (Colchicine in Recurrent Pericarditis, 2007) indicate the effectiveness of treatment with colchicine for up to 6 months in combination with aspirin; other NSAIDs or prednisolone are traditionally used; if such treatment is ineffective, with frequent relapses, immunopathological forms, the use of cyclophosphamide or azathioprine (at a dose of 50-100 mg / day) or intrapericardial administration of triamcinolone (at 300 mg / m ³ ) may be effective.

Pericardiectomy or pericardial window is indicated only in cases of frequent and clinically significant relapses that are resistant to medical treatment. Patients should not receive glucocorticoids for several weeks before pericardiectomy.

Information for patients

Patients should be informed about the clinical symptoms of worsening acute pericarditis and the threat of tamponade (increased dyspnea, decreased exercise tolerance), which require urgent medical attention due to the likely need for emergency treatment. Patients who have previously suffered from acute pericarditis should be informed about the possibility of a relapse of the disease and symptoms (chest pain, dyspnea, palpitations), which require medical attention and repeated examination.

How to prevent acute pericarditis?

Prevention of acute pericarditis is not carried out.

Prognosis for acute pericarditis

The outcome of acute pericarditis may be the resorption of effusion when the inflammation subsides, less often - the organization of effusion with the formation of pericardial adhesions, partial or complete obliteration of the pericardial cavity. In a small number of patients who have had this disease, constrictive pericarditis may subsequently develop. Mortality depends on the cause. Idiopathic and viral pericarditis have a self-limited favorable course without complications in almost 90% of patients. Purulent, tuberculous and tumor pericarditis have a more severe course: with tuberculous pericarditis, fatal outcomes are reported in 17-40% of cases, with untreated purulent pericarditis, mortality reaches 100%.