Fibrinous pericarditis

Various pathologies of the cardiovascular system can be complicated by such a disorder as fibrinous pericarditis. Such a complication requires immediate examination and treatment, which is necessary to prevent the further development of other serious consequences. If such treatment is timely and competent, then the majority of patients have a favorable outcome of the disease. [1]

Pericarditis is an inflammatory reaction involving the pericardium. Inflammation is most often due to primary systemic pathology or structural pericardial changes: injuries, infectious and non-infectious lesions.

They say about fibrinous pericarditis if a patient develops pericarditis with the deposition of fibrinous filaments in the cavity of the pericardial bursa, which is caused by an inflammatory reaction. The condition is manifested by chest pains, aggravated by deep breathing or coughing, as well as severe weakness, fever and auscultatory noise of pericardial friction. [2]

Epidemiology

In clinical practice, fibrotic pericarditis is diagnosed relatively rarely - in about 0.1% of patients. Post-mortem autopsy data in frequency range from 3 to 6%. In men, pathology develops one and a half times more often than in women aged 20 to 50 years. [3]

The "culprits" of the development of fibrous pericarditis most often become:

• viruses (up to 50% of cases);
• bacteria (up to 10% of cases);
• acute myocardial infarction (up to 20% of cases);
• metabolic disorders (failure of renal function, uremia, myxedema - up to 30% of cases), as well as autoimmune pathologies.

It is impossible to determine the cause of fibrous pericarditis in 3-50% of cases. Pathology is rarely diagnosed during the lifetime of patients, and mostly becomes a finding during autopsy.

Causes of the fibrinous pericarditis

Viral diseases are considered the most common cause of the development of fibrinous pericarditis: such a relationship is present in almost every second patient. Most often we are talking about enteroviruses, cytomegaloviruses, Coxsackie virus, as well as the causative agent of epidparotitis and HIV.

Fibrinous pericarditis can be provoked by:

• acute myocardial infarction;
• traumatic injury (including surgery);
• infectious disease;
• autointoxication (uremia);
• systemic pathologies;
• neoplasia processes.

If we consider the oncological causes of the appearance of fibrinous pericarditis, then most often we are talking about malignant pulmonary tumors and neoplasms of the mammary glands. Less common is leukemia and lymphoma, as well as infiltrative damage to the pericardial sac with non-lymphocytic leukemia.

In some situations, the exact origin of the disease cannot be established: neither tumor structures, nor bacterial microorganisms, nor viruses are histologically determined. Such cases are called idiopathic fibrinous pericarditis.

Risk factors

Etiological risk factors can be:

• autoimmune processes - in particular, systemic lupus erythematosus, rheumatoid arthritis, etc.;
• systemic infectious-allergic inflammation of the connective tissue (rheumatism);
• tuberculosis;
• bacterial infectious and inflammatory processes;
• chronic insufficiency of renal function (terminal stage);
• pneumonia;
• myocardial infarction;
• malignant tumors;
• septic conditions;
• traumatic injuries of the chest, surgical operations in the region of the heart.

Risk groups include:

• the elderly (after 55 years);
• patients with elevated blood lipids (triglycerides and cholesterol);
• patients suffering from hypertension;
• heavy smokers;
• people with limited physical activity, or with its absence;
• obese and/or diabetic individuals.

Adverse factors are also considered some eating habits (abuse of salty, fatty foods, convenience foods and fast food), alcohol consumption, frequent stress.

Pathogenesis

With fibrinous pericarditis, hemodynamic disturbances are not observed, since a gradual increase in fluid volume is accompanied by a slow stretching of the outer pericardial sheet. If the exudation is fast, then the supporting ability of the heart bag is activated, which consists in limiting the boundaries of the diastolic expansion of the heart chambers. [4]

The pericardial tissue is characterized by good elasticity, but this property is relatively quickly lost when the heart sac is strongly stretched.

Hemodynamic disorders in the form of a decrease in blood pressure, venostasis appear when the pressure inside the bursa reaches 50-60 mm. In. Art. Venous pressure indicators increase and begin to exceed intrapericardial indicators by 20-30 mm. Art. When a critical exudative volume is reached, causing severe squeezing of the heart, cardiac tamponade develops. The rate of its development depends on the intensity of the liquid accumulation. [5]

The etiology is often infectious, allergic or autoimmune, which is due to the trigger mechanism for the development of pathology. Direct damage to the heart membranes by viral and other agents is not excluded.

The pathogenetic scheme of the development of the disease can be described as follows: the pericardium becomes inflamed → vascular permeability increases → liquid blood fractions, fibrinogen, which is deposited in the form of fibrin, sweat into the pericardial sac → catarrhal pericarditis develops → fibrinous pericarditis develops. [6]

Pathoanatomy

The appearance of fibrous pericarditis is associated with increased exudation of blood components into the pericardial sac. The fluid collection is reabsorbed by non-inflamed pericardial areas. If vascular permeability is impaired, coarse plasma proteins sweat, fibrinogen precipitates, an inflammatory infiltrate forms, and limited or widespread fibrotic pericarditis develops.

Abundant fluid accumulations in the bag indicate an incorrect absorption process and the spread of an inflammatory reaction to the pericardium. If the pericarditis is compressive, then the processes of fibrous scarring and adhesion of the sheets entail the formation of a dense pericardial membrane. With a prolonged course of the disease, the pericardium is calcified, a continuous capsule is formed, which is called the "shell" heart. In advanced cases, the muscular layer of the ventricles is damaged, local pathological disorders are noted against the background of myocardiofibrosis. The myocardium becomes thinner, degenerates into adipose tissue and atrophies due to a decrease in the functional load on the ventricles. [7]

Symptoms of the fibrinous pericarditis

Symptomatic fibrous pericarditis may present with the following symptoms:

• Heart pain: [8]
  • growing over several hours;
  • different intensity (from small to strong);
  • aching, burning, stabbing, scratching, or squeezing, squeezing;
  • with localization in the zone of cardiac projection, in the epigastrium (usually not extending to the limb or shoulder, as in coronary heart disease, but with possible irradiation to the neck and liver area);
  • aggravated during swallowing, deep breathing, coughing shocks, when bending and turning, without a clear connection with physical activity;
  • disappearing as exudate accumulates;
  • relieved in the position on the right side with the knees brought to the chest;
  • disappearing after taking analgesics, non-steroidal anti-inflammatory drugs, but not responding to taking nitroglycerin.
• General weakness, increased sweating, high fever, headache, as well as signs of a general intoxication syndrome.
• Persistent hiccups, nausea (sometimes with vomiting, without subsequent relief), tachypnea, palpitations, arrhythmia.

First signs

The initial symptomatology of fibrous pericarditis usually manifests itself as an infectious process, which complicates the diagnosis of the disease. Patients have general weakness, increased sweating, loss of appetite, subfebrile temperature.

Symptoms grow and worsen, a characteristic pericardial pain syndrome joins:

• pain bothers in the epigastrium or behind the sternum;
• has a different intensity - from slight discomfort to a sharp "heart attack" pain;
• according to the description of patients, the pain is burning, tingling, scratching, cutting or pulling;
• aggravated by coughing, position on the left side;
• weakens in the position on the right side, with an anterior tilt, in the knee-elbow position;
• not relieved by nitroglycerin.

In addition to pain, excruciating coughing attacks that do not cause relief, as well as nausea, swallowing tension, may disturb. Respiratory movements are superficial, the patient complains of a lack of air. [9]

Stages

There are the following stages of pericarditis:

1. Acute stage - if the disease lasts up to 1-2 months from the start of the pathology. It is the acute course that is characteristic of exudative and fibrinous pericarditis.
2. Subacute stage - if the disease lasts from two to six months from the start of the pathology. Characteristic of exudative, adhesive and constrictive pericarditis.
3. Chronic stage - if the disease lasts more than six months from the start of the pathology. Characteristic for exudative, adhesive, constrictive pericarditis, as well as for calcification (armored heart).

Forms

Acute fibrinous pericarditis according to the etiological factor is divided into infectious and infectious-allergic. Subtypes of the disease are:

• tuberculosis;
• specific bacterial (syphilitic, gonorrheal, dysentery, etc.);
• nonspecific bacterial (streptococcal, pneumococcal, meningococcal, staphylococcal, etc.);
• viral (adenoviral, influenza, Coxsackie, etc.);
• rickettsial (in patients with Q fever, typhus);
• chlamydial (genitourinary infections, ornithosis);
• mycoplasma (pneumonic, acute respiratory infections);
• mycotic (candidiasis, actinomycosis, histoplasmosis, etc.);
• due to protozoa (amoebic, malarial);
• allergic;
• rheumatic;
• malignant;
• traumatic, etc.

Dry fibrinous pericarditis can be idiopathic - that is, without a specific cause of pathology.

Acute pericarditis can be dry (fibrinous), exudative (serous-fibrinous, fibrinous-purulent), with or without cardiac tamponade.

As fibrinous pericarditis progresses, exudative pericarditis may develop. For example, serofibrinous pericarditis is diagnosed when a significant amount of serofibrinous effusion accumulates in the pericardial cavity. If a purulent effusion forms in the pericardial sac, then a diagnosis of fibrinous-purulent pericarditis is made.

Complications and consequences

Fibrinous pericarditis, if left untreated, is often complicated by adhesion of the pericardial sheets, as well as impaired myocardial conduction. With a running pathological process, symptoms are present and aggravated for a long time. Pericardial murmur persists in many patients even after treatment.

Cardiac tamponade occurs when pressure in the pericardium is high enough to prevent the right heart from filling. [10]

Patients may complain of chest pain and shortness of breath after physical activity, which is due to an increase in the volume of the heart muscle and the contact of dense pericardial sheets. Most often, such a condition is not treated, but observed in dynamics.

Even after a favorable outcome of fibrotic pericarditis in patients, the appearance of arrhythmia attacks is not excluded. The inflammatory reaction changes the impulse susceptibility of the myocardium, which can provoke the appearance of paroxysmal tachycardia, atrial and ventricular fibrillation, blockades. With regular violations of the heart rhythm, the development of heart failure is possible.

Diagnostics of the fibrinous pericarditis

The diagnosis of acute fibrinous pericarditis can be made if the patient has a typical triad  [11]:, [12]

• heartache;
• noise of pericardial friction;
• typical ECG pattern.

Instrumental diagnosis is usually represented by ECG, echocardiography and chest x-ray - to exclude the presence of exudate.

The ECG shows a concordant ST wave convex down no more than 7 mm, with a transition to high T without accompanying reciprocal ST depression in other leads. Fibrinous pericarditis for 1-2 days is accompanied by a rise in the segment covering all standard leads with a limit in the second standard lead. [13]

The main auscultatory sign of fibrinous dry pericarditis is the friction rub of the pericardial sheets. It is felt in the area of the left lower edge of the sternum, in the area of absolute cardiac dullness. The noise is heard synchronously with the contractions of the heart, has no connection with respiratory movements, however, it has variability and a tendency to increase at the time of pressure with a phonendoscope. Disappears with the appearance of exudate. The nature of the noise - sometimes soft, more often - rough, scraping, can be felt when probing.

The pericardial friction murmur in fibrinous pericarditis can be continuous (systolic-diastolic), two-component (ventricular systole and rapid filling of the left ventricle), or three-component (the so-called "locomotive rhythm").

During the diagnosis of fibrinous pericarditis, it is necessary to obtain micro and macro preparations, which is possible only when performing a histological examination of a part of the biomaterial removed during a biopsy of the pericardium.

Micropreparation of fibrinous pericarditis:

• under low microscopic magnification, pronounced fibrin overlays with a characteristic lilac-pinkish color are visualized on the epicardial surface;
• leukocytes are noted between fibrinous fibers;
• epicardial vessels are dilated, plethoric.

Macropreparation of fibrinous pericarditis:

• thickening of the epicardium (visceral pericardial sheet);
• whitish-grayish color, croupous fibrous film;
• "hairy" heart;
• depending on the outcome of the disease: splitting of fibrin and resolution of the inflammatory process, or the formation of adhesions ("armored" heart).

The term fibrinous pericarditis is often associated with the concept of "hairy heart", which is due to the deposition of a large number of proteins and fibrinous filaments on the sheets of the pericardium, which gives the heart a kind of "hairiness".

Laboratory tests (particularly a complete blood count) are general in nature and can help determine the origin of the disease and assess the intensity of inflammation.

Differential diagnosis

Differential diagnosis of fibrinous pericarditis is carried out:

• with myocardial infarction;
• with dissecting aortic aneurysm;
• with pulmonary embolism;
• with spontaneous pneumothorax;
• with angina;
• with myopericarditis;
• with pleurisy;
• with herpes zoster;
• with esophagitis, spasm of the esophagus;
• with acute gastritis, gastric ulcer.

Differential ECG signs:

	With fibrinous pericarditis	With acute myocardial infarction
ST segment	The changes are diffuse, in combination with a positive T wave. A return to the isoline is noted for several days.	Changes are local, discoordinate, in combination with a negative T wave. In patients with an uncomplicated course, the ST segment returns to the isoline for several hours.
PQ or PR interval	Interval depression is noted.	There are no changes.
Q wave, QS complex	Atypically pathological Q wave.	The pathological Q wave develops rapidly.
Atrial and ventricular arrhythmias	Not typical.	Typical.

The difference between fibrinous pericarditis and acute coronary syndrome:

• With the development of fibrinous pericarditis, pain often appears sharply, with retrosternal or epigastric localization. The nature of the pain is acute, steady, dull, aching, sometimes squeezing, constant (increasingly decreasing). Nitroglycerin is ineffective.
• In acute coronary syndrome, the pain is growing, radiating to the shoulder, forearm, upper limb, back. Attacks of pain are characteristic: attacks last for about half an hour. The position of the patient's body does not affect the severity of the pain syndrome. After taking Nitroglycerin, the symptoms subside.

Treatment of the fibrinous pericarditis

The patient is prescribed strict bed rest for a period of up to 7-14 days (hereinafter - depending on the course of the disease), dietary table No. 10 (10A).

If it was possible to determine the cause of the development of fibrinous pericarditis, then, according to indications, antibiotics, antiparasitic, antifungal, and other agents are prescribed.

Antibiotics are used for a clear infectious factor - for example, with sepsis, pneumonia, tuberculosis, purulent foci, etc.

Antiviral drugs are prescribed with a proven viral origin of the disease:

• cytomegalovirus requires the use of immunoglobulin 1 time per day 2-4 ml / kg according to the scheme;
• Coxsackie virus requires the appointment of interferon-A;
• for adenovirus and parvovirus B19, immunoglobulin 10 g intravenously is used.

Pathogenetic treatment consists in the use of the following drugs:

• Non-steroidal anti-inflammatory drugs - have analgesic, anti-inflammatory, slight immunosuppressive effects. It is appropriate to use acetylsalicylic acid, Voltaren (0.05 g three times a day), Ibuprofen (0.4 g three times a day), Meloxicam (0.015 g twice a day). [14]
• Glucocorticosteroids - have a bright anti-inflammatory, anti-shock, immunosuppressive effect. They are prescribed for the ineffectiveness of non-steroidal anti-inflammatory drugs.

In the idiopathic variant of fibrinous pericarditis and the absence of active foci of inflammation, antibiotics do not become the drugs of choice. The treatment regimen includes non-steroidal anti-inflammatory drugs (Diclofenac 150 mg / day, Meloxicam 15 mg / day, Ibuprofen 200 mg three times a day), as well as Colchicine (1 mg / day), corticosteroid drugs (1 mg / kg). [15], [16]

Surgical treatment is appropriate if the patient develops compressive pericarditis, if serofibrinous pericarditis recurs, or if medical therapy fails. Pericardiocentesis is the method of choice for cardiac tamponade. If this recurs, a pericardial window may be performed. In constrictive pericarditis, pericardiectomy is the treatment of choice. [17]

Prevention

There is no specific prevention of the development of fibrinous pericarditis. Doctors suggest following the following recommendations that reduce the risk of such complications:

• Eliminate smoking, avoid visiting smoking rooms (passive smoke inhalation). It has been proven that smoking even five cigarettes daily increases the risk of developing cardiovascular diseases by almost 50%.
• Adhere to a low-cholesterol diet, reduce the intake of saturated fats (fatty meat, lard should be replaced with white meat, seafood), introduce cereals, vegetables, herbs, fruits, vegetable oils into the diet.
• Reduce salt intake to 3-5 g per day, which will reduce the risk of developing cardiovascular disease by 25%.
• Introduce foods rich in magnesium and potassium into the diet (seaweed, dried fruits, apricots, pumpkin, buckwheat, bananas).
• Watch your body weight, eat a balanced diet.
• Ensure adequate physical activity (walking, swimming, cycling - at least half an hour daily or five times a week).
• Regularly monitor the indicators of fat metabolism, visit a doctor for preventive diagnostics.
• Limit or eliminate the use of alcoholic beverages.
• Avoid deep and prolonged stress.

Even making small changes in lifestyle can significantly slow down the development of pathologies of the heart and blood vessels. At the same time, you need to understand that it is never too late to start adhering to a healthy lifestyle. If, nevertheless, there are any signs of cardiac pathology, then you should immediately consult a doctor, preventing the progression of the disease and aggravation of symptoms.

Forecast

It is difficult to assess the prognosis of the disease, since it is relatively rarely detected during the life of the patient. In general, the criteria for an unfavorable prognosis are:

• a significant increase in temperature (above 38 degrees);
• subacute onset of symptoms;
• intense exudation into the pericardial sac;
• development of cardiac tamponade;
• no positive response to acetylsalicylic acid or other non-steroidal anti-inflammatory drugs after at least 7 days of treatment.

If fibrinous pericarditis is not treated, then the risks of death increase significantly - primarily due to the development of complications and intoxication. [18] Patients who have had this disease should be under regular supervision of a cardiologist.