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Pericarditis

For medical students2 min readUpdated 2026-10-10

Pericarditis is an inflammatory condition affecting the visceral and parietal layers of the serous pericardium. In pathology, it is most frequently considered a secondary complication of mediastinal, pulmonary, or cardiac diseases, although it can also present as a primary, isolated process of unknown etiology.

EpidemiologyPrimary isolated inflammation of the pericardium accounts for 7% to 33% of all cases.

Clinical CourseThe primary idiopathic variant is characterized by a strong tendency toward frequent recurrences.

Rheumatic ProcessMicroscopically, specific *Aschoff-Talalov* bodies (granulomas) are identified within the pericardial layers.

Uremic InvolvementSevere uremia causes fibrinous inflammation, forming the classic "cor villosum" (hairy heart) appearance.

Classification by Origin

In pathology, the primary criterion for classifying pericarditis is its origin. Two main groups are distinguished:

Primary (Idiopathic) Isolated Pericarditis. This is a standalone inflammatory condition whose exact etiology remains unknown. It occurs significantly less frequently as a completely isolated pathology.
Secondary Pericarditis. This represents a complication of other systemic or local diseases. The inflammatory process extends to the pericardial sac from adjacent anatomical structures—most commonly pulmonary, cardiac, or mediastinal disorders. Secondary involvements are frequently infectious in nature and play a critical role in the pathogenesis of various systemic diseases.

Morphology of Primary Isolated Pericarditis

This form accounts for 7% to 33% of all diagnosed cases of pericardial inflammation. The clinical and morphological course can be either acute or chronic. A distinctive feature of this variant is its high propensity for frequent recurrences.

Depending on the nature of the inflammatory process, primary pericarditis may be serous, serous-fibrinous, or hemorrhagic. Pathology outlines a clear dynamic in the development of morphological changes:

Initial stage: characterized by marked edema and hyperemia (congestion) of both pericardial layers. Fibrinous exudate begins to actively accumulate in the pericardial cavity.
Development stage: gradual organization of the deposited exudate takes place.
Infiltration stage: an inflammatory cellular infiltrate forms within the pericardial tissues, predominantly represented by lymphoplasmacytic elements and macrophages.

Despite prominent morphological changes, the outcome of primary pericarditis is usually favorable. Resorption of the exudate occurs, leading to complete patient recovery. Obliteration (complete fusion and scarring) of the pericardial cavity is atypical for this form and extremely rare.

Etiology and Morphology of Secondary Pericarditis

Secondary forms exhibit a wide variety of morphological manifestations that directly depend on the underlying disease causing the inflammation:

Viral Pericarditis. Develops due to various viral agents. Proven pathogens include Coxsackie viruses, polioviruses, ECHO viruses, as well as influenza and infectious mononucleosis viruses. Serous-fibrinous inflammation is typical for this etiology.
Rheumatic Pericarditis. A classic manifestation of rheumatic fever. The nature of the inflammation is usually serous or serous-fibrinous. The main diagnostic criterion upon microscopic examination is the detection of specific cellular aggregates within the pericardial layers—Aschoff-Talalov granulomas.
Uremic Pericarditis. Occurs in the setting of severe renal failure. Characterized by prominent fibrinous or fibrinohemorrhagic inflammation. Due to massive deposition of dense fibrin strands on the epicardium, the heart acquires a characteristic villous appearance, macroscopically referred to as "cor villosum" (hairy heart).

Mnemonic

To quickly remember the type of exudate: Viruses and Rheumatism frequently produce Serous-fibrinous effusion (VRS), whereas Uremia leads to Fibrinous involvement ("hairy heart" — UF).

Frequently asked questions

What is concretio cordis ("armored heart") and in which outcome of pericarditis does it form?

Concretio cordis is the calcification of the pericardium that occurs during the organization of exudate with adhesion formation, obliteration of the pericardial cavity, and connective tissue calcification. This outcome is described, in particular, in rheumatic pericarditis and corresponds to pericardial constriction: constrictive pericarditis, or the "armored heart".

Which bacterial pathogens most frequently cause secondary purulent pericarditis?

For bacterial (purulent) pericarditis, the following pathogens are noted:

Staphylococcus aureus — the primary pathogen, causing 22–31% of primary abscess or purulent pericarditis cases.
Staphylococci, pneumococci, streptococci, Escherichia coli, Gram-negative bacteria — agents of nonspecific bacterial pericarditis.
Anaerobes: Prevotella spp., Peptostreptococcus spp., Propionibacterium acnes — their role is increasingly recognized.
Additionally, infectious causes include meningococci, salmonellae, chlamydia, and Borrelia burgdorferi.

Nonspecific bacterial pericarditis is often associated with septicopyemia; purulent pericarditis may occur in the setting of sepsis, following thoracic surgery, or as a complication of pneumonia.

What are the potential adverse outcomes of fibrinous pericarditis, aside from complete resolution of the exudate?

Adverse outcomes of fibrinous pericarditis are associated with the organization of the exudate when it fails to dissolve and is replaced by connective tissue. Potential outcomes include:

formation of adhesions (synechiae) and fibrous bands (shwarts);
obliteration of the pericardial cavity;
calcification of the connective tissue, forming an "armored heart";
development of pericardial constriction, i.e., constrictive pericarditis.

Which type of pericarditis is more common: primary or secondary?

Secondary pericarditis is diagnosed much more frequently. It arises as a complication of pre-existing cardiac, pulmonary, or mediastinal diseases, whereas primary pericarditis is a rarer standalone pathology.

How does primary idiopathic pericarditis typically resolve?

In most cases, complete resorption of the exudate and recovery occur. Obliteration (fusion) of the pericardial cavity is rare in this form.

What microscopic changes are characteristic of rheumatic pericarditis?

The primary morphological marker of rheumatic pericarditis is the detection of specific Aschoff-Talalov granulomas within the tissues of the pericardial sac.

What is a "hairy heart" in pathology?

This is the macroscopic description of uremic pericarditis. Due to fibrinous or fibrinohemorrhagic inflammation, thick fibrin strands deposit on the heart's surface, visually resembling hair.

Go deeper

Dynamics and mechanisms of fibrinous exudate organization in serous cavities.
Morphogenesis and cellular composition of Aschoff-Talalov granulomas in rheumatic fever.
Pathogenesis of "cor villosum" formation in end-stage uremia.
Mechanisms driving lymphoplasmacytic and macrophage infiltration in serous membranes.
Causes of frequent recurrences in idiopathic pericarditis.