Classification by origin
In pathological anatomy, the key criterion for dividing pericarditis is its origin. Two main groups are distinguished:
- Primary (idiopathic) isolated pericarditis. This is an independent inflammatory disease whose exact etiology remains unknown to date. As a completely isolated pathology, it occurs much less frequently.
- Secondary pericarditis. This represents a complication of other diseases. The inflammatory process spreads to the pericardial sac from adjacent anatomical structures—most commonly in pathologies of the lungs, the heart itself, or other mediastinal organs. Secondary lesions are often infectious in nature and play a crucial role in the pathogenesis of a number of systemic diseases.
Morphology of primary isolated pericarditis
In the overall incidence structure, this form accounts for 7% to 33% of all diagnosed cases of pericardial inflammation. The clinical and morphological course of the pathology can be either acute or chronic. A distinctive feature of this variant is a high tendency toward frequent relapses.
According to the nature of the inflammatory process, primary pericarditis can be serous, serofibrinous, or hemorrhagic. Pathological anatomy distinguishes a clear dynamics 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 cavity of the pericardial sac.
- Development stage: gradual organization of the deposited exudate takes place.
- Infiltration stage: an inflammatory cellular infiltrate forms in the pericardial tissues, represented predominantly by lymphoplasmacytic elements and macrophages.
Despite pronounced morphological changes, the outcome of primary pericarditis is usually favorable. The exudate is resorbed, leading to the complete recovery of the patient. Obliteration (complete fusion and adhesion of the layers) of the pericardial cavity is atypical for this form and occurs extremely rarely.
Etiology and morphology of secondary pericarditis
Secondary forms are characterized by a great diversity of morphological manifestations that directly depend on the underlying disease that caused the inflammation:
- Viral pericarditis. Develops under the influence of various viral agents. Proven pathogens include Coxsackie viruses, polioviruses, ECHO, as well as influenza and infectious mononucleosis viruses. The development of serofibrinous inflammation is typical for this etiology.
- Rheumatic pericarditis. Is a classical manifestation of rheumatic fever. The nature of the inflammation is usually serous or serofibrinous. The main diagnostic criterion upon microscopic examination is the detection of specific cell clusters in the pericardial layers — Aschoff-Talaalov granulomas.
- Uremic pericarditis. Occurs against the background of severe renal failure. Characterized by pronounced fibrinous or fibrinopericarditis (fibrinogen-hemorrhagic) inflammation. Due to the massive deposition of thick fibrin strands on the epicardium, the heart acquires a specific villous appearance, which in macroscopic diagnosis is figuratively called "hairy heart".
Briefly: answers to topical questions
What is a "concretio cordis" (armor heart) and in what outcome of pericarditis does it form?
An "armor heart" is calcification of the pericardium that occurs during the organization of exudate with the formation of adhesions, obliteration of the pericardial cavity, and calcification of connective tissue. Such an outcome is described, in particular, in rheumatic pericarditis and also corresponds to pericardial constriction: constrictive pericarditis, or "armor heart".
Which bacterial pathogens most commonly cause secondary purulent pericarditis?
For bacterial (purulent) pericarditis, sources indicate the following pathogens:
- Staphylococcus aureus — the main pathogen, accounting for 22–31% of cases of primary abscess or purulent pericarditis.
- Staphylococci, pneumococci, streptococci, Escherichia coli, Gram-negative bacteria — pathogens of nonspecific bacterial pericarditis.
- Anaerobes: Prevotella spp., Peptostreptococcus spp., Propionibacterium acnes — their role is increasing.
- Also among the infectious causes of pericarditis are meningococci, salmonellae, chlamydiae, and Borrelia burgdorferi.
Nonspecific bacterial pericarditis is more often associated with septicopyemia; purulent pericarditis can occur against the background of sepsis, after thoracic surgery, or as a complication of pneumonia.
What are the possible adverse outcomes of fibrinous pericarditis, apart from complete resorption of the exudate?
Adverse outcomes of fibrinous pericarditis are associated with the organization of the exudate if it does not dissolve and is replaced by connective tissue. Possible outcomes include:
- formation of adhesions (synechiae) and fibrous plaques;
- obliteration of the pericardial cavity;
- calcification of connective tissue with the formation of an "armor heart";
- development of pericardial constriction, i.e., constrictive pericarditis.
For quick memorization of the exudate nature: Viruses and Rheumatism more often produce a Serofibrinous effusion (VSF), while Uremia leads to Fibrinous involvement ("hairy heart" — UF).
Class and exam questions
Which type of pericarditis is more common: primary or secondary?
Secondary pericarditis is diagnosed much more frequently. It occurs as a complication of pre-existing heart, lung, or mediastinal diseases, whereas primary pericarditis is a rarer independent pathology.
How does primary idiopathic pericarditis usually end?
In most cases, complete resorption of the exudate and recovery occur. Obliteration (fusion) of the pericardial cavity is rare for this form.
What microscopic changes are characteristic of rheumatic pericardial involvement?
The main morphological marker of rheumatic pericarditis is the detection of specific Aschoff-Talaalov granulomas in the tissues of the pericardial sac.
What is a "hairy heart" in pathological anatomy?
This is a macroscopic description of uremic pericarditis. Due to fibrinous or fibrinohemorrhagic inflammation, thick strands of fibrin settle on the surface of the heart, visually resembling hair.
What else to study on this topic
- Dynamics and mechanisms of organization of fibrinous exudate in serous cavities.
- Morphogenesis and cellular composition of Aschoff-Talaalov granulomas in rheumatic fever.
- Pathogenesis of the formation of a "hairy heart" in the terminal stage of uremia.
- Mechanisms of development of lymphoplasmacytic and macrophage infiltration in serous membranes.
- Causes of frequent relapses in idiopathic pericarditis.
Master the entire topic in the "Pathological Anatomy" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Pericarditis" and 4,414 more pages of the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 153 video lessons on the subject
Other topics in the section "Pathology of the Cardiovascular System"
Free video lessons: pathological anatomyShort lessons with study notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.