Stages of polypoid changes formation
Changes in the valves and mural endocardium represent consecutive links of a single pathomorphological process. The inflammatory destruction of connective tissue goes through three main stages:
- Initial stage (Stage 1). Macroscopically, valve tissues appear thickened and edematous. Under the microscope, mucoid swelling of the endocardial interstitial substance is determined. Mild lymphocellular infiltration is observed, accompanied by fibroblast proliferation, and moderate focal sclerosis is formed.
- Stage of warty changes (Stage 2). Warts appear on the mural endocardium or strictly along the line of valve closure. They can be delicate and loose or dense and difficult to separate from the surface. The histological picture demonstrates fibrinoid transformations in the connective tissue. The heart stroma becomes edematous and loosened, perivascular hemorrhages and focal interstitial myocarditis occur.
- Stage of warty-polypoid changes (Stage 3). It is here that the morphological substrate of the "polyp" is formed. Massive polypoid-warty vegetations with ulceration form on the valves and mural endocardium. Septic endocarditis develops: ulcers appear, pyogenic bacteria accumulate on the cusps, leading to purulent melting of the valve. Importantly, the lesion site is not limited to the valvular apparatus alone — the pathological process involves blood vessels, fibrous rings, papillary muscles, and all layers of the heart (endocardium, myocardium, pericardium).
Myocardial changes during polyp formation
At the third, polypoid-warty stage, the myocardium undergoes major morphological alterations. Histologically, the following are revealed in the heart muscle tissue:
- Pronounced stromal edema.
- Massive lymphocellular infiltration.
- Fatty and protein degeneration of cardiomyocytes.
- Marked dilation of sinusoidal vessels, accompanied by blood stasis.
Both old and fresh areas of connective tissue disorganization are simultaneously present in the tissues, which emphasizes the continuity of the developing pathomorphological process.
Classification by anatomical substrate and activity
Polypoid-warty changes can develop against various backgrounds. Several variants of the lesion are distinguished:
- Primary endocarditis: inflammation affects previously healthy (intact) valves.
- Secondary endocarditis: the process develops against the background of pre-existing congenital or acquired changes in the great vessels, septa, and valves.
- Prosthetic valve endocarditis: infection affects artificial biological or mechanical implants. It is divided into early (occurring in the first 12 months after surgery) and late (developing after 12 months).
Based on the histology of the removed material and clinical data, the process is divided into active (there are symptoms, laboratory shifts, and morphological signs of tissue inflammation) and inactive (any signs of inflammation are absent).
Course and possible complications
The disease leading to the formation of polypoid vegetations is classified by its course into acute (up to 8 weeks) and subacute (more than 8 weeks). With massive antibiotic therapy, remission may occur. If a repeat attack by the same microorganism occurs 6 months after the initial episode, a relapse is diagnosed.
A formidable consequence of valve destruction is complications:
- Intracardiac: intracardiac abscesses, appearance of pathological shunts within the heart, embolic myocardial infarction.
- Extracardiac: systemic embolisms, mycotic aneurysms of peripheral vessels, infarction pneumonia, abscesses of parenchymatous organs. Disorders of cerebral circulation (ischemic, hemorrhagic, or mixed type) are also characteristic.
To memorize the histological stages of inflammatory valve destruction, use the mnemonic chain: "Muco — Fibra — Purulent Polyp" (Stage 1 — MUcoid swelling; Stage 2 — FIBRInoid transformations; Stage 3 — POLYPoid changes and pus).
Class and exam questions
What is the difference between early and late prosthetic valve endocarditis?
The difference lies in the timing of occurrence after surgery. Early prosthetic valve endocarditis occurs within the first 12 months after valve implantation, while late endocarditis occurs after 12 months.
How to determine that the process in the valve is active?
An active process is characterized by the presence of clinical symptoms, laboratory markers of inflammation, and, most importantly, clear morphological (histological) signs of inflammation in the tissue of the removed valve.
What happens to myocardial vessels at the polypoid-warty stage?
Dilation of sinusoidal blood vessels, accompanied by stasis (cessation of blood flow), along with pronounced stromal edema and degeneration, is observed in the myocardium.
What else to study on this topic
- Pathogenesis of mucoid and fibrinoid swelling of connective tissue
- Mechanisms of formation of intracardiac pathological shunts
- Histological differential diagnosis of protein and fatty myocardial degeneration
- Pathomorphological features of prosthetic infective endocarditis
- Morphology of extracardiac complications: mycotic aneurysms and infarction pneumonia
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