Tissue changes in P. are based on systemic disorganization of connective tissue (the deepest and most progressive in the heart and vessels) in combination with specific proliferative and non-specific exudative-proliferative reactions, as well as lesions of the microcirculatory channel vessels.
Since the 1950s, the evolution of clinical and morphological manifestations (pathomorphosis) of R. has been noted, which is primarily due to the active prevention and treatment of the disease. First of all, it refers to acute non-specific exudative-infiltrative inflammatory processes associated with hyperergic reactions. In particular, acute synovitis, polyserositis, rheumatic nodules and meningoencephalitis are much rarer. According to A.I. Lukina (1971), rheumocarditis pathomorphosis consists in a sharp decrease in the cases of exudative myocarditis and pericarditis, multi-valve heart defects, and rare detection of Ashoff-Talai granules. At the same time, isolated mitral valve defects became more frequent.
В. T. Talalaev (1929) first isolated exudative-alterative, granulomatous and sclerotic stages in the cycle of rheumatic process. Later, A. I. Strukov (1961, 1963) showed on the basis of histochemical analysis that the first stage is not only inflammation (see), but is manifested by a kind of disorganization (dystrophy) of connective tissue. He suggested dividing it into stages of mucoid swelling and fibrinoid changes.
Mucoid swelling (see Protein Dystrophy) is the earliest, surface reversible phase of connective tissue disorganization, characterized by mucoid (basophilic) oedema, spilled and focal metacheromasia (see), revealed when colored toluidin blue. In this case, there is not only true accumulation of acidic glycosaminoglycans due to their synthesis by cells, but also “disguise” of reactive groups of glycosaminoglycans due to dissociation of protein-carbohydrate complexes of connective tissue under the influence of activated proteolytic enzymes. The accumulation of free glycosaminoglycans, especially hyaluronic acid (see), causes increased hydration of the basic substance of connective tissue. Collagen fibers swell, they break up, but their colorful properties do not change. Fibers become unstable to the action of microbial collagenase, which is associated with changes in the cementing agent of the fibers (proteoglycans). Electron microscopy reveals fiber break-down into fibrils, less often – splitting of fibrils into subfibrils (Fig. 1), color enhancement by ruthenium red binding to carbohydrate components.
Fibrinoid changes (swelling, necrosis) represent the next, irreversible phase of connective tissue disorganization (fibrinoid). According to A. I. Strukov (1974), the fibrinoid in P. is associated with immunocomplex damage of the vascular channel and connective tissue. It is accompanied by plasma proteins, mainly globulins (see) and fibrinogen (see), which form pathological complexes with disorganized proteoglycans and destroyed collagen fibers. Fibrinoid foci are characterized by consistent swelling, homogenization, granular and bumpy decomposition of collagen fibers, weakening of their fuchsinophilia and strengthening of pycrinophilia in the Van-Guizon color, argyrophilia, SIC reaction, red color in Mallory or Heidengine (evidence of plasma proteins). A. I. Strukov (1961) extraction on the basis of colorful reaction to fibrin of two forms of fibrinoid (with and without fibrin) is conditional, because biochemical, immunohistochemical, polarization-optical and electron microscopic data indicate that the fibrin is detected in all forms of fibrinoid. In electron microscopy, all phases of destruction of collagen fibrils are detected in fibrinoid: adhesion, loss of leriodicity, fragmentation, splitting into sub and protofibrils with disorderly arrangement of the latter. In fibrinoid necrosis, the destruction of cellular elements is also detected (see Fibrinoid Transformation).