Visceral lesions in RA, on the one hand, are evidence of the systemic nature of the disease, on the other hand, they testify to the severity of its course and cause lethal outcomes. In fact, visceral lesions in RA develop as a result of immunopathological processes in the connective tissue and vessels with the accumulation of pathological immunoglobulins there and a tendency to develop amyloidosis (especially in the kidneys).
Heart manifestations of RA. Heart failure in rheumatoid arthritis is of interest in many respects, both theoretical and practical. First, it is important in terms of studying the relationship between RA and rheumatism and the differential diagnosis of these two diseases, and second, as evidence of the systemic nature of RA, which affects not only the joints, but also the internal organs.
For a long time it was believed that, unlike rheumatism, in RA, the heart is not affected. However, this view turned out to be deeply erroneous. Along with rheumatic heart disease and the “roar of the cardiac carditis”, there is undoubtedly a rheumatoid heart disease in the form of a “rheumatoid carditis”.
The frequency of heart damage in RA, according to sectional data, reaches 50-60%. In particular, the following changes were found in a clinical-anatomical study of 43 patients with RA on the side of the heart (M. Levin et al.).
There is no doubt that anatomical lesions of the heart are much more common than are diagnosed during the life of patients.
With severe articular syndrome, patients rarely complain about the heart.
The difference between rheumatoid carditis and rheumatic is less frequent involvement of the endocardial valve in the pathological process and relatively rare formation of malformations.
• heart, especially mitral stenosis. Diagnosis of rheumatoid carditis is difficult. In varying degrees, there may be a wide variety of cardiac symptoms and ECG changes of a non-specific nature.
A comprehensive examination of patients with RA makes it possible to diagnose rheumatoid myocarditis in at least 20% of cases. Roaring cardiac heart defects are in the form of mitral valve insufficiency or aortic valve insufficiency and are characterized by mild symptomatology. However, cases of severe rheumatoid heart defects that required aortic valve replacement have been described.
Aortic heart defects have to be differentiated from aortic aorticitis characteristic of RA. Aortitis is manifested by the expansion of the aorta and systolic murmur above the aorta, which has a diamond shape on the PCG. Unlike aortic stenosis, this noise is transient.
Adhesive pericarditis on the section is found not less than in 50% of cases, often in combination with pleurisy and more often in men. Clinically, rheumatoid pericarditis is latent and beneficial. The most common signs of them are – an increase in the size of the heart, pain in the heart and transient pericardial rub. On the ECG, a low voltage of the teeth or signs characteristic of a subepicardial lesion is observed: the layers of the myocardium, more often there are nonspecific changes of S and T.
An echocardiogram makes it possible to detect spikes and effusions in the pericardium even in the absence of clinical symptoms.
The development of kidney amyloidosis in RA is not uncommon and is marked by the terminal stage of the disease. The origin of amyloidosis in RA is associated with an intensive autoimmune process, hyper production of immune complexes and the development of dysproteinemia.
Circulating in the kidneys, immunoglobulins in the form of coarse protein molecules are deposited in the kidney vessels and, as a result, reactions with components of the connective tissue of the vessels lead to the formation of amyloidosis.
Amyloidosis usually develops 7–10 years from the onset of RA .. With a more malignant course of the disease it may be earlier. The earliest and most stable sign of amyloidosis is proteinuria. Urine sediment usually varies little. At first, proteinuria is moderate (1-3 g / l). Edema and renal function failure gradually appear, first the tubules (as a violation of urine concentration), and then the glomeruli (with nitrogen), anemia develops. As a result of amyloidosis, nephrotic syndrome can develop: proteinuria (up to 6–8 g / l), hypoproteinemia, hypercholesterolemia, anemia, and massive edema increase. Blood pressure may be elevated, but more often it remains normal.
The average life expectancy of patients from the onset of amyloi dose is 4 ± 1 year.
Rheumatoid glomerulonephritis is a manifestation of rheumatoid vasculitis, usually reflecting the high activity of the process. Morphologically rheumatoid glomerulonephritis occurs in two forms: membranous and membranous-proliferative.
Clinically, glomerulonephritis is characterized by proteinuria with hematuria. In this case, urinary syndrome is transient, depending on the activity of the underlying disease. Impaired renal function in rheumatoid glomerulonephritis is usually not observed.
Interstitial nephritis and necrosis of the papillae are most often associated with drug therapy: use of amidopirin, buta diene, gold salts, etc. Amidopyrine and butadione contribute to the development of renal vasculitis with a clinical picture of nephritis glomerular or isolated urinary syndrome.
Drug nephropathy most often ends favorably, but may contribute to the development of renal failure and death of the disease.