Autoimmune Valvular Carditis

Abstract

Autoimmune carditis is associated with many human rheumatic conditions, including rheumatic fever, systemic lupus erythematosous, and rheumatoid arthritis. The immune mechanisms that mediate the cardiovascular pathology connected to these diseases are poorly defined. Several animal models are used to recapitulate human pathophysiology in order to better characterize the immunopathogenic mechanisms driving autoimmune endocardial inflammation. These animal models point toward common mechanisms mediating autoimmune endocarditis; in particular, CD4+ T cells and pro-inflammatory macrophages play critical roles in directing the disease process. The goals of this review are to discuss the prevailing animal models of autoimmune endocarditis and their underlying immunologic mechanisms, and to provide insight regarding potential therapeutic targets in humans.

Rheumatic heart disease: A review of the current status of global research activity

“…Fibrotic scarring is accompanied by neovascularisation, which provides additional routes of access to valve tissue for activated T-cells and macrophages [15]. Persistence of cross-reactive anti-M T-cells in valvular tissues, epitope spreading and T-cell receptor (TCR) degeneracy are thought to perpetuate the autoimmune response, leading to alternating cycles of valvulitis and attempts at repair by fibrosis [20,88,89,92]. This cycle of tissue damage and repair leads to the formation of macroscopic nodules and microscopic granulomas known as Aschoff bodies (or nodules), which are considered pathognomonic for rheumatic carditis and RHD [23,95].…”

Triggers of Inflammatory Heart Disease

“…Endocarditis can be seen in patients with RA, SLE, and rheumatic fever, in which both joint and cardiovascular systems could be affected. RA patients can also carry cardiac-specific antibodies (Breed and Binstadt, 2015). To study the immunepathogenic mechanism of inflammatory arthritis, the K/BxN TCR transgenic mouse model has been developed (Monach et al, 2008).…”

Combined Use of Immunological and Ultrasound Methods of Estimation of Valve Heart Status in Patients With Inflammatory Rheumatic Diseases

“…У больных РА в подавляющем большинстве случаев выявляли недостаточность митрального и/или аортального клапанов, существенно реже -стеноз аорты. Высокая частота митрального пролапса у больных РА по мнению ряда исследователей [4,5] может быть связанна с наличием хронического воспалительного процесса, который способен ускорять развитие атеросклероза и сердечных заболеваний у больных с данной патологией [6].…”