Immune-Mediated Heart Disease

Abstract

The heart involvement in systemic autoimmune diseases represents a growing burden for patients and health systems. Cardiac function can be impaired as a consequence of systemic conditions and manifests with threatening clinical pictures or chronic myocardial damage. Direct injuries are mediated by the presence of inflammatory infiltrate which, even though unusual, is one of the most danger manifestations requiring prompt recognition and treatment. On the other hand, a not well-managed inflammatory status leads to accelerated atherosclerosis that precipitates ischemic disease. All cardiac structures may be damaged with different grades of intensity; moreover, lesions can appear simultaneously or more frequently at a short distance from each other leading to the onset of varied clinical pictures. The pathogenesis of heart damages in systemic autoimmune conditions is not yet completely understood for the great part of situations, even if several mechanisms have been investigated. The principal biochemical circuits refer to the damaging role of autoantibodies on cardiac tissues and the precipitation of immune complexes on endocardium. These events are finally responsible of inflammatory infiltration which leads to subsequent worsening of the previous damage. For these reasons, it appears of paramount importance a regular and deepened cardiovascular assessment to prevent a progressive evolution toward heart failure in patient affected by autoimmune diseases.

Кардиоваскулярные Манифестации У Пациентов С Антифосфолипидным Синдромом: Вопросы Диагностики И Менеджмента

“…Ураження клапанів може супроводжуватися такими клінічними наслідками, як серцева недостатність, протезування клапанів і кардіоваскулярна смерть [8]. Патогенетичні механізми ураження клапанів до цього часу остаточно невідомі.…”

“…Патогенетичні механізми ураження клапанів до цього часу остаточно невідомі. Є докази, що саме аФЛ-АТ відіграють важливу роль у розвитку цих станів [8]. Ці імунологічні маркери сприяють утворенню тромбів на стулках клапанів, крім того, виходячи з даних мікроскопії, при АФС відбувається субендотеліальна депозиція імуноглобулінів (Ig), включаючи аФЛ-АТ (головним чином IgG), і компонентів комплементу (C1q, C3c, C4) [9].…”

Cardiac Manifestations of Antiphospholipid Syndrome: Clinical Presentation, Role of Cardiac Imaging, and Treatment Strategies

“…APS can also cause myocardial damage, pulmonary arterial hypertension (PAH), and both left ventricular (LV) and right ventricular dysfunction. 14,[17][18][19] Among this spectrum, VHD is the most common cardiac manifestation in patients with APS, with a prevalence of about 30%. [12][13][14]…”

“…[17][18][19][20][21] The pathogenic mechanisms involved in VHD are unknown, but there is evidence that aPL exert a role in the development of these lesions. [17][18][19][20] The aPL may promote the formation of valve thrombi, but these antibodies could also be involved in other mechanisms, as supported by evidence at microscopy of valve subendothelial deposits of Ig, including aCL (mainly IgG), and of complement components (C1q, C3c, C4). 17 Microinjuries due to mechanical stress may induce the exhibition of negative PL on valve surfaces and endothelial cells of intravalve capillaries, leading to interaction with aPL.…”

Diagnostic and prognostic value of autoantibodies against β1‑adrenoreceptors in patients with heart failure following acute myocardial infarction: A 5‑year prospective study

“…An autoimmune response against the myocardium may contribute to the pathogenesis of dilated cardiomyopathy (DCM), heart failure, myocarditis, rheumatic fever, idiopathic recurrent pericarditis and atherosclerosis (3,4). Autoantibodies against β 1 -adrenoreceptors (β 1 R-AAbs) are amongst the most important autoantibodies to cardiovascular receptors and have been proven to be associated with myocardial enlargement and cardiac dysfunction.…”