Toll-like receptors (TLRs) have a critical role in the pathogenesis and disease course of viral infections. The induced pro-inflammatory responses result in the disturbance of the endovascular surface layer and impair vascular homeostasis. The injury of the vessel wall further promotes pro-thrombotic and pro-coagulatory processes, eventually leading to micro-vessel plugging and tissue necrosis. Moreover, TLRs have a direct role in the sensing of viruses and platelet activation. TLR-mediated upregulation of von Willebrand factor release and neutrophil, as well as macrophage extra-cellular trap formation, further contribute to (micro-) thrombotic processes during inflammation. The following review focuses on TLR signaling pathways of TLRs expressed in humans provoking pro-thrombotic responses, which determine patient outcome during viral infections, especially in those with cardiovascular diseases.

Granulomatosis with polyangiitis is an immunologically mediated small to medium vessel vasculitis associated with the formation of antineutrophil cytoplasmic antibodies. Advances in immunosuppressive therapy have expanded patients’ life expectancy in recent decades and have required an expansion of clinical attention to include management of chronic disease manifestations and long-term comorbidities. Though the heart and coronary arteries specifically are typically not primarily affected in GPA, studies have shown that patients are at an increased risk of cardiovascular and thromboembolic events. In many patients, metabolic risk factors promoting the formation of atherosclerotic plaques are not sufficiently controlled or screened for and potentially exacerbated by undesired treatment effects. This review aims to provide clinical physicians with an overview of the current literature on epidemiology, pathophysiology and prevention of coronary artery disease in the context of granulomatosis with polyangiitis and help to identify and lower the risk of cardiovascular events in this high-risk population.

Inflammation has a critical role in the development and progression of atherosclerosis. On the molecular level, inflammatory pathways negatively impact endothelial barrier properties and thus tissue homeostasis. Conformational changes and destruction of the glycocalyx further promote proinflammatory pathways also contributing to procoagulability and a prothrombotic state. In addition, changes in the extracellular matrix composition lead to (peri-)vascular remodelling and alterations of the vessel wall, e.g., aneurysm formation. Moreover, progressive fibrosis leads to reduced tissue perfusion due to loss of functional capillaries. The present review aims at discussing molecular and clinical effects of inflammatory processes on the micro- and microvas-culature with a focus on peripheral artery disease.