Background/Objectives: This study investigated the effect of the consumption of carnosine-enriched chicken meat on endothelium-dependent and independent microvascular reactivity and inflammatory mediators in patients with chronic coronary syndrome (CCS). Materials and Methods: In total, 38 CCS participants were randomized to two groups: the Control group (N = 19), who consumed regular chicken meat, and the Carnosine group (N = 19), who consumed carnosine-enriched chicken meat for 3 weeks. Skin microvascular reactivity in response to vascular occlusion (PORH), acetylcholine (ACh ID), sodium nitroprusside (SNP ID), and local thermal hyperemia (LTH) was measured. Arterial blood pressure (BP), heart rate (HR), biochemical parameters, anti- and proinflammatory cytokine levels, and markers of oxidative stress were assessed before and after the intervention. Results: The consumption of carnosine-enriched chicken meat improved endothelium-dependent (PORH, LTH) and endothelium-independent vasodilation (SNP ID). Systolic BP (SBP), diastolic BP (DBP), and mean BP (MAP), as well as serum concentrations of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and endoglin, decreased from the initial measurements. Conclusion: The consumption of carnosine-enriched chicken meat enhances microvascular endothelium-dependent and independent vasodilatation. Patients with CCS can benefit from carnosine-enriched chicken meat consumption through improved hemodynamic parameters, reduced inflammation, and enhanced microvascular relaxation.

The coexistence of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) and infective endocarditis (IE) represents a diagnostic challenge because of substantial overlap in clinical, serological, and cardiac manifestations. We report the case of a patient with prolonged ear, nose, and throat manifestations, pulmonary nodules and cavitary lesions, markedly elevated PR3-ANCA, and small lesions adjacent to the aortic valve initially considered suspicious for infective vegetations. Despite repeatedly negative blood cultures, culture-negative IE remained an important diagnostic consideration, and antimicrobial therapy was continued. The patient subsequently developed rapidly progressive pulmonary disease and severe systemic inflammation despite broad-spectrum antimicrobial treatment. The combination of characteristic upper respiratory tract disease, pulmonary involvement, markedly elevated PR3-ANCA, and a marked clinical and radiological response to immunosuppressive therapy supported the diagnosis of granulomatosis with polyangiitis (GPA). Glucocorticoids and plasma exchange were initiated, followed by rituximab for remission induction. Conservative cardiac management with regular follow-up was chosen. This case highlights the diagnostic challenge of distinguishing PR3-ANCA-positive IE from AAV and the importance of integrating microbiological, imaging, and clinical findings to establish the diagnosis.