RESUMO
The key side effects of antiplatelet therapy are associated with the damage of the upper gastrointestinal tract (GIT) mucous that can lead to erosions or ulcers and specifically complicated by bleeding. AIM: To assess the upper gastrointestinal mucosal condition by endoscopic and histological methods in patients with stable coronary arteries disease receiving long-term antiplatelet therapy with gastrointestinal bleeding (GIB) history or with high risk of this complication. MATERIALS AND METHODS: The study included patients from the single-center prospective registry of long-term antithrombotic therapy REGATTA-1. The gastric mucosa endoscopic examination with biopsy was performed in 20 patients with gastrointestinal bleeding history less than 1 year ago and in 24 patients without GIB, which have concomitant risk factors such as erosions and ulcers history and/or persistent dyspepsia clinical signs. The mucosal condition (erosions and ulcers) was estimated using a modified Lanz scale. The presence of Helicobacter pylori was determined by Histological verification. The inflammatory process characteristics were evaluated according to the modified Sydney classification. All participants received antithrombotic therapy at the time of esophagogastroduodenoscopy; 81.8% of patients received proton pump inhibitors. RESULTS: Chronic inflammation (93.2%), atrophy (59.1%), multiple erosions (45.5%) or ulcers (18.2%) were the most frequent endoscopic finding. H. pylori infection, found in mucosal samples in 90.9% of patients was one of the most important pathogenesis mechanism, which support the gastrointestinal mucosa damage. CONCLUSION: Mucosal damage endoscopic signs remains despite long-term proton pump inhibitors therapy in patients with coronary arteries disease and concomitant GIB risk factors, receiving antithrombotic therapy. H. pylori contamination may be the cause of these changes. Therefore, its active screening and eradication is necessary in such patients.
Assuntos
Doença da Artéria Coronariana , Infecções por Helicobacter , Helicobacter pylori , Gastropatias , Humanos , Inibidores da Bomba de Prótons/uso terapêutico , Doença da Artéria Coronariana/complicações , Doença da Artéria Coronariana/diagnóstico , Doença da Artéria Coronariana/tratamento farmacológico , Úlcera/complicações , Úlcera/tratamento farmacológico , Úlcera/patologia , Fibrinolíticos/farmacologia , Fibrinolíticos/uso terapêutico , Inibidores da Agregação Plaquetária/uso terapêutico , Anti-Inflamatórios não Esteroides/uso terapêutico , Infecções por Helicobacter/complicações , Infecções por Helicobacter/tratamento farmacológico , Mucosa Gástrica , Hemorragia Gastrointestinal/induzido quimicamente , Hemorragia Gastrointestinal/diagnóstico , Hemorragia Gastrointestinal/epidemiologiaRESUMO
Reduced expression of the key regulator of cardiac metabolism, transcription factor PPARα, in surgical samples of the auricles from patients with coronary heart disease and heart failure was detected by real-time quantitative PCR. These changes indicate reduced activity of this factor and a shift of energy metabolism from oxidative phosphorylation to glycolysis typical of dedifferentiated cells. Electron microscopy revealed dedifferentiated cardiomyocytes with disassembled contractile apparatus and disorganized sarcomeres. In the examined specimens from patients with heart failure, severe myocardial fibrosis was revealed.
Assuntos
Metabolismo Energético/fisiologia , Coração/fisiologia , Miócitos Cardíacos/metabolismo , PPAR alfa/fisiologia , Regeneração/fisiologia , Biópsia , Desdiferenciação Celular/genética , Doença das Coronárias/genética , Doença das Coronárias/metabolismo , Doença das Coronárias/patologia , Doença das Coronárias/fisiopatologia , Fibrose Endomiocárdica/genética , Fibrose Endomiocárdica/metabolismo , Fibrose Endomiocárdica/patologia , Fibrose Endomiocárdica/fisiopatologia , Metabolismo Energético/genética , Regulação da Expressão Gênica , Glicólise/genética , Insuficiência Cardíaca/genética , Insuficiência Cardíaca/metabolismo , Insuficiência Cardíaca/patologia , Insuficiência Cardíaca/fisiopatologia , Humanos , Miocárdio/metabolismo , Miocárdio/patologia , Miócitos Cardíacos/patologia , Miócitos Cardíacos/fisiologia , Fosforilação Oxidativa , PPAR alfa/genética , PPAR alfa/metabolismoRESUMO
Critical illness - related corticosteroid insufficiency (CIRCI) is associated with elevated level of circulating biomarkers of inflammation, pro - coagulant effects, deterioration of systemic inflammatory response syndrome (SIRS) and, consequently, prolonged in - hospital stay and increased mortality of intensive care patients. Incidence of CIRCI widely varies depending on specific patient's population and applied diagnostic thresholds being as high as 30% among postoperative patients on inotropes. CIRCI is a complex clinical and pathophysiological condition with substantial influence on immediate survival and prognosis. Clinical impact of CIRCI as well as pathogenetically based therapy arouse keen interest of intensive care specialists and clinical pathologists. The specific issues of CIRCI in patients after cardiac surgery and cardiology emergencies remain largely under - recognized, so further scrutinization is needed.