Key result
Increasing severity of chronic heart failure in patients with CAD was associated with more diffuse gastroduodenal inflammatory changes, suppressed gastric secretion, and H. pylori in 63.2% of cases.
Observational (n=74)
The severity of gastroduodenal inflammatory and atrophic changes, including microcirculatory disorders and secretory suppression, increases with the progression of chronic heart failure in patients with CAD.
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Gastroduodenal evaluation may be warranted as CHF severity increases in CAD; leaves open causal role of H. pylori and need for prospective trials.
AIM: To study the clinical features of inflammatory and atrophic changes (IAls) in the gastroduodenal zone (GDZ) in people with varying severity of chronic heart failure (CHF) associated with coronary artery disease (CAD) and to determine gastric secretion, local microcirculation, and the presence of Helicobacter pylori. SUBJECTS AND METHODS: Seventy-four patients with CHF and gastric duodenal (GD) IAls who were divided into 2 groups according to its severity were examined. The specific features of impaired gastric secretory function and blood flow in the GD mucosa and its contamination with H. pylori were elucidated. RESULTS: GD IAls were ascertained to be mainly focal in the patients with Stages I-Ila CHF and focal or diffuse in those with Stages IIb-III. According the clinical findings, these changes were generally shown in the concurrence of transient and unstable (in early- stage circulatory insufficiency) and prolonged and persistent (during severe congestive events) phenomena. The development of IAls in the GDZ was linked to its thrombohemorrhagic microcirculatory disorders, the severity of which increased as the symptoms of CHF progressed. In Stages I-Ila circulatory insufficiency, this was accompanied by the normal activity of acid-peptic factor, by the decreased production gastromucoproteins, and, in 58.3% of cases, by H. pylori. The patients with Stages IIb-III showed the suppressed production of all constituents of gastric secretion and H. pylori in 63.2% of cases. CONCLUSION: The clinical manifestations and mechanisms of GD IAIs in CHF associated with CAD have a number of substantial differences in relation to its severity, which should be kept in mind when elaborating therapeutic and diagnostic measures.
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Osadchiy et al. (2015) conducted an observational in Chronic heart failure associated with coronary artery disease (n=74). Stages IIb-III chronic heart failure vs. Stages I-IIa chronic heart failure was evaluated on Presence of Helicobacter pylori. Increasing severity of chronic heart failure in patients with CAD was associated with more diffuse gastroduodenal inflammatory changes, suppressed gastric secretion, and H. pylori in 63.2% of cases.
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