Erosive-Ulcerative Gastrointestinal Lesions in Coronary Artery Disease: The Role of Helicobacter pylori and Prevention Strategies in Different Clinical Scenarios

Aim: to assess the prevalence and characteristics of erosive-ulcerative lesions of the gastrointestinal tract in patients with chronic coronary artery disease and acute myocardial infarction, determining the role of Helicobacter pylori (H. pylori) and other independent risk factors in their pathogenesis.

Materials and methods. A single-center prospective cohort study analyzed data from 110 patients divided into two groups based on the clinical form of coronary artery disease (CAD). Group 1 (n = 56) included patients with acute myocardial infarction (AMI) after primary percutaneous coronary intervention (mean age — 62.0 years) and consisted predominantly of men (n = 41; 73.21 %). Group 2 (n = 54) included patients with stable CAD who had undergone percutaneous coronary intervention within the preceding year (mean age — 67.5 years), and there was also a predominance of men (n = 37; 72.55 %). All patients underwent a comprehensive examination, including the collection of clinical and anamnestic data and laboratory diagnostics. Esophagogastroduodenoscopy (EGD) was performed at different time points depending on clinical status: patients with stable CAD underwent EGD at the time of hospitalization, while for patients with AMI, the examination was conducted in a delayed manner to minimize risks. H. pylori infection was diagnosed using the ¹³C-urea breath test in AMI patients and via biopsy during EGD in stable CAD patients. The one-month follow-up examination included: esophagogastroduodenoscopy to assess the condition of the upper gastrointestinal mucosa, and the ¹³C-urea breath test for patients with baseline H. pylori infection to evaluate the efficacy of eradication therapy.

Results. The prevalence of H. pylori was 46.4 % in the AMI group and 31.5 % in the stable CAD group. Planned EGD in patients with stable CAD before treatment revealed erosive-ulcerative lesions of the upper gastrointestinal tract in 51.9 % of cases, with 46.4 % of these lesions being associated with active H. pylori infection (p = 0.012). The application of active screening and preventive H. pylori eradication strategy in AMI patients resulted in successful eradication in 92.3 % of cases. At the 1-month follow-up EGD, mucosal changes persisted in 30.9 % of AMI patients; however, the majority of these findings were minimal and clinically insignificant (superficial gastritis, catarrhal bulbitis). True erosive-ulcerative lesions were detected in only 18.2 % of patients, indicating the role of the ulcerogenic effect of antiplatelet therapy in their pathogenesis. In patients with stable CAD, targeted therapy (eradication of H. pylori and prescription of proton pump inhibitors) led to a significant reduction in the frequency of erosive-ulcerative lesions from 51.9 to 7.4 % (p < 0.001). Multivariate analysis confirmed that in stable CAD, active H. pylori infection is an independent risk factor for gastrointestinal lesions (adjusted odds ratio [OR] — 4.32; 95 % CI: 1.22–18.20; p = 0.023). In contrast, in the AMI group after preventive eradication, this association completely lost statistical significance (OR = 0.84; 95 % CI: 0.22–3.20; p = 0.79).

Conclusions. Erosive-ulcerative gastrointestinal lesions in patients with CAD are closely associated with H. pylori infection and can be effectively prevented through its early diagnosis and eradication. In patients with AMI, preventive H. pylori eradication is a mandatory but insufficient element of prophylaxis and must be complemented by measures to mitigate the risks associated with dual antiplatelet therapy. Thus, an individualized approach to gastroprotection, tailored to the clinical form of coronary artery disease, enhances the safety and efficacy of pharmacotherapy in these patient groups.

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