Helicobacter pylori active infection in patients with acute coronary heart disease

Antonio Aceti1, Riccardo Are, Giuseppe Sabino

  • 1Department of Infectious Diseases, II Faculty of Medicine, University of Rome La Sapienza, Sant'Andrea Hospital, Via di Grottarossa 1035, 00189 Rome, Italy. professoraceti@tiscali.it

Insights

Active Helicobacter pylori infection, identified by H. pylori stool antigen (HpSA), is linked to acute coronary heart disease (CHD). This suggests H. pylori may trigger cardiovascular events.

Area of Science:

  • Cardiology
  • Infectious Diseases
  • Gastroenterology

Background:

  • Helicobacter pylori (H. pylori) infection is a common cause of gastritis and peptic ulcers.
  • The potential link between H. pylori infection and cardiovascular diseases is an area of ongoing research.
  • Acute coronary heart disease (CHD) represents a significant global health burden.

Purpose of the Study:

  • To investigate the association between active H. pylori infection and the occurrence of acute coronary heart disease (CHD).
  • To determine if H. pylori infection acts as a trigger factor for acute cardiovascular events.

Main Methods:

  • A study involving 40 patients with acute coronary syndromes and two control groups (40 patients with non-H. pylori infections and 40 healthy subjects).
  • Participants were pair-matched for age, sex, and CHD risk factors.
  • H. pylori stool antigen (HpSA) and serum anti-CagA were tested in all participants.

Main Results:

  • A significantly higher prevalence of HpSA positivity was observed in patients with acute CHD (28/40) compared to control group A (14/40) and control group B (16/40) (p=0.00095).
  • No significant difference in anti-CagA positivity was found between the CHD group and control groups.
  • Concomitant positivity for HpSA and anti-CagA was significantly higher in patients with acute CHD (13/40) compared to controls (p=0.017).

Conclusions:

  • The findings indicate a higher rate of active H. pylori infection in patients experiencing acute CHD.
  • A significant association between HpSA and anti-CagA positivity in acute CHD patients suggests a potential role for H. pylori.
  • Active H. pylori infection may serve as a trigger factor for acute cardiovascular events.
Abstract

Related Concept Videos

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy01:16

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy

Helicobacter pylori, a resilient gram-negative bacterium, can thrive in the stomach's harsh, acidic environment. Infection with H. pylori leads to a cascade of events within the stomach lining. One of the critical disruptions caused by this bacterium is the interference with somatostatin production, a hormone responsible for regulating acid secretion. This interference tips the balance, escalating acid secretion and diminishing bicarbonate levels. This imbalance compromises the defensive...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies01:28

Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies

Peptic ulcer disease (PUD) presents with diverse symptoms depending on the location and severity of the ulcer. Clinical manifestations of peptic ulcer include dull pain and a burning sensation in the mid-epigastric region.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...