Related Experiment Video

Updated: Jul 9, 2026

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability
09:05

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability

Published on: November 21, 2014

Helicobacter pylori infection and coronary artery disease

Aleksandar Vcev1, Dario Nakić, Anamarija Mrden

  • 1Department of Internal Medicine, School of Medicine, University "J.J. Strossmayer", Osijek, Osijek, Croatia. vcev.aleksandar@kbo.hr

Collegium Antropologicum
|November 29, 2007
PubMed

Insights

Helicobacter pylori infection is more common in coronary artery disease (CAD) patients. However, H. pylori seropositivity did not correlate with traditional CAD risk factors in this study.

Area of Science:

  • Cardiology
  • Infectious Diseases
  • Epidemiology

Background:

  • Coronary artery disease (CAD) is a leading cause of mortality worldwide.
  • The potential role of infections, including Helicobacter pylori (H. pylori), in CAD pathogenesis is under investigation.
  • Understanding the association between H. pylori and CAD is crucial for public health.

Purpose of the Study:

  • To investigate the seroprevalence of H. pylori infection in patients diagnosed with coronary artery disease (CAD).
  • To examine the association between H. pylori seropositivity and established cardiovascular risk factors in CAD patients and controls.

Main Methods:

  • A randomized, multi-centre study involving 90 patients with CAD and 90 controls.
  • Serological assessment for H. pylori infection.
  • Analysis of traditional CAD risk factors: age, gender, diabetes mellitus, hypertension, smoking, hypercholesterolemia, and socioeconomic status.

Main Results:

  • A significantly higher seroprevalence of H. pylori was observed in CAD patients (78.8%) compared to controls (58.3%), with p < 0.05.
  • H. pylori seropositivity showed no significant association with CAD risk factors, including smoking, BMI, diabetes, hypertension, cholesterol levels, or socioeconomic status (P > 0.05).

Conclusions:

  • The findings suggest a potential link between H. pylori infection and the presence of coronary artery disease.
  • However, H. pylori infection does not appear to be associated with common cardiovascular risk factors.
  • Further research is warranted to elucidate the exact role of H. pylori in the development and progression of CAD.

More Related Videos

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance05:23

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance

Published on: March 7, 2025

Related Concept Videos

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 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...
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...
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...
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.