Related Experiment Video

Updated: Jul 13, 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 in coronary artery disease

M Kowalski1, M Pawlik, J W Konturek

  • 1Schüchterman - Klinik, Heart - Center Osnabrück - Bad Rothenfelde, Witten/Herdecke - University, Germany.

Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society
|October 13, 2006
PubMed

Insights

Inflammation plays a key role in coronary artery disease (CAD) development. Helicobacter pylori (Hp) infection may contribute to CAD progression through local inflammation, with eradication potentially reducing restenosis.

Area of Science:

  • Cardiovascular Medicine
  • Immunology
  • Infectious Diseases

Background:

  • Inflammation is increasingly implicated in coronary artery disease (CAD) pathogenesis.
  • Systemic inflammatory markers and infectious agents are linked to atherosclerosis.
  • The precise mechanisms initiating atherosclerotic vascular disease remain under investigation.

Purpose of the Study:

  • To explore the role of inflammation in CAD progression.
  • To investigate the controversial link between Helicobacter pylori (Hp) infection and CAD.
  • To assess Hp infection's potential contribution to CAD via local inflammatory processes.

Main Methods:

  • Review of existing literature on inflammation, atherosclerosis, and infectious agents in CAD.
  • Analysis of seroepidemiological and eradication studies concerning Hp infection and coronary heart disease.
  • Examination of evidence for Hp DNA in coronary plaques and the impact of Hp eradication on restenosis.

Main Results:

  • Growing evidence supports active inflammation in atherosclerosis, including coronary circulation.
  • Studies suggest a potential causal relationship between Hp infection and coronary heart disease, though controversial.
  • Detection of Hp DNA in coronary plaques and reduced restenosis post-eradication suggest Hp involvement in CAD progression.

Conclusions:

  • Inflammation is a significant factor in the pathogenesis and progression of CAD.
  • Helicobacter pylori infection may contribute to CAD progression through localized inflammatory responses.
  • Eradication of Hp infection shows potential in reducing coronary restenosis, indicating a role in CAD management.

More Related Videos

Quantitative Polymerase Chain Reaction (qPCR)-Based Rapid Diagnosis of Helicobacter pylori Infection and Antibiotic Resistance06:40

Quantitative Polymerase Chain Reaction (qPCR)-Based Rapid Diagnosis of Helicobacter pylori Infection and Antibiotic Resistance

Published on: July 28, 2023

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

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...
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...
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.
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...
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 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...