Infection by Helicobacter pylori and acute myocardial infarction. Do cytotoxic strains make a difference?

R Pellicano1, P P Parravicini, R Bigi

  • 1Department of Gastro-Hepatology, Molinette Hospital, Turin, Italy.

The New Microbiologica
|August 14, 2002
PubMed

Insights

Helicobacter pylori infection is significantly more common in men with acute myocardial infarction (AMI) than in controls. This bacterial infection, not necessarily the virulent strains, is linked to increased AMI risk, independent of traditional risk factors.

Area of Science:

  • Cardiology
  • Infectious Diseases
  • Epidemiology

Background:

  • Classical risk factors for acute myocardial infarction (AMI) do not fully explain disease epidemiology.
  • Infectious agents are emerging as potential contributors to AMI risk.
  • Helicobacter pylori (H. pylori) infection, particularly virulent strains, is suspected to be associated with AMI.

Purpose of the Study:

  • To investigate the prevalence of H. pylori infection and its virulent strains in male patients with AMI compared to a control group.
  • To assess the association between H. pylori infection and AMI, independent of traditional risk factors.

Main Methods:

  • A case-control study involving 223 male patients with AMI and 223 age-matched male controls admitted to emergency care.
  • H. pylori seroprevalence was determined by detecting IgG antibodies against H. pylori and anti-CagA.
  • Classical risk factors (hypertension, cholesterol, glucose, fibrinogen, smoking) were evaluated.

Main Results:

  • H. pylori infection was significantly more prevalent in AMI patients (84.7%) than in controls (61.8%) (p < 0.0001).
  • Prevalence of anti-CagA antibodies (virulent strains) did not significantly differ between AMI patients (33.8%) and controls (26.8%) (p=0.17).
  • Classical risk factors for AMI did not differ between patients with and without H. pylori infection.

Conclusions:

  • Patients with AMI exhibit a significantly higher prevalence of H. pylori infection compared to the control group.
  • The association between H. pylori and AMI appears to be independent of traditional cardiovascular risk factors.
  • Further research may be warranted to elucidate the precise role of H. pylori in the pathogenesis of AMI.

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: Pathophysiology01:17

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Myocarditis I: Introduction01:21

Myocarditis I: Introduction

Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
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...