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ROCHESTER, MINNESOTA. In 2005 Italian researchers reported that patients with atrial fibrillation tended to have a higher level of IgG antibodies
to Helicobacter pylori (seropositive) than did healthy volunteers. They speculated that the H pylori bacterium may adversely affect the NA+/K+-ATPase pump
responsible for maintaining homeostatic balance in individual heart cells. A disturbance of this balance may trigger AF by creating abnormal
automaticity or triggered activity that causes a depolarization delay, which can result in very rapid premature atrial contractions (PACs), a forerunner for a full-blown afib episode.[1]
Researchers at the Mayo Clinic have now followed up on these findings. Their study included 743 patients who were admitted to the clinic because of suspected
cardiovascular disease and underwent coronary angiography or an electrophysiologic study. All patients were also tested for IgG antibodies to H pylori.
Those who had one or more electrocardiograms showing afib during the study period (1994 to 2001) were included in the AF group (83 patients in total).
The researchers found that patients with afib were more likely to seropositive for H pylori than were non-afibbers (65% vs. 55%).
Paroxysmal afibbers (62% of group) were seropositive in 65% of cases, persistent afibbers (22%) were seropositive in 67% of cases, and permanent afibbers (67%)
were seropositive in 67% of cases.
The association between seropositivity and AF varied significantly with age. In patients less than 50 years of age, the incidence of AF was 8% in the
seropositive group versus 0% in the seronegative group; however, in older patients (more than 70 years of age), there was no significant
difference in incidence (17.5% among seropositive versus 15.4% among seronegative patients).
There was no association between the level of the systemic inflammation marker CRP (C-reactive protein) and H pylori status,
which is somewhat surprising since H pylori infection causes chronic gastric inflammation. Nevertheless, the researchers
conclude that ectopy within pulmonary veins may be aggravated by inflammation in the esophagus or stomach caused by a
chronic H pylori infection. They suggest further studies and routine assessment of H pylori status in younger patients with atrial fibrillation.
Bunch, TJ, et al. Frequency of Helicobacter pylori seropositivity and C-reactive protein increase in atrial fibrillation in patients undergoing coronary angiography.
American Journal of Cardiology, Vol. 101, 2008, pp. 848-51
Editor�s comment: There is little question that H pylori is a bad actor when it comes to stomach ulcers and perhaps,
stomach cancer. However, whether its elimination will �cure� or prevent afib is still very much an open question,
but one that further Mayo Clinic studies will, hopefully, help answer. In the meantime, routine elimination of H pylori,
except in the case of stomach ulcers, may not be the smartest idea for an afibber.
Nine years ago Dr. Martin Blaser of the Department of Veterans Affairs warned that
a lack of H pylori may be behind the recent increase in the incidence of gastroesophageal reflux disease (GERD),
Barrett's esophagus, and esophageal cancer. Dr. Blaser points out that the human stomach and H pylori have
lived in harmony for millions of years. However, recently the incidence of H pylori colonization has declined in the
Western world because of, among other reasons, the excessive use of antibiotics in children.
This decline has been accompanied by a substantial increase in GERD and esophageal cancer.
GERD is uncommon in countries where most people are colonized ("infected") by H pylori. Dr. Blaser believes
that the most common strain of H pylori (cag+) is protective against GERD, Barrett's esophagus, and
esophageal cancer but can promote stomach ulcers and cancer. He believes H pylori exerts its effect by regulating acid secretion in different parts of the stomach.[2]
[1] Montenero, AS, et al. Helicobacter pylori and atrial fibrillation: a possible pathogenic link. Heart, Vol. 91, July 2005, pp. 960-61
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