Key result
Helicobacter pylori infection in patients with gastritis was associated with a higher rate of lower standing postprandial blood pressure compared to uninfected controls (41.7% vs 0%, p=0.045).
Why the study?
Does Helicobacter pylori infection alter the cardiovascular autonomic response to food ingestion in patients with chronic gastritis?
Observational (n=21)
Does Helicobacter pylori infection alter the cardiovascular autonomic response to food ingestion in patients with chronic gastritis?
Absolute Event Rate: 41.7% vs 0%
p-value: p=0.045
Helicobacter pylori infection in patients with chronic gastritis is associated with a blunted sympathetic and exacerbated vagal cardiovascular response to feeding.
H. pylori gastritis may alter postprandial autonomic responses; hypothesis-generating and should not yet change practice.
BACKGROUND: Feeding evokes a cardiovascular response associated to an increased sympathetic drive. The role of the parasympathetic component in this regard is less clear. Improvement of postprandial vasovagal complaints after Helicobacter pylori eradication in three cases led us to assess autonomic response to feeding in H. pylori-positive patients in search for an exacerbated parasympathetic response. MATERIAL AND METHODS: Patients with mild or moderate chronic histologic gastritis were studied. Subjects with the same diagnosis but testing negative for H. pylori were used as controls. Noninvasive cardiovascular tests were applied before and after feeding. RESULTS: On sympathetic tests, standing postprandial blood pressure was lower than preprandially in 5/12 H. pylori-positive patients and in 0/9 controls, p = .045. Resting postprandial BP on handgrip test was significantly lower than preprandially only in H. pylori-positive patients (71 +/- 8 versus 76 +/- 6 mmHg, p = .0068). Regarding parasympathetic tests, the 4-s unloaded exercise revealed greater initial heart rate response to unloaded cycling after feeding than preprandially again only in H. pylori-positive patients (1.40 +/- 0.20 versus 1.33 +/- 0.17, p = .0195). On tests influenced by both branches of the autonomic system, a difference was seen in the chronotropic response to handgrip. Postprandial heart rate on effort of H. pylori-positive patients was not higher than preprandially in contrast to controls [intervals between 2 consecutive R waves on electrocardiogram (R-R intervals) of 666 +/- 39 versus 685 +/- 62 ms, p = .0195], suggesting blunted sympathetic activation in the former. CONCLUSION: Supporting the observations that motivate the study, our findings indicate blunted sympathetic reactivity and exacerbated vagal response to feeding in H. pylori-positive patients.
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Lugon et al. (2006) conducted an observational in Mild or moderate chronic histologic gastritis (n=21). Helicobacter pylori infection vs. H. pylori-negative was evaluated on Lower standing postprandial blood pressure compared to preprandial levels (p=0.045). Helicobacter pylori infection in patients with gastritis was associated with a higher rate of lower standing postprandial blood pressure compared to uninfected controls (41.7% vs 0%, p=0.045).
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