PPIs lowered high blood pressure in hypertensive patients with GERD

Hypertension is significantly correlated with gastroesophageal reflux disease (GERD), according to a new study published in the Journal of Clinical Gastroenterology. The investigators also found that proton-pump inhibitors lowered hypertension in these patients. 

“Our results clearly demonstrated that anti-acid drug therapy could reduce systolic and diastolic blood pressure (BP) of patients with both GERD and essential hypertension,” wrote authors led by Zhi-tong Li, MD, Department of Interventional Radiology and GERD, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

GERD and hypertension share common risk factors, including obesity, male sex, and alcohol intake. Nevertheless, findings from studies examining any potential association have been mixed. However, the availability of 24-hour BP monitoring, esophageal impedance, and pH monitoring have facilitated efforts to assess this relationship.

“The aim of this study was to determine whether there was a relationship between GERD and episodes of high BP in patients with essential hypertension, and to assess whether short-term anti-acid therapy for GERD could lower BP,” the authors wrote.

This study included 86 patients with essential hypertension; of these, 38 (44.2%) had GERD. The investigators excluded patients with obstructive sleep apnea and large hernias—conditions that could confound BP results.

Patients were assessed using endoscopy, simultaneous 24-hour continuous BP monitoring, esophageal impedance, and pH monitoring. Patients were asked to discontinue all forms of anti-acid therapy at least 2 weeks before the study; hypertensive medications, however, were not withheld or altered during the trial.

The authors employed regression analysis to assess the relationship between GERD and hypertension.

Dr. Li and colleagues observed 494 episodes of pathologic reflux (PR) and 684 episodes of elevated BP levels among the 38 patients with GERD. PR was defined as reflux associated with the onset of symptoms, including heartburn, regurgitation, and chest pain, and was indicated by a drop in esophageal pH to

In total, 102 of 684 episodes (14.9%) of elevated BP levels occurred at the same time as PR. Of the 38 patients with GERD and hypertension, only 24 met the criteria of at least one episode of elevated BP levels being time-dependent on the occurrence of PR. Investigators administered a 14-day course of proton-pump inhibitor (PPI) therapy as 20 mg omeprazole twice daily, and analyzed its effect on BP levels.

Patients with GERD had higher night-time BP levels than patients without GERD. Also, PPI treatment in patients with GERD decreased systolic and diastolic BP levels, as well as esophageal monitoring parameters.

“Anti-acid therapy restored esophageal pH to normal and significantly lowered elevated BP, which suggested that treatment of GERD could be useful for normalizing BP in essential hypertension patients,” the authors concluded.

In this study, use of 24-hour continuous BP monitoring provided a better understanding of the relationship between GERD and hypertension because this diagnostic approach is uninfluenced by “white coat hypertension,” permits the identification of hidden hypertension, and assesses brief variations in BP levels and the circadian rhythm. Moreover, 24-hour esophageal impedance and pH monitoring measures differences between weak acid reflux and nonacid reflux instead of merely the presence of acid reflux.

The authors suggested that one mechanism that could underlie the relationship between GERD and hypertension involves relaxed tonicity of the lower esophageal sphincter and decreased esophageal clearance secondary to beta blockers and calcium channel blockers.

Researchers acknowledged that a limitation of the study was that they did not assess potential confounders—including high alcohol intake, stress, and lifestyle choices—which can both elevate BP levels and heighten GERD symptoms and severity. Furthermore, the study had low power, with the small sample size not permitting subgroup analyses for different factors.