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The Contribution of Gastroesophageal Reflux to Chest Pain in Patients with Coronary Artery Disease

Swarnjit Singh, MD; Joel E. Richter, MD; Edward G. Hewson, MD; Jane W. Sinclair, PA-C; and Barry T. Hackshaw, MD
[+] Article, Author, and Disclosure Information

Requests for Reprints: Joel E. Richter, MD, Division of Gastroenterology, University of Alabama at Birmingham, UAB Station, Zeigler Building 635, Birmingham, AL 35294.

Current Author Addresses: Drs. Singh and Richter: Division of Gastroenterology, University of Alabama at Birmingham, UAB Station, Birmingham, Alabama 35294.

Dr. Hewson: 48 Denison Street, New Castle, New South Wales, Australia 2303.

Ms. Sinclair: Division of Gastroenterology, Bowman Gray School of Medicine, 300 South Hawthorne Road, Winston-Salem, NC 27103.

Dr. Hackshaw: Desert Cardiology Consultants' Medical Group, Wright Building, Suite 401, 39-000 Bob Hope Drive, Rancho Mirage, CA 92270.

© 1992 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1992;117(10):824-830. doi:10.7326/0003-4819-117-10-824
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Objective: To describe the effectiveness of investigating and treating the cause of refractory chest pain in patients with coronary artery disease who are receiving optimal antianginal therapy.

Design: Cohort study.

Setting: Tertiary referral center.

Patients: Between January 1988 and December 1989,34 patients were identified as having angiographically proven coronary artery disease and atypical chest pain symptoms despite their having received aggressive medical or surgical antianginal therapy, or both.

Intervention: Patients with confirmed acid-related symptoms were treated with high-dose histamine-2 (H2) blockers or omeprazole for 8 weeks in an open-label study.

Measurements: Esophageal manometry and simultaneous 24-hour pH and Holter studies; global improvement in or disappearance of chest pain.

Results: Of the 34 patients, 30 (88%) experienced their identical chest pain symptoms during the study. A total of 164 pain episodes was recorded: 38 (23.2%) correlated with acid reflux; 6 (3.7%) were related to cardiac ischemia; and the remaining 120 (73.2%) had no identifiable cause. Of these 30 patients, 20 (67%) had some of their episodes of chest pain (range, 14% to 100%) secondary to acid reflux. After 8 weeks of vigorous acid suppression, 13 of these 20 patients had marked improvement or resolution of chest pain. Four other patients had ischemia-related episodes of chest pain that responded to more aggressive antianginal therapy. No episodes of acid reflux were clearly followed by ischemic chest pain. One patient had both acid- and ischemic-related episodes of chest pain that were indistinguishable. Overall, 24 of 34 (71%) patients had a definite cause of chest pain identified by combined pH and Holter monitoring.

Conclusions: Gastroesophageal reflux disease is a common, treatable cause of chest pain in patients with coronary artery disease who have atypical symptoms and remain symptomatic despite aggressive antianginal therapy. Combined Holter and 24-hour esophageal pH studies are complementary investigations for elucidating the cause of chest pain in these patients.





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