Coronary Artery Disease and Barrett’s Esophagus: Is There Any Association?

Abstract

Introduction: Coronary artery disease (CAD) and Barrett’s esophagus (BE) share similar risk factor profile and CAD is highly prevalent in BE patients. In fact, CAD is the most common cause of mortality in BE patients. It is not known if CAD is associated with increased incidence of esophageal adenocarcinoma (EAC). Our aim was to identify patients with BE and CAD and see if there is any increased prevalence of dysplasia and EAC. Methods: All patients in our Barrett’s registry database from 2002 to 2013 with biopsy confirmed intestinal metaplasia were included. Variables such as age, gender, race, BMI, BE length, hiatal hernia size and biopsy findings were recorded. E-research services were utilized to identify patients with CAD, use of aspirin, NSAIDs and PPIs. Results: A total of 2341 subjects were included in the analysis. Average age was 60 ± 13 years and 75% were male and 95.8% were Caucasian. Average BMI was 29.7±6. Mean BE length was 3.23.5± cm and hiatal hernia size was 22.2± cm. CAD was identified in 110 (4.7%) patients. ASA use was documented in 413 (17.6%), and PPIs in 825 patients (35.2%). There were no significant differences in prevalence of dysplasia (Table 1). A total of 1034 subjects without high-grade dysplasia (HGD) or EAC at baseline, i.e. 836 with no dysplasia and 198 with low-grade dysplasia (LGD) were included in the follow-up. No dysplasia: During median follow-up of 47 [24, 90] months, 22% had progression (134 to LGD, 26 to HGD and 21 to EAC). After adjusting for age, gender, BE length and hernia size, CAD was associated with lower hazard of progression to HGD/EAC (HR=0.22; p= 0.038). Similarly, use of aspirin was associated with 55% lower risk of progression to HGD/EAC (HR=0.45, P=0.024) and use of PPIs with 23% lower risk (HR=0.77, p=0.4). LGD group: During median follow-up time of 30 [9, 56] months, 24% had progression (16 to HGD and 33 to EAC). CAD, use of asprin and PPIs was not associated with progression to HGD/EAC (HR=0.87, 0.64, 0.76 with p values of 0.79, 0.18 and 0.35, respectively).Table 1: Prevalence of Dysplasia in BE SubgroupsConclusion: CAD is not associated with any increased prevalence of dysplasia or cancer in BE patients. In fact, there is lower risk of progression in patients with no dysplasia at baseline. This may be perhaps due to concurrent aspirin and PPI use. However, the protective effect of CAD or ASA and PPIs was not observed in LGD patients with BE.