Gastroesophageal Reflux Disease, Esophagitis, and Barrett's Esophagus 3 to 4 Years Post Sleeve Gastrectomy.

BACKGROUND: Sleeve gastrectomy (SG) has become the most popular bariatric procedure worldwide. However, SG is associated with de novo gastroesophageal reflux (GERD) and esophagitis, with concerns for progression into Barrett's esophagus (BE). The purpose of this study is to assess the clinical and endoscopic progression of GERD, esophagitis, and BE 3 to 4 years after SG. METHODS: Fifty-eight patients (pts) were assessed with endoscopy preoperative and at 3 to 4 years post SG, representing 44.9% follow-up. Endoscopy was offered to all SG pts regardless of symptoms. Outcomes including percent total weight loss (%TWL), PPI use, esophagitis progression, de novo reflux, and BE formation. RESULTS: At post-op follow-up, the %TWL was 23%. The average BMI dropped from 49.07 to 37.5. De novo reflux developed in 13 pts (30.9%). Of the 16 pts with GERD pre-op, 37.5% improved, 25% had stable disease, and 37.5% had worsening symptoms. The rate of esophagitis nearly doubled from 37.9% pre-op to 70.6% post-op. A majority of post-op pts had mild esophagitis (87.8%), with 12.1% with LA classes C and D. Asymptomatic esophagitis was found in 68.2% of post-op pts. The incidence of BE was 12.7% post-op, with de novo BE developing in 4 pts, representing 7.2%. CONCLUSION: SG is associated with increased rates of asymptomatic esophagitis and de novo reflux at 3 to 4 years post-op. De novo BE was detected as well, highlighting the importance of post-op screening. The majority of pts with GERD pre-op have stable disease or improve.

Losartan inhibits myosin isoform shift after myocardial infarction in rats.

Hypertrophy and heart failure following a myocardial infarction in rodents are accompanied by a switch of myosin isoforms from V1 to V3. The angiotensin II receptor blocker, Losartan, has been demonstrated to improve cardiac function and long-term survival after myocardial infarction. In this study we have investigated whether chronic Losartan treatment affects myosin isoform composition in the hearts of rats following a myocardial infarction. Rats were subjected to coronary artery ligation and received either Losartan (1 g/L) in the drinking water or water only. Four months after myocardial infarction, rats were classified as having either congestive heart failure (cMI) or uncomplicated myocardial infarction (uMI) based on their lung weight to body weight ratio (LW/BW). Compared with sham operated rats, uMI rats showed a 68.5% increase in the relative contribution of V3 and a 33.7% decrease in the relative contribution of V1 (p < 0.05). Untreated cMI showed 39.7% more V3 and 38.2% less V1 when compared with untreated uMI (p < 0.05). Losartan treatment after myocardial infarction reduced the incidence of cMI from 30.4 to 4.5% and scar size from 1.52 +/- 0.07 to 0.94 +/- 0.11 cm2 respectively. The percentage of V1 in Losartan treated uMI (LuMI) was 25.2% higher than the percentage of V1 in untreated uMI (p < 0.05), whereas the percentage of V3 in LuMI was 24.2% lower than that in untreated uMI (p < 0.05). A positive correlation of V3 myosin and scar area was observed. Our study suggests that expression of V3 myosin in the left ventricle is associated with scar size and the progress of hemodynamic changes after myocardial infarction. Losartan treatment reduces scar size and wall stress of the heart after the infarct, and therefore inhibits the signals shifting myosin isoform expression from V1 to V3 after a myocardial infarction.