Research Spotlight

Tjaden, B. L., Jr., H. Sandhu, C. Miller, D. Gable, S. Trimarchi, F. Weaver and A. Azizzadeh (2018). “Outcomes from the Gore Global Registry for Endovascular Aortic Treatment in patients undergoing thoracic endovascular aortic repair for type B dissection.” J Vasc Surg 68(5): 1314-1323.

Full text of this article.

OBJECTIVE: The Global Registry for Endovascular Aortic Treatment (GREAT) is a prospective multicenter registry collecting real-world data on the performance of W. L. Gore (Flagstaff, Ariz) aortic endografts. The purpose of the present study was to analyze the implementation and outcomes of thoracic endovascular aortic repair (TEVAR) in GREAT patients with type B aortic dissection (TBAD). METHODS: From 2010 to 2016, >5000 patients were enrolled in the GREAT from 113 centers in 14 countries across 4 continents. The study population comprised those treated for TBAD. The primary outcomes of interest were mortality and freedom from aortic events (AEs). RESULTS: A total of 264 patients (80% male; mean age, 62 years) underwent TEVAR for the treatment of 170 (64%) acute and 94 (36%) chronic cases of TBAD. Chronic TBAD patients required significantly longer endograft coverage than did acute TBAD patients (P = .05). Early postoperative complications occurred in 9% of patients, with no difference in chronic vs acute dissection (P = .11). The 30-day aortic mortality and all-cause mortality were 1.5% and 2.3%, respectively, with no differences based on chronicity. During a mean follow-up of 26 months, the total aortic mortality was 2.7% and the total all-cause mortality was 12.5%. The all-cause mortality was significantly greater for chronic vs acute TBAD (19.2% vs 8.8%, respectively; P = .02). On multivariate analysis, patients with acute uncomplicated dissections had significantly improved overall survival compared with all other categories of dissections (93% vs 83% at 2 years; P < .05). A proximal landing zone diameter >40 mm was associated with an increased risk of retrograde type A dissection (18% vs 2%; P = .02). Patients undergoing left subclavian artery (LSA) coverage experienced a twofold greater rate of AEs compared with noncoverage patients (P < .01). Patients who underwent LSA revascularization experienced a 1.5-fold greater rate of AEs compared with patients covered without revascularization (P = .04). CONCLUSIONS: TEVAR for TBAD using the conformable GORE TAG thoracic endoprosthesis device can be performed with a low incidence of aortic mortality and complications. Acute uncomplicated TBAD patients had a significantly lower mortality rate than that of other patients. Larger proximal landing zones were associated with more frequent retrograde type A dissection. LSA involvement (coverage and/or revascularization) was associated with an increased risk of AEs during follow-up.

Spechler, S. J., V. Konda and R. Souza (2018). “Can Eosinophilic Esophagitis Cause Achalasia and Other Esophageal Motility Disorders?” Am J Gastroenterol Oct 12. [Epub ahead of print].

Full text of this article.

Eosinophilic esophagitis (EoE), a disorder identified by its esophageal mucosal features, often is associated with esophageal motility abnormalities, which are manifestations of esophageal muscle dysfunction. Those motility abnormalities sometimes normalize with treatments that reduce esophageal eosinophilia, suggesting that eosinophils can cause reversible esophageal motility disturbances, perhaps by releasing myoactive and neuroactive eosinophil products. Although achalasia uncommonly is associated with EoE as currently defined, most achalasia patients have evidence of an abnormal accumulation of eosinophils and/or their degranulation products in the esophageal muscularis propria, a location inaccessible to routine endoscopic evaluation. Achalasia is an idiopathic condition resulting from destruction of neurons in the myenteric plexus of the esophagus, and degranulating eosinophils release toxic proteins capable of destroying those neurons, thereby causing the irreversible motility abnormalities of achalasia. This report reviews data on the association of esophageal eosinophilia with achalasia and other esophageal motility abnormalities. Based on this review, we propose that EoE, like eosinophilic gastroenteritis, might have mucosal-predominant and muscle-predominant forms with different clinical manifestations. A muscle-predominant form of EoE could underlie a variety of reversible and irreversible esophageal motility disorders, including achalasia. The concept that esophageal motility abnormalities might develop from a muscle-predominant form of EoE warrants serious consideration and further investigation.

Schiller, L. R. (2018). “Response to: The Significance of Mast Cell Activation in The Era of Precision Medicine.” Am J Gastroenterol Oct 17. [Epub ahead of print].

Full text of this article.

To the Editor: I thank Drs. Weinstock, Rezaie and Afrin for their thoughtful letter commenting on my paper about the evaluation of patients with chronic diarrhea and irritable bowel syndrome with diarrhea (IBS-D) [1]. Mast cell activation syndrome (MCAS) should be considered in patients with multi-system symptoms, including those with IBS-D. The role of mast cells in more ordinary cases of IBS-D is still unresolved. Like Rodney Dangerfield, intestinal mucosal mast cells “don’t get no respect,” probably related to their poor uptake of commonly used histological stains, such as hematoxylin and eosin, which lets them blend in with other cells during routine histological analysis. With the use of appropriate stains, it is apparent that the intestine has plenty of mast cells, with up to 55 per high-power field in healthy subjects one study. While earlier studies claimed that IBS-D patients had greater numbers of mast cells than healthy subjects, there is substantial overlap between these two groups and attention has been focused on hyperresponsiveness of mast cells in IBS-D patients. Current studies indicate that this can happen and that therapy aimed at mast cells or their mediators with drugs such as disodium cromoglycate or antihistamines may modify symptoms in some IBS-D patients. What is not known is how often this happens and what role mast cells might play with other etiologies of IBS-D, such as food intolerances or post-infectious IBS. Future studies should clear this up. Until they do, as suggested by Drs. Weinstock, Rezaie and Afrin, clinicians should keep this mechanism in mind when dealing with patients with chronic diarrhea or IBS-D. (Text of Author’s reply to the comment of Weinstock et al. on Schiller LR. Evaluation of chronic diarrhea and irritable bowel syndrome with diarrhea in adults in the era of precision medicine. Am J Gastroenterol. 2018;113:660–9.)

Rossler, K. L., K. Hardin, M. Hernandez-Leveille and K. Wright (2018). “Newly licensed nurses’ perceptions on transitioning into hospital practice with simulation-based education.” Nurse Educ Pract 33: 154-158.

Full text of this article.

Highlights: 1) Transition into practice with simulation-based education was explored; 2) Themes of Gaining Comfort with Relationships and Talking It Out were evident; 3) Newly licensed registered nurses need guidance with role socialization; 4) The simulated environment encouraged the development of collective competence.

Ramires, F. J. A., F. Martinez, E. A. Gomez, C. Demacq, C. R. Gimpelewicz, J. L. Rouleau, S. D. Solomon, K. Swedberg, M. R. Zile, M. Packer and J. J. V. McMurray (2018). “Commentary: Post hoc analyses of SHIFT and PARADIGM-HF highlight the importance of chronic Chagas’ cardiomyopathy.” ESC Heart Fail Oct 9. [Epub ahead of print].

Full text of this article.

We read with interest the report by Bocchi and colleagues of their post hoc analysis of the Systolic Heart failure treatment with the If inhibitor ivabradine Trial (SHIFT), examining the effect of study drug in the 38 patients with chronic chagasic cardiomyopathy (CCC). The authors reported that study drug lowered heart rate and improved New York Heart Association class. The sample size was too small to allow estimation of the effect of treatment on mortality or hospitalization. However, this analysis did suggest that patients with CCC experienced high event rates, despite excellent background therapy. We examined outcomes in patients with CCC in the Prospective comparison of Angiotensin Receptor Neprilysin Inhibitor with Angiotensin Converting Enzyme Inhibitor to Determine Impact on Global Mortality and morbidity in Heart Failure (PARADIGM‐HF) and the Aliskiren trial to Minimize OutcomeS in Patients with Heart failure (ATMOSPHERE). These trials included 195 CCC patients from among a total of 2552 recruited in Latin America. Despite being younger and having less co‐morbidity, the CCC patients had higher hospitalization and mortality rates, compared with other aetiologies, despite similarly good treatment. We also conducted an exploratory post hoc analysis of the effect of sacubitril/valsartan (formerly known as LCZ696) in CCC patients in PARADIGM‐HF. Of a total of 113 patients, 58 were randomized to sacubitril/valsartan and 55 to enalapril. The two treatment groups were similar in terms of demographics, co‐morbidity, and heart failure (HF) severity. Patients with CCC treated with sacubitril/valsartan, as compared with enalapril, had a lower risk of experiencing cardiovascular death or HF hospitalization, the primary composite endpoint, and each of its components (Figure). The point estimate for risk reduction was comparable with or greater than that seen with the drug vs. enalapril in the entire study population. This analysis is underpowered and should be interpreted with caution. CCC is a major health issue in Latin America and is now recognized in the USA and Europe, reflecting contemporary migration patterns.5-8 Indeed, a recent study from Brazil concluded that the population attributable mortality risk from CCC increased between 2002/2004 and 2012/2014.9 Future trials should consider recruiting larger numbers of patients with CCC to allow adequately powered subgroup analysis and even trials specifically in CCC would be justified, given the magnitude of this problem. Until that time, patients with CCC should be treated empirically with therapies recommended by guidelines, on the assumption that treatments for patients with reduced ejection fraction are effective, irrespective of aetiology. (Text of letter concerning Bocchi. 2018. Safety profile and efficacy of ivabradine in heart failure due to Chagas heart disease: a post hoc analysis of the SHIFT trial.)