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Cardiac involvement portends a poor prognosis in patients with sarcoidosis. However, due to the nonspecific clinical manifestations of the disease, patchy myocardial involvement, and the limited diagnostic yield of diagnostic tests, early diagnosis of cardiac sarcoidosis has been exceedingly difficult. As a result, there is no standardized approach for the early diagnosis of cardiac sarcoidosis. Imaging modalities that can both identify disease and predict response to therapy are paramount to improve management of cardiac sarcoidosis. 18F-FDG PET has many practical advantages in assessing disease activity and monitoring treatment response in patients with cardiac sarcoidosis. Accumulating data support the growing role of 18F-fluorodeoxyglucose (18F-FDG) PET in the diagnosis and risk stratification of patients with cardiac sarcoidosis.

With the development of reliable endoscopic closure techniques and tools, endoscopic full-thickness resection (EFTR) is emerging as a therapeutic option for the treatment of subepithelial tumors and epithelial neoplasia with significant fibrosis. EFTR may be categorized as “exposed” and “nonexposed.” In exposed EFTR, the full-thickness resection is undertaken with a tunneled or nontunneled technique, with subsequent closure of the defect. In nonexposed EFTR, a secure serosa-to-serosa apposition is achieved before full-thickness resection of the isolated lesion. This document reviews current techniques and devices used for EFTR and reviews clinical applications and outcomes.

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Obesity is one of the most significant health problems worldwide. Bariatric surgery has become one of the fastest growing operative procedures and has gained acceptance as the leading option for weight-loss. Despite improvement in the performance of bariatric surgical procedures, complications are not uncommon. There are a number of unique complications that arise in this patient population and require specific knowledge for proper management. Furthermore, conditions unrelated to the altered anatomy typically require a different management strategy. As such, a basic understanding of surgical anatomy, potential complications, and endoscopic tools and techniques for optimal management is essential for the practicing gastroenterologist. Gastroenterologists should be familiar with these procedures and complication management strategies. This review will cover these topics and focus on major complications that gastroenterologists will be most likely to see in their practice.

Chest CT scans are being performed more frequently on postoperative cancer patients and have resulted in an increased diagnosis of peripheral PE. The clinical significance of, and optimal treatment for, diagnosed subsegmental PE are incompletely defined.

The benefit of the ␤ 2 -adrenergic agonist, clenbuterol, in left ventricular assist device patients with dilated cardiomyopathy has been reported, but its effect on ischemic heart failure (HF) is unknown. We investigated whether clenbuterol improves left ventricular remodeling, myocardial apoptosis and has synergy with a ␤ 1 antagonist, metoprolol, in a model of ischemic HF. Rats were randomized to: 1) HF only; 2) HF ϩ clenbuterol; 3) HF ϩ metoprolol; 4) HF ϩ clenbuterol ϩ metoprolol; and 5) rats with sham surgery. HF was induced by left anterior descending artery (LAD) artery ligation and confirmed by decreased left ventricular fractional shortening, decreased maximum left ventricular dP/dt (dP/dt max ), and elevated left ventricular end-diastolic pressure (LVEDP) compared with sham rats (p Ͻ 0.01). After 9 weeks of oral therapy, echocardiographic, hemodynamic, and ex vivo end-diastolic pressure-volume relationship (EDPVR) measurements were obtained. Immunohistochemistry was performed for myocardial apoptosis and DNA damage markers. Levels of calcium-handling proteins were assessed by Western blot analysis. Clenbuterol-treated HF rats had increased weight gain and heart weights versus HF rats (p Ͻ 0.05). EDPVR curves revealed a leftward shift in clenbuterol rats versus metoprolol and HF rats (p Ͻ 0.05). The metoprololtreated group had a lower LVEDP and higher dP/dt max versus the HF group (p Ͻ 0.05). Clenbuterol and metoprolol groups had decreased myocardial apoptosis and DNA damage markers and increased DNA repair markers versus HF rats (all p Ͻ 0.01). Protein levels of the ryanodine receptor and sarcoplasmic reticulum calcium-ATPase were improved in clenbuterol-, metoprolol-, and clenbuterolϩmetoprolol-treated groups versus HF rats. However, as a combination therapy, there were no synergistic effects of clenbuterolϩmetoprolol treatment. We conclude that clenbuterol ameliorates EDPVR, apoptosis, and calcium homeostasis but does not have synergy with metoprolol in our model of ischemic HF.Clenbuterol is a ␤ 2 -adrenergic receptor agonist first used in the mid-1970s to treat asthma and is approved for this indication in Europe (Salorinne et al., 1975). The drug bears structural similarity to albuterol but has enhanced oral absorption and ␤ 2 -selectivity. Clenbuterol also increases muscle bulk (Choo et al., 1992;Maltin et al., 1993;Carter and Lynch, 1994) because of an anabolic effect that may be mediated via long-term ␤ 2 -activation (MacLennan and Edwards, 1989;Choo et al., 1992). Because of this anabolic action, oral clenbuterol has been abused by athletes to enhance size and strength (Beckett, 1992;Perry, 1993). Article, publication date, and citation information can be found at http://jpet.aspetjournals.org.