Adenocarcinoma of the distal esophagus and esophagogastric junction continues to rise in incidence. An intestinal metaplasia (Barrett esophagus)-dysplasia-carcinoma sequence induced by gastroesophageal reflux disease is well established. However, a significant number of adenocarcinomas in the vicinity of the esophagogastric junction are seen in the background of gastric/cardiac-type mucosa without intestinal metaplasia. Thus, the aim of this study was to investigate the role of Barrett esophagus (intestinal-type mucosa) in the classification and prognosis of tumors of the distal esophagus and esophagogastric junction. Clinicopathological and molecular characteristics were examined in 157 consecutively resected adenocarcinomas of the distal esophagus and esophagogastric junction and were compared between tumors arising in association with intestinal-type and cardiac-type mucosa. Intestinal-type mucosa-associated adenocarcinomas were more likely to be associated with younger age (P ¼ 0.0057), reflux symptoms (Po0.0001), proximal location (P ¼ 0.0009), lower T stage (Po0.0001), fewer nodal metastases (P ¼ 0.0001), absence of lymphatic (Po0.0001), venous (P ¼ 0.0060) or perineural (Po0.0001) invasion. Histologically, intestinal-type mucosa-associated tumors were more likely to be low-grade glandular tumors (P ¼ 0.0095) of intestinal or mixed immunophenotype (P ¼ 0.015) and express nuclear b-catenin (P ¼ 0.0080), whereas tumors arising in a background of cardiac-type mucosa were more frequently associated with EGFR amplification (P ¼ 0.0051). Five-year overall survival rate was significantly higher in patients with intestinal-type mucosa-associated tumors (28 vs 9%, P ¼ 0.0015), although no survival benefit was seen after adjusting for potential confounders. Our findings support the theory that multiple distinct pathways of tumorigenesis exist in the vicinity of the esophagogastric junction, including one in which tumors arise from dysplastic intestinal metaplasia (intestinal pathway), and one potentially involving dysplasia of the cardiac-type mucosa (non-intestinal pathway). Additional studies are warranted to further clarify their pathogenesis and the molecular mechanisms involved.

Ischemic heart disease (IHD) affects about 16 million adults in the USA. Many more individuals likely harbor subclinical coronary disease. Hypertension (HTN) continues to be a potent and widespread risk factor for IHD. Among other Framingham risk factors of tobacco use, diabetes mellitus, dyslipidemia, and left ventricular hypertrophy, HTN plays an independent role in augmenting IHD risk, as well as a multiplicative role with respect to adverse outcomes when HTN is present concurrently with the other major IHD risk factors listed above. Over the past two decades, numerous studies and guideline reports have been presented with the aims of (a) elucidating the pathophysiology of IHD, (b) delineating an ideal blood pressure (BP) threshold at which to institute pharmacotherapy, and (c) defining the optimal pharmacologic elements of a therapeutic regimen. While there are active debates surrounding the existence and relevance of the J curve in IHD patients who have HTN, as well as the numerical level of the BP cutoff justifying drug therapy in the general population, there is a general consensus that the BP target in IHD patients should be lower than 140/90 mmHg. The most appropriate class (or classes) of medication recommended will depend on the comorbid conditions associated with each individual patient. Overall, however, there is no major evidence underscoring a significant difference between drug classes, provided the target BP is achieved, although it should be pointed out that the most recent (2015) American Heart Association (AHA)/American College of Cardiology (ACC)/American Society of Hypertension (ASH) guideline statement now elevates beta-blockers (BB) to the same level of recommendation as other classes of hypertension drugs in the treatment of patients who have hypertension and ischemic heart disease. Although most agents that reduce blood pressure will correspondingly lower myocardial workload, BB may exhibit a special advantage in IHD patients because BB (as well as verapamil and diltiazem subclasses of calcium channel blockers or CCB) act to lower HR as well as cardiac inotropy. Moreover, BB will remain an integral if not indispensable part of the management of IHD, especially in those with history of angina pectoris or MI, based on decades of favorable clinical as well as trial experience. This extensive salutary historical background has served as a foundation for the 2015 committee's decision to bring BB into the front rank of BP agents for those hypertensive individuals suffering simultaneously from IHD.

Background: Prior cardiac magnetic resonance (CMR) studies have reported abnormal T1 mapping, reflective of diffuse myocardial fibrosis, in patients with mitral valve prolapse (MVP) and ventricular arrhythmias. However, T1 mapping was derived from conventional Look-Locker sequences and/or obtained in selected MVP patients with severe mitral regurgitation (MR) and a clinical indication for CMR. Hypothesis: We hypothesize that extracellular volume (ECV) fraction, a marker of diffuse fibrosis derived from research-based, MOLLI T1 mapping sequences, is increased in MVP subjects with ventricular arrhythmias, even in the absence of significant MR. Methods: We performed CMRs in 10 consecutive, randomly selected MVP patients identified through our echocardiographic database, age/gender matched to 10 controls free of significant cardiac disease. All 10 MVPs underwent ambulatory EKG monitoring. CMR images were acquired using a GE 3.0T Discovery MR750w scanner. Global ECV fraction was calculated using pre- and 10 minutes post-contrast T1 times after administration of 0.1 mmol/kg of gadobutrol (Gadavist). Late gadolinium enhancement (LGE) was also obtained. MR fraction was quantified by velocity encoded CMR. Mild MR was defined as MR fraction < 16%. Results: MVP patients had significantly higher ECV fraction compared to controls (mean ECV (%) 32 ± 4 vs 20 ± 6, p = 0.0002), with 5/10 demonstrating non-sustained VT on ambulatory EKG monitoring. The majority (9/10 or 90%) of MVPs had mild or no MR (MR fraction < 16%), and 1/10 or 10% had moderate MR (MR fraction 18%). Only one individual in the MVP group had late gadolinium enhancement (LGE) in the papillary muscles. Conclusion: MVP with ventricular arrhythmias is associated with increased global ECV reflective of diffuse myocardial fibrosis, even in the absence of significant MR or LGE. Our preliminary findings highlight for the first time a primary interstitial derangement in MVP. Larger studies are needed to understand the mechanisms and prognostic significance of primary diffuse fibrosis in MVP.

Paravalvular aortic regurgitation affects some patients after surgically implanted prosthesis. The number of patients affected is likely to increase with increased utilization of nonsurgical valve replacement techniques. These patients are at increased risk of persistent clinical symptoms often requiring repair. Clinical and procedural outcomes are of importance when performing these procedures and managing these patients. We describe a case where two different leaks around an aortic prosthesis improved with closure of one defect.