Pulmonary hypertension secondary to valvular heart disease: a state-of-the-art review.

Pulmonary hypertension (PH) is a common disease affecting up to 1% of the population and at least 50% of patients diagnosed with heart failure (HF) (Hoeper et al. in Lancet Respir Med 4(4):306-322, 2016). It is estimated that PH is present in 15% to 60% of patients with valvular heart disease (VHD) which can result from an increase in pulmonary blood flow and subsequently in pulmonary venous congestion and pulmonary vascular resistance (PVR). It is important to identify the severity of PH in patients with VHD to appropriately risk stratify and manage these patients (Magne et al. in JACC Cardiovasc Imaging 8(1):83-99, 2015). In this review, we examine the diagnostic criteria for PH and its pathophysiology. We also focus on the growing evidence supporting the presence of PH secondary to VHD and describe the contemporary surgical and medical therapeutic interventions in this patient population (Fig. 1).

Outpatient Endovascular Tibial Artery Intervention in an Office-Based Setting Is as Safe and Effective as in a Hospital Setting.

PURPOSE: To compare outcomes of outpatient tibial artery procedures between an office endovascular center and a hospital angiography suite. METHODS: A retrospective review was conducted of 204 outpatient tibial interventions performed on 161 patients (mean age 72±11.5 years; 81 men) in either an office (n=100) or hospital (n=104) angiography suite from April 2011 through September 2013. Patients who had an existing ipsilateral bypass that was completely proximal to the tibial trifurcation were eligible, as were patients with prior proximal endovascular interventions. Exclusion criteria included previous ipsilateral bypass involving the infrapopliteal vessels, in-patient status at the time of the procedure, planned admission after the procedure, and infrapopliteal stenting. Treatment included percutaneous transluminal angioplasty (PTA) or PTA with atherectomy. Primary outcomes were unplanned admission, emergency room visits, acute complications, and patency. RESULTS: There were no significant differences in demographics or baseline Rutherford category between patients treated in an office endovascular suite vs a hospital angiography suite. Factors more prevalent in the hospital group included chronic obstructive pulmonary disease (16% vs 8%, p=0.045), renal insufficiency (37% vs 25%, p=0.017), and previous proximal bypass (12% vs 4%, p=0.045). Of the 100 office procedures, 25 involved PTA and 75 were PTA with atherectomy, while in the 104 hospital procedures, PTA was applied in 68 patients and PTA with atherectomy in 36. Thirty-day local complication rates (7% vs 11%, p=0.368), systemic complication rates (4% vs 8%, p=0.263), and mortality (1% vs 2%, p=0.596) in the office vs hospital setting were not statistically different. Unplanned postprocedure hospital admission rates for medical reasons were lower in the office group (2% vs 11%, p=0.01). Kaplan-Meier estimates of the 1-year follow-up data were better in the office group for primary patency (69% vs 53%, p=0.050), assisted primary patency (90% vs 89%, p=0.646), and amputation-free survival (89% vs 83%, p=0.476), but the differences were not statistically significant. CONCLUSION: Efficacy and safety of outpatient endovascular tibial artery interventions between office and hospital settings were similar, with lower unplanned admission rates and better patency. With appropriate patient selection, the office endovascular suite can be a safe alternative to the hospital angiography suite.

Is It Time for Noncontinuous Therapy for Gastroesophageal Reflux Disease?

Gastroesophageal reflux disease (GERD) is a chronic disorder characterized by the reflux of gastric contents into the esophagus, leading to symptoms and potential long-term complications such as Barrett esophagus and esophageal adenocarcinoma. Currently, there are various medical, endoscopic, and surgical therapeutic strategies for GERD. However, proton pump inhibitors (PPIs), which effectively suppress acid secretion but require daily administration, remain the mainstay of treatment. Noncontinuous therapy for GERD includes on-demand and different variations of intermittent administration of antireflux medication. Attributes that make an antireflux medication a good candidate for noncontinuous therapy for GERD include potent acid suppression, rapid effect, durability of antisecretory effect, and flexibility of administration. Noncontinuous therapy for GERD is appealing to patients because it is convenient, reduces cost, and alleviates concerns about complications of long-term PPI use. Patients with nonerosive esophageal reflux disease or low-grade erosive esophagitis who have episodic heartburn are probably best suited for such treatment. Although PPIs have been shown to be efficacious as on-demand or intermittent therapy for GERD, their usefulness as on-demand treatment for episodic heartburn has been limited by their slow maximal effect on intragastric acid secretion. In contrast, potassium-competitive acid blockers (P-CABs) demonstrate the pharmacokinetic and pharmacodynamic characteristics that make this class of drugs a good candidate for noncontinuous treatment of GERD. Early studies using P-CABs for noncontinuous treatment of GERD have demonstrated promising results. Future studies are needed to further establish the value of P-CABs for such a therapeutic approach. This article reviews the current evidence on the use of PPIs and P-CABs in noncontinuous therapy for GERD.

Role of microbial dysbiosis in the pathogenesis of esophageal mucosal disease: A paradigm shift from acid to bacteria?

Genomic sequencing, bioinformatics, and initial speciation (e.g., relative abundance) of the commensal microbiome have revolutionized the way we think about the "human" body in health and disease. The interactions between the gut bacteria and the immune system of the host play a key role in the pathogenesis of gastrointestinal diseases, including those impacting the esophagus. Although relatively stable, there are a number of factors that may disrupt the delicate balance between the luminal esophageal microbiome (EM) and the host. These changes are thought to be a product of age, diet, antibiotic and other medication use, oral hygiene, smoking, and/or expression of antibiotic products (bacteriocins) by other flora. These effects may lead to persistent dysbiosis which in turn increases the risk of local inflammation, systemic inflammation, and ultimately disease progression. Research has suggested that the etiology of gastroesophageal reflux disease-related esophagitis includes a cytokine-mediated inflammatory component and is, therefore, not merely the result of esophageal mucosal exposure to corrosives (i.e., acid). Emerging evidence also suggests that the EM plays a major role in the pathogenesis of disease by inciting an immunogenic response which ultimately propagates the inflammatory cascade. Here, we discuss the potential role for manipulating the EM as a therapeutic option for treating the root cause of various esophageal disease rather than just providing symptomatic relief (i.e., acid suppression).