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P Rangachari,1 KC Dellsperger,2 RK Rethemeyer31Department of Interdisciplinary Health Sciences, College of Allied Health Sciences, Augusta University, Augusta, GA 30912, USA; 2Cardiovascular Division, AU Health, Department of Medicine, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA; 3Rockefeller College of Public Affairs and Policy, University at Albany, Albany, NY 12222, USABackground: In fall 2016, a 2-year grant was secured to pilot a Social Knowledge Networking (SKN) system pertaining to Electronic Health Record (EHR) Medication Reconciliation (MedRec), to enable Augusta University Health System to progress from “limited use” of EHR MedRec technology, to “meaningful use” (MU). A total of 50 “SKN users” (practitioners), participated in discussing practice issues related to EHR MedRec, over a 1-year period. These discussions were moderated by five “SKN moderators” (senior administrators). The pilot study, completed in fall 2018, found that inter-professional knowledge exchanges on the SKN, enabled several collective learning (“aha”) moments to emerge. These learning dynamics in turn, were associated with distinct improvement trends in two measures of MU of EHR MedRec technology, identified for the study. A key takeaway was that an SKN could be a valuable tool in enabling MU of EHR MedRec technology.Purpose: The study’s key findings related to the content and dynamics of inter-professional knowledge exchange on the SKN system, and their association with trends in measures of MU of EHR MedRec technology, have been described in a separate publication. This paper seeks to describe the structure of inter-professional knowledge exchange (or the pattern of connections) related to EHR MedRec, over the 1-year SKN period.Methods: Social network analysis (SNA) techniques were used to describe the structure of inter-professional knowledge exchange on the SKN system.Results: Results revealed that three of the five SKN moderators played a strong “collective brokerage” role in facilitating inter-professional knowledge exchange related to EHR MedRec, to enable learning and practice change. Together, they played complementary roles in reinforcing best-practice assertions, providing IT system education, and synthesizing collective learning moments, to enable “champions for change” to emerge from among SKN users.Conclusion: Results provide insight into the structure of effective knowledge-sharing networks for enabling inter-professional learning and practice change in health care organizations.Keywords: inter-professional learning, social network analysis, electronic health records, medication reconciliation, meaningful use, change implementation

Pavani Rangachari,1 Kevin C Dellsperger,2 R Karl Rethemeyer31Department of Interdisciplinary Health Sciences, College of Allied Health Sciences, Augusta University, Augusta, GA 30912, USA; 2Cardiovascular Division, AU Health, Department of Medicine, Medical College of Georgia, Augusta University, Augusta, GA, 30912, USA; 3Rockefeller College of Public Affairs and Policy, University at Albany, State University of New York, Albany, NY, 12222, USABackground: Similar to issues faced in health systems across the USA, AU Health faced a scenario of low physician engagement in and limited use of its Electronic Health Record (EHR) Medication Reconciliation (MedRec) technology, which translated to high rates of medication discrepancies and low accuracy of the patient’s active medication list, during transitions of care. In fall 2016, a 2-year research grant was secured to pilot a Social Knowledge Networking (SKN) system on “EHR MedRec” to enable AU Health to progress from “limited use” of EHR MedRec technology to “meaningful use.”Purpose: The aims of this study were to 1) examine dynamics of interprofessional knowledge exchange and learning related to EHR MedRec on the SKN system and 2) explore associations between “SKN Use” and “Meaningful Use (MU) of EHR MedRec,” with the latter being assessed in terms of adherence to best practices in EHR MedRec.Methods: Over a 1-year period, 50 SKN Users (practitioners from inpatient and outpatient medicine settings), participated in discussing issues related to EHR MedRec, moderated by five SKN Moderators (senior administrators). Qualitative analysis was used to understand dynamics of interprofessional knowledge exchange and descriptive analysis was used to examine trends in two measures of MU of EHR MedRec, identified for the study.Results: Interprofessional knowledge exchanges related to EHR MedRec on the SKN system, progressed from “problem statements” to “problem-solving statements” to “IT system education” to “best-practice assertions” to “culture change assertions” to “collective learning (aha) moments” to lay a foundation for practice change. These interprofessional learning dynamics were associated with distinct improvement trends in both measures of MU of EHR MedRec technology.Conclusion: Results suggest that an SKN system could be a valuable tool in enabling MU of EHR MedRec technology. The study helps identify strategies for the creation of “learning health systems,” to enable successful change implementation in healthcare organizations.Keywords: interprofessional learning, qualitative analysis, electronic health records, medication reconciliation, meaningful use, change implementation

Acute left ventricular (LV) dysfunction is common in the critical care setting and more frequently affects the elderly and patients with comorbidities. Because of increased mortality and the potential for significant improvement with early revascularization, the practitioner must first consider acute coronary syndrome. However, variants of stress (takotsubo) cardiomyopathy may be more prevalent in ICU settings than previously recognized. Early diagnosis is important to direct treatment of complications of stress cardiomyopathy, such as dynamic LV outflow tract obstruction, heart failure, and arrhythmias. Global LV dysfunction occurs in the critically ill because of the cardio-depressant effect of inflammatory mediators and endotoxins in septic shock as well as direct catecholamine toxicity. Tachycardia, hypertension, and severe metabolic abnormalities can independently cause global LV dysfunction, which typically improves with addressing the precipitating factor. Routine troponin testing may help early detection of cardiac injury and biomarkers could have prognostic value independent of prior cardiac disease. Echocardiography is ideally suited to quantify LV dysfunction and determine its most likely cause. LV dysfunction suggests a worse prognosis, but with appropriate therapy outcomes can be optimized. [ABSTRACT FROM AUTHOR]

Objectives: Tracheostomy-related pressure injuries (TRPI) have been demonstrated to occur in approximately 10% of tracheostomy patients. In this study, we present TRPI outcomes after implementation of a standardized tracheostomy care protocol., Methods: A tracheostomy care protocol was developed by an interdisciplinary quality improvement program and implemented on July 1, 2016. The protocol was designed to minimize factors that contribute to the development of TRPI. Rates of TRPI over the subsequent 20 months were compared to the year before implementation., Results: 9 out of 85 patients (10.6%) developed TRPI in the pre-protocol cohort compared to 0 of 137 (0%) in the post-protocol cohort, which was a statistically significant decrease by Fisher's exact test with a p-value of 0.0001. Pearson's correlation coefficient demonstrated a negative correlation between age and post-operative day of diagnosis (r = -0.641, p = 0.063), indicating that older patients develop TRPI more quickly., Conclusions: Interdisciplinary peri-operative tracheostomy care protocols can be effective in decreasing rates of TRPI., Competing Interests: Declaration of competing interest None., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Background: Nonactionable alarms comprise over 70% of alarms and contribute a threat to patient safety. Few studies have reported approaches to translate and sustain these interventions in clinical settings., Purpose: This study tested whether an interprofessional team-based approach can translate and implement effective alarm reduction interventions in the adult intensive care unit., Methods: The study was a prospective, cohort, pre- and postdesign with repeated measures at baseline (preintervention) and post-phase I and II intervention periods. The settings for the most prevalent nonactionable arrhythmia and bedside parameter alarms were adjusted during phases I and II, respectively., Results: The number of total alarms was reduced by 40% over a 14-day period after both intervention phases were implemented. The most prevalent nonactionable parameter alarms decreased by 47% and arrhythmia alarms decreased by 46%., Conclusions: It is feasible to translate and sustain system-level alarm management interventions addressing alarm fatigue using an interprofessional team-based approach.

In fall 2016, a two-year grant was secured from AHRQ, to pilot a mobile Social Knowledge Networking (SKN) system on Electronic Health Record (EHR) Medication Reconciliation (MedRec), to enable Augusta University (AU) Health System, to progress from "limited-use" of EHR-MedRec technology, to "meaningful-use." The rationale is that an SKN system would enable knowledge exchange on practice issues related to EHR-MedRec, across diverse provider subgroups and settings-of-care, which, in turn, is expected to increase provider engagement, promote inter-professional learning of best-practices, and provide a foundation for practice change (e.g., Meaningful Use of EHR-MedRec technology). Over a one-year period, 50 SKN Users (physicians, nurses, and pharmacists from outpatient-and-inpatient-medicine services), participated in discussing issues-related-to-EHR-MedRec, moderated by 5 SKN Moderators (senior administrators). This paper describes the health system's experiences with this pilot initiative; and discusses lessons learned, in regard to the potential of a mobile SKN system to enable Meaningful Use of EHR-MedRec technology., (©2019 AMIA - All rights reserved.)

Similar to issues faced in health systems across USA, AU Health, based in Augusta, Georgia, faced a scenario of low physician engagement in, and limited-use of its Electronic Health Record (EHR) Medication Reconciliation (MedRec) technology, which translated to high rates of medication discrepancies and low accuracy of the patient's active medication list, during transitions of care. In fall 2016, a two-year grant was secured from the U.S. Agency for Healthcare Research and Quality (AHRQ), to pilot a Social Knowledge Networking (SKN) system pertaining to "EHR-MedRec," to enable AU Health to progress from "limited use" of EHR MedRec technology, to "meaningful use." The rationale behind an SKN system, is that it could provide a platform for inter-professional knowledge exchange on practice issues related to EHR MedRec, across diverse provider subgroups and care settings, to highlight adverse consequences of gaps in practice for patient safety, and emphasize the value of adhering to best-practices in EHR MedRec. This, in turn, is expected to increase provider engagement in addressing issues related to EHR MedRec, and promote inter-professional learning of best-practices, to create a foundation for practice change or improvement (e.g., Meaningful Use of EHR MedRec technology). This Case Report describes AU Health's experiences with this novel initiative to pilot an SKN system for enabling Meaningful Use of EHR MedRec technology. It also discusses lessons learned in regard to the potential of an SKN system to enable inter-professional learning and practice improvement in the context of EHR MedRec, which, in turn, helps identify strategies and practice implications for healthcare managers., Competing Interests: Conflicts of Interest: None to declare.

Background: In an effort to reduce medication discrepancies during transitions of care and improve accuracy of the patient's medication list, AU Health conducted a study to identify a comprehensive set of issues related to electronic health record (EHR) medication reconciliation (MedRec) from the perspective of practitioners directly involved in the EHR MedRec process., Methods: An exploratory mixed-method design was used. The 2-round study included 15 individual interviews, followed by a survey of 200 practitioners (ie, physicians, nurses, and pharmacists) based in the outpatient and inpatient medicine service at AU Health., Results: Thematic analysis of interview data identified 55 issue items related to EHR MedRec under 9 issue categories. The survey sought practitioners' importance rating of all issue items identified from interviews. A total of 127 (63%) survey responses were received. Factor analysis served to validate the following 6 of the 9 issue categories, all of which were rated "important" or higher (on average), by over 70% of all respondents: (1) care coordination (CCI); (2) patient education (PEI); (3) ownership and accountability (OAI); (4) processes-of-care (PCI); (5) IT-related (ITRI); and (6) workforce training (WTI). Significance testing of importance rating by professional affiliation revealed no statistically significant differences for CCI and PEI, and some statistically significant differences for OAI, PCI, ITRI, and WTI., Conclusion: There were 2 key gleanings from the issues related to EHR MedRec unearthed by this study: (1) there was an absence of shared understanding among practitioners, of the value of EHR MedRec in promoting patient safety, which contributed to workarounds, and suboptimal use of the EHR MedRec system; and (2) there was a sociotechnical dimension to many of the issues, creating an added layer of complexity. These gleanings, in turn, provide insights into best practices for managing both (1) clinical transitions of care in the EHR MedRec process and (2) sociotechnical challenges encountered in EHR MedRec implementation.

Background: In fall 2016, Augusta University received a two-year grant from AHRQ, to implement a Social Knowledge Networking (SKN) system for enabling its health system, AU-Health, to progress from "limited use" of EHR Medication Reconciliation (MedRec) Technology, to "meaningful use." Phase 1 sought to identify a comprehensive set of issues related to EHR MedRec encountered by practitioners at AU-Health. These efforts helped develop a Reporting Tool , which, along with a Discussion Tool , was incorporated into the AU-Health EHR, at the end of Phase 1. Phase 2 (currently underway), comprises a 52-week pilot of the EHR-integrated SKN system in outpatient and inpatient medicine units. The purpose of this paper is to describe the methods and results of Phase 1., Methods: Phase 1 utilized an exploratory mixed-method approach, involving two rounds of data collection. This included 15 individual interviews followed by a survey of 200 practitioners, i.e., physicians, nurses, and pharmacists, based in the outpatient and inpatient medicine service at AU Health., Results: Thematic analysis of interviews identified 55 issue-items related to EHR MedRec under 9 issue-categories. The survey sought practitioners' importance-rating of all issue-items identified from interviews. A total of 127 (63%) survey responses were received. Factor analysis served to validate the following 6 of the 9 issue-categories, all of which, were rated "Important" or higher (on average), by over 70% of all respondents: 1) Care-Coordination (CCI); 2) Patient-Education (PEI); 3) Ownership-and-Accountability (OAI); 4) Processes-of-Care (PCI); 5) IT-Related (ITRI); and 6) Workforce-Training (WTI). Significance-testing of importance-rating by professional affiliation revealed no statistically significant differences for CCI and PEI; and some statistically significant differences for OAI, PCI, ITRI, and WTI., Conclusion: There were two key gleanings from the issues related to EHR MedRec unearthed by this study: 1) there was an absence of shared understanding among practitioners, of the value of EHR MedRec in promoting patient safety, which contributed to workarounds, and suboptimal use of the EHR MedRec system; and 2) there was a socio-technical dimension to many of the issues, creating an added layer of complexity. These gleanings in turn, provide insights into best practices for managing both clinical transitions-of-care in the EHR MedRec process; and socio-technical challenges encountered in EHR MedRec implementation.

Background: Diagnosis of constrictive pericarditis (CP) can be challenging. It can be nearly impossible to distinguish CP from other causes of right heart failure. Although various imaging modalities help in the diagnosis, no test is definitive. Several reviews have addressed the role of various imaging techniques in the diagnosis of CP but a systematic review has not yet been published., Objective: Our intention was to study the ability of various non-invasive imaging modalities to diagnose CP in patients with surgically confirmed disease and to apply our findings to develop a clinically useful diagnostic algorithm., Methods: A PubMed (NLM) search was performed with MeSH term "constrictive pericarditis". Original articles that investigated the ability of various cardiovascular imaging modalities to noninvasively diagnose surgically confirmed CP were included in our review. Investigations that included any cases without surgical confirmation were excluded., Results: The PubMed search yielded 3001 results with MeSH term "constrictive pericarditis" (January 8, 2016). We identified (40) studies on CP that matched our inclusion criteria. We summarized our results sorted by individual non-invasive CV imaging modalities - echocardiography, cardiac computed tomography (CT), and magnetic resonance imaging (MRI). Under each imaging modality, we grouped our discussion based on different parameters useful in CP diagnosis., Conclusions: In conclusion, contemporary diagnosis of CP is based on clinical features and echocardiography. Cardiac MRI is recommended in patients where echocardiography is not diagnostic. Both cardiac MRI and CT can guide surgical planning but we prefer MRI as it provides both structural and functional information., (Copyright © 2016. Published by Elsevier B.V.)

Objective: Short-term exercise training improves glycemic control, but the effect of short-term training on postprandial satiety peptide responses or perceived satiety remains unknown. We tested the hypothesis that short-term aerobic exercise training (15 days) would alter postprandial pancreatic and gut peptide (pancreatic polypeptide (PP) and peptide YY (PYY)) responses and perceived appetite and satiety in obese individuals., Subjects: Thirteen healthy obese men and women (age: 42±2 years; body mass index: 30-45 kg m(-2))., Measurements: Subjects were studied before and after 15 days of training (walking 1 h at 70-75% VO(2peak)). On the study day, subjects consumed 1500 kcal as six meals (250 kcal: 9 g protein, 40 g carbohydrate, 6 g fat), while blood samples and satiety measurements were taken at baseline and every 20 min for 12 h. Blood was analyzed for PP, PYY, glucose and insulin levels. Appetite and satiety was assessed with a visual analog scale throughout the day., Results: Incremental area under the curve (iAUC) for PP increased significantly with training (pre: 2788±753; post: 3845±830 pg ml(-1)·per min for 12 h; P<0.001), but there was no difference in the PP response to each meal. The initial PP response to the first meal increased (ΔPP(min 20-0): pre 86±25; post 140±36 pg ml(-1); P<0.05) with training. PYY iAUC showed no significant changes with training but showed a significant main effect of time across meals, with the largest response being to the first meal (P<0.005). There were no changes in satiety, glucose or insulin levels with training., Conclusion: Short-term exercise training increases postprandial PP concentrations in obese individuals; however, PYY levels and glycemic control remain unaffected. Both PP and PYY show meal-induced increases at all meals, but PYY has a greater response at the first meal with reduced responses at subsequent meals.

We recently reported that mitochondrial dysfunction, characterized by increased mitochondrial permeability transition (MPT), was present in a translational swine model of heart failure with preserved ejection fraction (HFpEF). Cyclophilin D is a key component of the MPT pore, therefore, the purpose of this study was to test the efficacy of a novel cyclosporine (CsA) dosing scheme as a therapeutic alternative for HFpEF. Computed tomography (CT), two-dimensional speckle tracking two-dimensional speckle tracking (2DST), and invasive hemodynamics were used to evaluate cardiac function. CT imaging showed 14 weeks of CsA treatment caused eccentric myocardial remodeling (contrasting concentric remodeling in untreated HF animals) and elevated systemic pressures. 2DST detected left ventricular (LV) mechanics associated with systolic and diastolic dysfunction prior to the onset of significantly increased LV end diastolic pressure including: (1) decreased systolic apical rotation rate, longitudinal displacement, and longitudinal/radial/circumferential strain; (2) decreased early diastolic untwisting and longitudinal strain rate; and (3) increased late diastolic radial/circumferential mitral strain rate. LV mechanics associated with systolic and diastolic impairment was enhanced to a greater extent than seen in untreated HF animals following CsA treatment. In conclusion, CsA treatment accelerated the development of heart failure, including dilatory LV remodeling and impaired systolic and diastolic mechanics. Although our findings do not support CsA as a viable therapy for HFpEF, 2DST was effective in differentiating between progressive gradations of developing HF and detecting diastolic impairment prior to the development of overt diastolic dysfunction.

In this review, we discuss the physiology, diagnosis and treatment of dyslipidemia in patients with chronic and end-stage renal disease. The recent important clinical trials in patients with chronic kidney disease and dyslipidemia are reviewed. Because of the lack of evidence in treating lipid abnormalities in this specific patient population, we propose that future studies should focus on the pathophysiological mechanisms and treatment of dyslipidemia in this special patient population.

Purpose: The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) help regulate postprandial triacylglycerol (TAG) and insulin concentrations, but the effects of acute aerobic exercise on GLP-1 or GIP responses are unclear. The purpose of this study was to determine whether reductions in postprandial TAG and insulin with exercise are associated with GLP-1 and GIP responses., Methods: Thirteen normal-weight (NW) and 13 obese (Ob) individuals participated in two, 4-d trials in random order including an exercise (EX) and a no exercise (NoEX) trial. Diet was controlled during both trials. The EX trial consisted of 1 h of treadmill walking (55%-60% of V˙O2peak) during the evening of day 3 of the trial, 12 h before a 4-h mixed meal test on day 4, during which frequent blood samples were collected to assess postprandial lipemia, glycemia, insulin, C-peptide, GIP, and GLP-1 responses. Insulin secretion was estimated using the insulinogenic index, and insulin clearance was estimated using the ratio of insulin to C-peptide., Results: Postprandial TAG were 29% lower after EX in Ob individuals (P < 0.05) but were not significantly altered in NW individuals (P > 0.05). The drop in postprandial HDL cholesterol was attenuated with EX in Ob individuals (P < 0.05). Insulin responses were 14% lower after EX in Ob individuals (P < 0.05), and this was associated with reduced insulin secretion (P < 0.05), with no change in insulin clearance (P > 0.05). Glucose, C-peptide, GIP, and GLP-1 were not different between trials., Conclusion: A 1-h bout of moderate-intensity aerobic exercise the night before a mixed meal attenuates TAG and insulin responses in Ob but not NW individuals, an effect not associated with altered GLP-1 or GIP responses.

Adiposity alters acylated ghrelin concentrations, but it is unknown whether adiposity alters the effect of exercise and feeding on acylated ghrelin responses. Therefore, the purpose of this study was to determine whether adiposity [normal-weight (NW) vs. obese (Ob)] influences the effect of exercise and feeding on acylated ghrelin, hunger, and fullness. Fourteen NW and 14 Ob individuals completed two trials in a randomized counterbalanced fashion, including a prior exercise trial (EX) and a no exercise trial (NoEX). During the EX trial, the participants performed 1 h of treadmill walking (55-60% peak O2 uptake) during the evening, 12 h before a 4-h standardized mixed meal test. Frequent blood samples were taken and analyzed for acylated ghrelin, and a visual analog scale was used to assess perceived hunger and fullness. In NW individuals, EX, compared with NoEX, reduced fasting acylated ghrelin concentrations by 18% (P = 0.03), and, in response to feeding, the change in acylated ghrelin (P = 0.02) was attenuated by 39%, but perceived hunger and fullness were unaltered. In Ob individuals, despite no changes in fasting or postprandial acylated ghrelin concentrations with EX, postprandial fullness was attenuated by 46% compared with NoEX (P = 0.05). In summary, exercise performed the night before a meal suppresses acylated ghrelin concentrations in NW individuals without altering perceived hunger or fullness. In Ob individuals, despite no changes in acylated ghrelin concentrations, EX reduced the fullness response to the test meal. Acylated ghrelin and perceived fullness responses are differently altered by acute aerobic exercise in NW and Ob individuals.

Objectives: This study sought to determine if simvastatin impairs exercise training adaptations., Background: Statins are commonly prescribed in combination with therapeutic lifestyle changes, including exercise, to reduce cardiovascular disease risk in patients with metabolic syndrome. Statin use has been linked to skeletal muscle myopathy and impaired mitochondrial function, but it is unclear whether statin use alters adaptations to exercise training., Methods: This study examined the effects of simvastatin on changes in cardiorespiratory fitness and skeletal muscle mitochondrial content in response to aerobic exercise training. Sedentary overweight or obese adults with at least 2 metabolic syndrome risk factors (defined according to National Cholesterol Education Panel Adult Treatment Panel III criteria) were randomized to 12 weeks of aerobic exercise training or to exercise in combination with simvastatin (40 mg/day). The primary outcomes were cardiorespiratory fitness and skeletal muscle (vastus lateralis) mitochondrial content (citrate synthase enzyme activity)., Results: Thirty-seven participants (exercise plus statins: n = 18; exercise only: n = 19) completed the study. Cardiorespiratory fitness increased by 10% (p < 0.05) in response to exercise training alone, but was blunted by the addition of simvastatin resulting in only a 1.5% increase (p < 0.005 for group by time interaction). Similarly, skeletal muscle citrate synthase activity increased by 13% in the exercise-only group (p < 0.05), but decreased by 4.5% in the simvastatin-plus-exercise group (p < 0.05 for group-by-time interaction)., Conclusions: Simvastatin attenuates increases in cardiorespiratory fitness and skeletal muscle mitochondrial content when combined with exercise training in overweight or obese patients at risk of the metabolic syndrome. (Exercise, Statins, and the Metabolic Syndrome; NCT01700530)., (Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Right atrial intracardiac tumours are uncommonly seen during echocardiography. Our patient presented with primary mediastinal large B-cell lymphoma with intracardiac involvement. The tumour was seen by echocardiography and the extent of the tumour was defined by CT scan of the chest. Following chemotherapy directed to her specific tumour cell type, there was complete resolution of the intracardiac mass.

Objective: The purpose of this study was to compare postprandial satiety regulating hormone responses (pancreatic polypeptide (PP) and peptide tyrosine tyrosine (PYY)) and visual analog scale- (VAS) assessed perceived appetite and satiety between liquid high-protein (HP) and high-carbohydrate (HC) meals in obese women during acute (24-h) caloric restriction., Design: Eleven obese premenopausal women completed two conditions in random order in which they consumed 1500 calories as six 250-calorie HP meals or six 250-calorie HC meals over a 12-h period. Blood samples were taken at baseline and every 20 min thereafter and analyzed for PP and PYY concentrations. At these same points, perceived hunger and fullness were assessed with a VAS. The incremental area under the curve (iAUC) was used to compare postprandial responses., Results: The 12-h PP and PYY iAUC were greater (P≤0.05) during the HP condition (PP: 4727±1306 pg/ml×12 h, PYY: 1373±357 pg/ml×12 h) compared with the HC condition (PP: 2300±528 pg/ml×12 h, PYY: 754±246 pg/ml×12 h). Perceived hunger and fullness were not different between conditions (P>0.05). The greatest changes in PYY and perceived fullness occurred after the morning meals during both conditions., Conclusions: These data suggest that in obese women during acute caloric restriction before weight loss, i) liquid HP meals, compared with HC meals, result in greater postprandial PP and PYY concentrations, an effect not associated with differential appetite or satiety responses, and ii) meal-induced changes in PYY and satiety are greatest during the morning period, regardless of dietary macronutrient composition.

Background: Studies assessing the timing of percutaneous coronary interventions (PCI) in patients with Non-ST segment elevation Acute Coronary Syndromes (NSTE-ACS) have failed to generate a consensus on how early PCI should be performed in such patients., Purpose: This meta-analysis compares clinical outcomes at 30 days in NSTE-ACS patients undergoing PCI within 24 hours of presentation (early PCI) with those receiving PCI more than 24 hours after presentation (delayed PCI)., Data Sources: Data were extracted from searches of MEDLINE (1990-2010) and Google scholar and from scrutiny of abstract booklets from major cardiology meetings (1990-2010)., Study Selection: Randomized clinical trials (RCTs) that included the composite endpoint of death and non-fatal myocardial infarction (MI) at 30 days after PCI were considered., Data Extraction: Two independent reviewers extracted data using standard forms. The effects of early and delayed PCI were analyzed by calculating pooled estimates for death, non-fatal MI, bleeding, repeat revascularization and the composite endpoint of death or non-fatal MI at 30 days. Univariate analysis of each of these variables was used to create odds ratios., Data Synthesis: Seven studies with a total of 13,762 patients met the inclusion criteria. There was no significant difference in the odds of the composite endpoint of death or non-fatal MI at 30 days between patients undergoing early PCI and those receiving delayed PCI (OR-0.83, 95%CI 0.62-1.10). Patients receiving delayed PCI experienced a 33% reduction in the odds of repeat revascularization at 30 days compared to those undergoing early PCI (OR-1.33, 95%CI 1.14-1.56, P=0.0004).Conversely, patients undergoing early PCI experienced lower odds of bleeding than those receiving delayed PCI (OR-0.76, 95%CI 0.63-0.91, P = 0.0003)., Conclusions: In NSTE-ACS patients early PCI doesn't reduce the odds of the composite endpoint of death or non-fatal MI at 30 day. This strategy is associated with lower odds of bleeding and higher odds of repeat revascularization at 30 days than a strategy of delayed PCI., (Copyright © 2012 Wiley Periodicals, Inc.)

Objective: The aim of this study was to compare postprandial lipemia, oxidative stress, antioxidant activity, and insulinemia between a three and six isocaloric high-carbohydrate meal frequency pattern in obese women., Design and Methods: In a counterbalanced order, eight obese women completed two, 12-h conditions in which they consumed 1,500 calories (14% protein, 21% fat, and 65% carbohydrate) either as three 500 calorie liquid meals every 4-h or six 250 calorie liquid meals every 2-h. Blood samples were taken every 30 min and analyzed for triacylglycerol (TAG), total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, oxidized low-density lipoprotein cholesterol, myeloperoxidase, paraoxonase-1 activity, and insulin., Results: The TAG incremental area under the curve (iAUC) during the three meal condition (321 ± 129 mg/dl · 12 h) was significantly lower (P = 0.04) compared with the six meal condition (481 ± 155 mg/dl · 12 h). The insulin iAUC during the three meal condition (5,549 ± 1,007 pmol/l · 12 h) was significantly higher (P = 0.05) compared with the six meal condition (4,230 ± 757 pmol/l(.) 12 h). Meal frequency had no influence on the other biochemical variables., Conclusions: Collectively, a three and six isocaloric high-carbohydrate meal frequency pattern differentially alters postprandial TAG and insulin concentrations but has no effect on postprandial cholesterol, oxidative stress, or antioxidant activity in obese women., (Copyright © 2012 The Obesity Society.)

We have previously reported chronic low-intensity interval exercise training attenuates fibrosis, impaired cardiac mitochondrial function, and coronary vascular dysfunction in miniature swine with left ventricular (LV) hypertrophy (Emter CA, Baines CP. Am J Physiol Heart Circ Physiol 299: H1348-H1356, 2010; Emter CA, et al. Am J Physiol Heart Circ Physiol 301: H1687-H1694, 2011). The purpose of this study was to test two hypotheses: 1) chronic low-intensity interval training preserves normal myocardial oxygen supply/demand balance; and 2) training-dependent attenuation of LV fibrotic remodeling improves diastolic function in aortic-banded sedentary, exercise-trained (HF-TR), and control sedentary male Yucatan miniature swine displaying symptoms of heart failure with preserved ejection fraction. Pressure-volume loops, coronary blood flow, and two-dimensional speckle tracking ultrasound were utilized in vivo under conditions of increasing peripheral mean arterial pressure and β-adrenergic stimulation 6 mo postsurgery to evaluate cardiac function. Normal diastolic function in HF-TR animals was characterized by prevention of increased time constant of isovolumic relaxation, normal LV untwisting rate, and enhanced apical circumferential and radial strain rate. Reduced fibrosis, normal matrix metalloproteinase-2 and tissue inhibitors of metalloproteinase-4 mRNA expression, and increased collagen III isoform mRNA levels (P < 0.05) accompanied improved diastolic function following chronic training. Exercise-dependent improvements in coronary blood flow for a given myocardial oxygen consumption (P < 0.05) and cardiac efficiency (stroke work to myocardial oxygen consumption, P < 0.05) were associated with preserved contractile reserve. LV hypertrophy in HF-TR animals was associated with increased activation of Akt and preservation of activated JNK/SAPK. In conclusion, chronic low-intensity interval exercise training attenuates diastolic impairment by promoting compliant extracellular matrix fibrotic components and preserving extracellular matrix regulatory mechanisms, preserves myocardial oxygen balance, and promotes a physiological molecular hypertrophic signaling phenotype in a large animal model resembling heart failure with preserved ejection fraction.

Adiponectin (APN) can confer protection against metabolism-related illnesses in organs such as fat, the liver, and skeletal muscle. However, it is unclear whether APN improves endothelial-dependent nitric oxide-mediated vasodilation in type 2 diabetes and, if so, by what mechanism. We tested whether exogenous APN delivery improves endothelial function in type 2 diabetic mice and explored the mechanisms underlying the observed improvement. To test the hypothesis, we injected adenovirus APN (Ad-APN) or adenovirus β-galactosidase (Ad-βgal; control virus) via the tail vein in control (m Lepr(db)) and diabetic (Lepr(db); db/db) mice and studied vascular function of the aorta ex vivo. Ad-APN improved endothelial-dependent vasodilation in db/db mice compared with Ad-βgal, whereas Ad-APN had no further improvement on endothelial function in control mice. This improvement was completely inhibited by a nitric oxide synthase inhibitor (N(G)-nitro-l-arginine methyl ester). Serum triglyceride and total cholesterol levels were increased in db/db mice, and Ad-APN significantly reduced triglyceride levels but not total cholesterol levels. Immunoblot results showed that interferon-γ, gp91(phox), and nitrotyrosine were markedly increased in the aorta of db/db mice. Ad-APN treatment decreased the expression of these proteins. In addition, mRNA expression of TNF-α, IL-6, and ICAM-1 was elevated in db/db mice, and Ad-APN treatment decreased these expressions in the aorta. Our findings suggest that APN may contribute to an increase in nitric oxide bioavailability by decreasing superoxide production as well as by inhibiting inflammation and adhesion molecules in the aorta in type 2 diabetic mice.

We discuss the current state of knowledge related to the pathogenesis of myocardial stunning as well as the potential mechanisms responsible for the clinical presentation of myocardial stunning in hemodialysis patients. We suggest future research areas for this critical and clinically important condition in this high-risk patient population. In consideration of acute and chronic changes secondary to dialysis, especially in patients with risk for coronary artery disease, the prevalence of myocardial stunning and its role in the natural history of these patients' disease progression is considered. We propose a paradigm: that the majority of the pathophysiologic mechanisms by which hemodialysis may induce myocardial stunning falls into two categories with (1) vascular and/or (2) metabolic contributions. In order to prevent eventual myocardial hibernation, myocardial remodeling, scarring, and loss of contractile function with aberrant electrical conductivity that could lead to sudden death, it is imperative to identify the risk factors associated with myocardial stunning during hemodialysis. Further understanding of these mechanisms may lead to novel clinical interventions and pharmacologic therapeutic agents.

Background/objectives: Moderate, long-term weight loss results in the loss of bone mass in overweight or obese premenopausal women. However, whether these changes persist during weight maintenance or regain remains to be determined., Subjects/methods: Overweight or obese (body mass index: 25.8-42.5 kg/m(2)) women (n=40) with at least two risk factors for the metabolic syndrome participated in this 12-month study that examined the effects of prescribed weight loss and regain, with or without exercise, on bone turnover and on bone mineral density (BMD) in a subset of participants (n=24). During the first 6 month, participants lost ≈ 10% of their initial body weight via energy restriction and supervised aerobic exercise. Following weight loss, participants were randomly assigned to either an exercise or a no exercise treatment for the regain (+50% of weight lost) phase. A one-way (time) repeated measures one-factor analysis of variance (RMANOVA) tested the effects of weight loss on BMD and bone turnover, and a two-way RMANOVA (time, exercise) was used to examine the effects of exercise during weight regain., Results: Hip (P=0.007) and lumbar spine (P=0.05) BMD decreased with weight loss, and remained reduced after weight regain with or without exercise. Likewise, the weight-loss-associated increases in osteocalcin (P<0.001) and C-terminal peptide of type I collagen (P<0.001) persisted following weight regain, independent of exercise., Conclusions: The results of the present study, which is the first to examine changes in bone mass and turnover during carefully controlled weight regain, suggest that weight-loss-induced perturbations in bone mass and turnover persist after partial weight regain, regardless of whether regular weight-bearing aerobic exercise was continued.

In their broad spectrum, cardiovascular diseases are, collectively, the major cause of death in patients on dialysis. The population of patients treated with peritoneal dialysis and hemodialysis are not only subject to the traditional risk factors for heart disease, but also to certain uremia-associated risk factors that are unique in this population. In the dialysis population, data regarding the effectiveness of routine pharmacologic and procedural interventions on cardiovascular outcomes are limited. Most dialysis patients are excluded from clinical trials, and so data from randomized controlled trials investigating outcomes in patients undergoing peritoneal dialysis or hemodialysis are almost absent. In this review, we discuss some of the major cardiovascular problems in the dialysis population, the impact of those problems on survival, and when data are available, the impact of therapeutic strategies.

Despite abundant clinical evidence linking metabolic abnormalities to diabetic vasculopathy, the molecular basis of individual susceptibility to diabetic vascular complications is still largely undetermined. Endothelial dysfunction in diabetes-associated vascular complications is considered an early stage of vasculopathy and has attracted considerable research interests. Type 2 diabetes is characterized by metabolic abnormalities, such as hyperglycemia, excess liberation of free fatty acids (FFA), insulin resistance and hyperinsulinemia. These abnormalities exert pathological impact on endothelial function by attenuating endothelium-mediated vasomotor function, enhancing endothelial apoptosis, stimulating endothelium activation/endothelium-monocyte adhesion, promoting an atherogenic response and suppressing barrier function. There are multiple signaling pathways contributing to the adverse effects of glucotoxicity on endothelial function. Insulin maintains the normal balance for release of several factors with vasoactive properties. Abnormal insulin signaling in the endothelium does not affect the whole-body glucose metabolism, but impairs endothelial response to insulin and accelerates atherosclerosis. Excessive level of FFA is implicated in the pathogenesis of insulin resistance. FFA induces endothelial oxidative stress, apoptosis and inflammatory response, and inhibits insulin signaling. Although hyperglycemia, insulin resistance, hyperinsulinemia and dyslipidemia independently contribute to endothelial dysfunction via various distinct mechanisms, the mutual interactions may synergistically accelerate their adverse effects. Oxidative stress and inflammation are predicted to be among the first alterations which may trigger other downstream mediators in diabetes associated with endothelial dysfunction. These mechanisms may provide insights into potential therapeutic targets that can delay or reverse diabetic vasculopathy.

Type 2 diabetes (T2D) is a leading risk factor for a variety of cardiovascular diseases including coronary heart disease and atherosclerosis. Exercise training (ET) has a beneficial effect on these disorders, but the basis for this effect is not fully understood. This study was designed to investigate whether the ET abates endothelial dysfunction in the aorta in T2D. Heterozygous controls (m Lepr(db)) and type 2 diabetic mice (db/db; Lepr(db)) were either exercise entrained by forced treadmill exercise or remained sedentary for 10 wk. Ex vivo functional assessment of aortic rings showed that ET restored acetylcholine-induced endothelial-dependent vasodilation of diabetic mice. Although the protein expression of endothelial nitric oxide synthase did not increase, ET reduced both IFN-γ and superoxide production by inhibiting gp91(phox) protein levels. In addition, ET increased the expression of adiponectin (APN) and the antioxidant enzyme, SOD-1. To investigate whether these beneficial effects of ET are APN dependent, we used adiponectin knockout (APNKO) mice. Indeed, impaired endothelial-dependent vasodilation occurred in APNKO mice, suggesting that APN plays a central role in prevention of endothelial dysfunction. APNKO mice also showed increased protein expression of IFN-γ, gp91(phox), and nitrotyrosine but protein expression of SOD-1 and -3 were comparable between wild-type and APNKO. These findings in the aorta imply that APN suppresses inflammation and oxidative stress in the aorta, but not SOD-1 and -3. Thus ET improves endothelial function in the aorta in T2D via both APN-dependent and independent pathways. This improvement is due to the effects of ET in inhibiting inflammation and oxidative stress (APN-dependent) as well as in improving antioxidant enzyme (APN-independent) performance in T2D.

Background: Doppler echocardiography using the ratio of early diastolic transmitral velocity to early diastolic mitral annular tissue velocity (E/E') is routinely used to evaluate left ventricular (LV) filling pressures at rest. We tested the hypothesis that measurement of E/E' in patients undergoing dobutamine stress echocardiography (DSE) will detect changes in LV filling pressures., Methods: In this prospective study, 16 patients with normal LV ejection fraction and normal coronary arteries by angiography underwent a standard DSE protocol with simultaneous LV filling pressure monitoring with a fluid filled pigtail catheter. Doppler echocardiographic assessment of LV diastolic function was performed using E/E' at rest and during DSE., Results: The average age of the study participants was 57 ± 8 years. Average heart rate was 61 ± 11 bpm at baseline and 141 ± 12 bpm at peak stress. LV mean diastolic pressure decreased from 12.3 ± 2.6 mmHg at baseline to 9.0 ± 2.3 mmHg at peak stress (P = 0.0001). Baseline E/E' at the septum and lateral annulus were 8.7 ± 2.2 and 7.5 ± 1.9 and during peak stress were 8.3 ± 3.1 and 7.9 ± 3.5, respectively. There was no significant change in E/E' at either the septum or the lateral annulus (P = 0.55, P = 0.66). There was no significant correlation between LV mean diastolic pressure and E/E' with dobutamine stress., Conclusions: In patients with normal LV ejection fraction and no significant coronary artery disease undergoing DSE, the ratio of early diastolic transmitral velocity to early diastolic tissue velocity (E/E') at peak stress with dobutamine does not predict changes in LV filling pressures., (© 2011, Wiley Periodicals, Inc.)

The term cardiorenal syndrome has evolved over the years. The understanding of the interactions between these two organ systems has led to better recognition and treatment strategies. As cardiovascular mortality is high in individuals with renal dysfunction, it is imperative to understand the pathophysiology behind the disease process. This knowledge may better serve these patients with this syndrome and improve their outcomes. In this review, we examine the key issues of the cardiorenal syndrome from a cardiologist's perspective., (© 2011 S. Karger AG, Basel.)

Our understanding of the cardiorenal syndrome continues to progress. Decades of research have led to a better definition of the clinical cardiorenal syndrome and have laid the groundwork for understanding its pathophysiology. Although improvements have been made, there are still knowledge gaps concerning the interactions of these two organ systems. In the present review, we examine those interactions in the setting of acute and chronic cardiac decompensation and the resulting impacts on renal dysfunction. Recognition and prevention of this syndrome may help to better serve a growing patient population.

Telmisartan, an angiotensin receptor blocker, may have unique benefits as it possesses partial peroxisome proliferator-activated receptor (PPAR)-γ agonist activity in addition to antihypertensive effects. In this study, we test whether treatment with telmisartan ameliorates cardiovascular abnormalities to a greater extent than olmesartan, which has little PPAR-γ activity. The hypertensive rodent model of tissue renin-angiotensin system activation, transgenic (mRen2)27 (Ren2) rats and their littermate Sprague-Dawley controls were used. Rats were treated with telmisartan (2 mg · kg(-1) · day(-1)), olmesartan (2.5 mg · kg(-1) · day(-1)), or vehicle via drinking water for 3 wk; these doses achieved similar blood pressure control, as measured by telemetry. Ren2 rats displayed impaired diastolic and systolic function using left ventricular (LV) pressure-volume (P-V) analysis. Load-independent diastolic indexes, including the time constant of isovolumic relaxation and the slope of the end-diastolic P-V relationship, as well as systolic indexes, including preload recruitable stroke work, the dP/dt(max)-end-diastolic volume (EDV) relationship, and the P-V area-EDV relationship, were elevated in Ren2 rats compared with Sprague-Dawley controls (P < 0.05). The Ren2 myocardium exhibited parallel increases in the oxidant markers NADPH oxidase and 3-nitrotyrosine. The increase in the prohypertrophic protein Jak2 in Ren2 rats was associated with cardiac structural abnormalities using light microscopic and ultrastructural analysis, which included interstitial fibrosis, cardiomyocyte and LV hypertrophy, and mitochondrial derangements. Both angiotensin receptor blockers attenuate these abnormalities to a similar extent. Our data suggest that the beneficial effect of telmisartan and olmesartan on cardiac structure and function may be predominantly pressor-related or angiotensin type 1 receptor dependent in this model of renin-angiotensin system activation.

Recent data implicate oxidative stress as a mediator of pulmonary hypertension (PH) and of the associated pathological changes to the pulmonary vasculature and right ventricle (RV). Increases in reactive oxygen species (ROS), altered redox state, and elevated oxidant stress have been demonstrated in the lungs and RV of several animal models of PH, including chronic hypoxia, monocrotaline toxicity, caveolin-1 knock-out mouse, and the transgenic Ren2 rat which overexpresses the mouse renin gene. Generation of ROS in these models is derived mostly from the activities of the nicotinamide adenine dinucleotide phosphate oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase. As disease progresses circulating monocytes and bone marrow-derived monocytic progenitor cells are attracted to and accumulate in the pulmonary vasculature. Once established, these inflammatory cells generate ROS and secrete mitogenic and fibrogenic cytokines that induce cell proliferation and fibrosis in the vascular wall resulting in progressive vascular remodeling. Deficiencies in antioxidant enzymes also contribute to pulmonary hypertensive states. Current therapies were developed to improve endothelial function, reduce pulmonary artery pressure, and slow the progression of vascular remodeling in the pulmonary vasculature by targeting deficiencies in either NO (PDE-type 5 inhibition) or PGI(2) (prostacyclin analogs), or excessive synthesis of ET-1 (ET receptor blockers) with the intent to improve patient clinical status and survival. New therapies may slow disease progression to some extent, but long term management has not been achieved and mortality is still high. Although little is known concerning the effects of current pulmonary arterial hypertension treatments on RV structure and function, interest in this area is increasing. Development of therapeutic strategies that simultaneously target pathology in the pulmonary vasculature and RV may be beneficial in reducing mortality associated with RV failure.

Resveratrol is a natural phytophenol that exhibits cardioprotective effects. This study was designed to elucidate the mechanisms by which resveratrol protects against diabetes-induced cardiac dysfunction. Normal control (m-Lepr(db)) mice and type 2 diabetic (Lepr(db)) mice were treated with resveratrol orally for 4 wk. In vivo MRI showed that resveratrol improved cardiac function by increasing the left ventricular diastolic peak filling rate in Lepr(db) mice. This protective role is partially explained by resveratrol's effects in improving nitric oxide (NO) production and inhibiting oxidative/nitrative stress in cardiac tissue. Resveratrol increased NO production by enhancing endothelial NO synthase (eNOS) expression and reduced O(2)(·-) production by inhibiting NAD(P)H oxidase activity and gp91(phox) mRNA and protein expression. The increased nitrotyrosine (N-Tyr) protein expression in Lepr(db) mice was prevented by the inducible NO synthase (iNOS) inhibitor 1400W. Resveratrol reduced both N-Tyr and iNOS expression in Lepr(db) mice. Furthermore, TNF-α mRNA and protein expression, as well as NF-κB activation, were reduced in resveratrol-treated Lepr(db) mice. Both Lepr(db) mice null for TNF-α (db(TNF-)/db(TNF-) mice) and Lepr(db) mice treated with the NF-κB inhibitor MG-132 showed decreased NAD(P)H oxidase activity and iNOS expression as well as elevated eNOS expression, whereas m-Lepr(db) mice treated with TNF-α showed the opposite effects. Thus, resveratrol protects against cardiac dysfunction by inhibiting oxidative/nitrative stress and improving NO availability. This improvement is due to the role of resveratrol in inhibiting TNF-α-induced NF-κB activation, therefore subsequently inhibiting the expression and activation of NAD(P)H oxidase and iNOS as well as increasing eNOS expression in type 2 diabetes.

Left ventricular (LV) pseudoaneurysm (PS) is an uncommon, often fatal complication associated with myocardial infarction, cardiothoracic surgery, trauma, and, rarely, infective endocarditis. A 28-year-old man with prior history of bioprosthetic mitral valve replacement presented with congestive heart failure and bacteremia with Abiotrophia granulitica. Transesophageal echocardiogram showed bioprosthesis dysfunction, large vegetations, mitral regurgitation, and probable PS. Cardiac and chest CT confirmed a PS communicating with the left ventricle Patient had pulseless electrical activity and died. Autopsy showed a giant PS with layered thrombus and pseudo-endothelialized cavity. Our case highlights the importance of multimodality imaging as an important tool in management of PS., (Copyright 2010 Society of Cardiovascular Computed Tomography. Published by Elsevier Inc. All rights reserved.)

Weight loss improves metabolic syndrome (MetS) factors, but risk may return with weight regain. This study was designed to determine if exercise training can maintain improvements in MetS risk factors during weight regain. In a randomized control trial,102 overweight or obese (body mass index 25.0-39.9 kg/m(2)) men and women (age 21-52 yr), with characteristics of the MetS, lost 10% of body weight with supervised walking/jogging at 60% of maximal oxygen consumption (Vo(2 max)) (-400 kcal/session), 5 days/wk, and caloric restriction (-600 kcal/day) over a 4- to 6-mo period. After weight loss, 77 remaining subjects underwent programmed weight regain (+50% of lost weight) for 4-6 mo with random assignment to two groups: no exercise (NoEX) or continued supervised exercise (EX). Blood pressure, regional fat, glucose homeostasis, lipids, and inflammatory markers were assessed at baseline, post-weight loss, and post-weight regain. Groups were compared by two-way repeated-measures ANOVA on the 67 subjects. After weight loss (9.7 +/- 0.2% of body weight), significant (P < 0.05) improvements were observed in almost all parameters assessed. Following weight regain (54.4 +/- 1.6% of lost weight), the NoEX group exhibited deterioration in most metabolic markers, while the EX group maintained improvements in Vo(2 max), blood pressures, glucose homeostasis, high- and low-density lipoprotein cholesterol (HDL-C and LDL-C), oxidized LDL, and other markers of inflammation, but did not maintain improvements in triglyceride and cholesterol concentrations or abdominal fat. Results of this design of controlled human weight regain suggest that aerobic exercise can counter the detrimental effects of partial weight regain on many markers of disease risk.

Widespread use of echocardiography has contributed to more frequent recognition of takotsubo stress cardiomyopathy. Initial presentation is similar to acute coronary syndrome and the acute course can be complicated by heart failure, arrhythmias, dynamic left ventricular outflow tract obstruction, hypotension and death. We briefly review the clinical presentation and propose a unified diagnostic algorithm for cardiologists acutely managing this cardiac emergency. We highlight the central role of echocardiography and emphasize the nuances of this peculiar acute cardiomyopathy from an echocardiographers' perspective.

Objectives: In an effort to improve patient safety attitudes and skills among third-year medical students, two patient safety training sessions were added to their curriculum, complementing a previously implemented second-year curriculum on quality improvement, patient safety and teamwork., Methods: Safety attitudes and skills were assessed before and after students completed the medicine clerkship training and were compared with historical controls. Students identified and reported on observed safety events, with their reports matched to event type and harm score with contemporaneous safety reports from University of Missouri's Patient Safety Network (PSN). Comparisons were assessed by five internal safety experts using criteria for report submission "worthiness", blame tone, target of blame and presence/strength of proposed solutions., Results: Students completing the third-year safety booster conferences expressed statistically higher comfort levels with identifying the cause of an error than did the student control group (p<0.05). Medical students proposed safety interventions that were more robust than those suggested by event reporters regarding similar events within our health system (p<0.0001). The worthiness and blame tone of medical student reports were not statistically different than event reports in PSN., Conclusions: Completion of two 1-h patient safety booster conferences in the third year of medical school led to increased student comfort in safety event analysis. Students documented stronger resolution robustness scores, suggesting similar training should be offered to PSN reporters. Medical students represent an underutilised resource for identifying and proposing solutions for patient safety issues.

Hypertension, diabetes and obesity cause cardiac diastolic dysfunction (DD) which could reduce exercise capacity. Our aim was to determine if 10% weight loss by exercise at 60% VO(2max) five days/week (approximately -375 kcal/session) and caloric restriction (approximately -600 kcal/d) over 6 months improves exercise capacity and DD in Metabolic syndrome (MetS). Eighteen subjects (40 +/- 1y, women = 6, BMI = 33.5 +/- 1.0 kg/m(2)) successfully completed the study. Maximal treadmill stress echocardiography was performed at baseline and post weight loss to determine VO(2max), resting and stress DD as the ratio of peak early diastolic mitral inflow velocity (E) to tissue Doppler early diastolic annular decent (E'). After weight loss (mean = 9.5 +/- 0.2%), all metabolic parameters improved. Resting and stress E/E' values remained normal before and after weight loss. Exercise intolerance is likely due to general deconditioning and not cardiac dysfunction in early MetS as VO(2max) increases significantly with lifestyle while cardiac function remains unchanged.

Background: The lungs of patients with pulmonary arterial hypertension (PAH) exhibit decreased bioavailability of nitric oxide and downstream signaling through cyclic guanosine monophosphate (cGMP). Therapies that enhance cGMP-mediated vasodilation have shown efficacy in treating PAH. We tested the hypothesis that combination therapy with sildenafil, a cGMP phosphodiesterase type 5 inhibitor, and brain natriuretic peptide (BNP), a receptor-mediated guanosine cyclase stimulator, synergistically attenuates monocrotaline-induced PAH in rats compared with either monotherapy., Methods: Adult male Sprague-Dawley rats were subcutaneously injected with monocrotaline (n = 41, 50 mg/kg). After approximately 4 weeks, the rats were infused intravenously with vehicle solution, sildenafil (42 and 85 microg/kg/min), or BNP (50 and 100 ng/kg/min), alone and in varied combination. The primary endpoint was the relative change in right ventricular systolic pressure (RVSP) and mean arterial systemic pressure (MAP). Secondary endpoints included heart rate and dP/dt., Results: Vehicle infusions did not alter hemodynamic variables. Sildenafil85 (85 microg/kg/min) alone decreased RVSP (-16.6 +/- 5.6%) and decreased MAP (-4.0 +/- 4.7%). BNP50 (50 ng/kg/min) and BNP100 (100 ng/kg/min) decreased RVSP (-23.3 +/- 5.7% and -27.1 +/- 2.9%, respectively) and MAP (-6.4 +/- 5.8% and -14.3 +/- 4.1%, respectively). Combination therapy with sildenafil42 and BNP50 decreased RVSP (-20.7 +/- 5.6%) and showed a lessened systemic effect (MAP = -11.6 +/- 5.9%). Combination therapy with sildenafil85 and BNP100 decreased RVSP (-27.6 +/- 3.2%, P = NS) and showed increased systemic effect (MAP = -20.7 +/- 3.1%, P < 0.05) in comparison with sildenafil85., Conclusions: This study suggests that intravenous administration of both sildenafil and BNP monotherapy produces significant improvement in RVSP, making them potentially viable options for the treatment of PAH, whereas combination therapy produces no additional improvement in pulmonary hemodynamics.

To determine whether resistance training effectively maintains improvements in cardiometabolic syndrome risk factors during weight regain, 9 individuals lost 4% to 6% of their body weight during an 8- to 12-week diet- and aerobic exercise-induced weight loss phase followed by a controlled weight regain phase (8-12 weeks), during which they regained approximately 50% of the lost weight while participating in a supervised resistance training program. Following weight loss (6.0%+/-0.3%), body mass index, body fat percentage, waist circumference, all abdominal adipose tissue depots, total cholesterol, low-density lipoprotein cholesterol, insulin, and homeostasis model assessment (HOMA) were significantly reduced, while quantitative insulin-sensitivity check index (QUICKI) and cardiorespiratory fitness (maximal oxygen consumption) significantly increased. During weight regain (48.3%+/-3.3% of lost weight), body fat percentage, waist circumference, and maximal oxygen consumption were maintained and muscular strength and lean body mass significantly increased. Abdominal adipose tissue depots, insulin, HOMA, and QUICKI did not significantly change after weight regain. Resistance training was effective in maintaining improvements in metabolic health during weight regain.

Cardiovascular diseases, in their broad spectrum, are collectively the major cause of death in patients on dialysis. The population of patients treated with peritoneal and hemodialysis are not only subject to the traditional risk factors for heart disease, but also to certain uremia-associated risk factors that are unique in this population. Limited data are available on the effectiveness of routine interventions on cardiovascular outcomes in dialysis patients. Because most dialysis patients are excluded from clinical trials, data from randomized controlled trials regarding outcomes in patients undergoing peritoneal dialysis are almost absent. The present review discusses some of the major cardiovascular problems in the dialysis population, the impact of those problems on survival, and the available therapeutic strategies.

Coronary artery disease is the number one cause of death in patients with chronic kidney disease (CKD). However,patients with impaired renal function are much less likely than patients with normal renal function to undergo left heart catheterization and coronary intervention. Patients that do receive invasive strategies experience more bleeding and higher rates of ischemic events. In this review, we examine advances in percutaneous coronary intervention--including antiplatelet therapy and drug-eluting stents--and their impact on patients with CKD.

We have recently reported that transgenic (mRen2)27 rats (Ren2 rats) exhibit pulmonary arterial hypertension (PAH), which is, in part, mediated by oxidative stress. Since 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors (statins) exhibit beneficial vascular effects independent of cholesterol synthesis, we hypothesized that rosuvastatin (RSV) treatment ameliorates PAH and pulmonary vascular remodeling in Ren2 rats, in part, by reducing oxidative stress. Six-week-old male Ren2 and Sprague-Dawley rats received RSV (10 mg x kg(-1) x day(-)1 ip) or vehicle for 3 wk. After treatment, right ventricular systolic pressure (RVSP) and mean arterial pressure (MAP) were measured. To evaluate treatment effects on pulmonary arteriole remodeling, morphometric analyses were performed to quantitate medial thickening and cell proliferation, whereas whole lung samples were used to quantitate the levels of 3-nitrotyrosine, superoxide, stable nitric oxide (NO) metabolites [nitrates and nitrites (NO(x))], and expression of NO synthase isoforms. In the Ren2 rat, RVSP is normal at 5 wk of age, PAH develops between 5 and 7 wk of age, and the elevated pressure is maintained with little variation through 13 wk. At 8 wk of age, left ventricular function and blood gases were normal in the Ren2 rat. Ren2 rats exhibited elevations in medial hypertrophy due to smooth muscle cell proliferation, 3-nitrotyrosine, NO(x), NADPH oxidase activity, and endothelial NO synthase expression compared with Sprague-Dawley rats. RSV significantly blunted the increase in RVSP but did not reduce MAP in the Ren2 rat; additionally, RSV significantly attenuated the elevated parameters examined in the Ren2 rat. These data suggest that statins may be a clinically viable adjunct treatment of PAH through reducing peroxynitrite formation.

Morbid obesity and diabetes cause diastolic dysfunction that can be detected by Doppler echocardiography. Patients with the metabolic syndrome could demonstrate early diastolic dysfunction that may influence effort tolerance. A total of 32 patients (17 men) who fulfilled >/=2 of the 5 metabolic syndrome criteria were studied. The average age of patients was 37+/-2 years. All patients were overweight/obese (mean body mass index of 34.4+/-0.7 kg/m(2)), 15 had blood pressure >130/85 mm Hg, 19 had elevated triglyceride levels (>150 mg/dL), and 17 had low high-density lipoprotein cholesterol levels (men <40 mg/dL, women <50 mg/dL). Maximal exercise was performed using Bruce treadmill protocol with standard stress echocardiography and tissue Doppler. Maximal oxygen consumption (VO(2max)) was measured using indirect calorimetry. Left ventricular filling pressure was indirectly derived from dividing pulse Doppler early mitral inflow velocity (E) by tissue Doppler early diastolic mitral annular motion (E') or E/E'. The group's average treadmill time was 8.06+/-0.28 minutes, VO(2max) was 28.6+/-1.1 mL/kg/min, and 8.2+/-0.3 metabolic equivalents. None had evidence of myocardial ischemia or systolic or diastolic dysfunction with exercise. Mean "resting" E/E' and "post-exercise" E/E' were 7.01+/-0.04 and 7.41+/-0.41, respectively. There was no significant correlation between resting E/E' and VO(2max) (r=-0.266; P=.14). The post-exercise E/E' significantly correlated with VO(2max) (r=-0.483; P=.005) and metabolic equivalents (r=-0.487; P=.005). Diastolic function is preserved in early metabolic syndrome. Even in the normal diastolic function range, exercise E/E' is inversely related to VO(2max). Further longitudinal studies are needed to determine whether they develop diastolic dysfunction and related heart failure.