Citations

ABSTRACTObjectivesIdentifying the distributions and determinants of fluoroscopy time for invasive coronary angiography (ICA) and percutaneous coronary intervention (PCI).BackgroundICA and PCI are significant contributors to radiation exposure from medical imaging in the US. Fluoroscopy time is a potentially modifiable determinant of radiation exposure for these procedures, but has not been well characterized in contemporary practice.MethodsWe evaluated the distribution of fluoroscopy time in patients undergoing ICA and/or PCI in the CathPCI Registry®, stratifying patients by numerous clinical scenarios. Hierarchical models were used to determine patient, procedure, operator and hospital‐level factors associated with fluoroscopy time for these procedures.ResultsOur study included a total of 3,295,348 ICA and PCI procedures performed by 9,600 operators from January 2005 through June 2009. There was wide variation in fluoroscopy times for these procedures with median [IQR] fluoroscopy times of 2.6 [1.7–4.5] minutes for ICA, 6.7 [4.2–10.8] minutes for ICA in patients with prior coronary artery bypass grafting (CABG), 10.1 [6.0–17.4] minutes for PCI, 10.7 [7.0–16.9] minutes for PCI with ICA, and 16.0 [10.6–24.0] minutes for PCI and ICA in patients with prior CABG. Prolonged fluoroscopy times (>30 minutes) were rare for ICA, but occurred in 6.7% of PCIs and 14.7% of PCIs in patients with prior CABG. After accounting for patient characteristics and procedure complexity, operator and hospital‐level factors explained nearly 20% of the variation in fluoroscopy time.ConclusionsFluoroscopy times vary widely during ICA and PCI with operator and hospital‐level factors contributing substantially to these differences. A better understanding of potentially modifiable sources of this variation will elucidate opportunities for enhancing the radiation safety of these procedures. © 2013 Wiley Periodicals, Inc.

AbstractObjectivesPatient satisfaction is tied to outcome, but there is scant literature on the relationship of patient perceived outcome and attributes of the pain clinic visit, including the patient interaction with the pain management specialist. The primary purpose of this study is to identify attributes of the patient–provider interaction most strongly associated with patient perceived outcome of their clinic visit. The secondary aim is to correlate patient perceived outcome with patient self‐rated overall health.MethodsA patient satisfaction survey conducted via phone approximately 3 weeks after the patient's pain clinic visit.ResultsThe response rate was 60.2%; 987 patient surveys collected between 2006 and 2010 were used in the analysis. Four factors were significantly associated with the outcome: (1) Explanations by the physician of the patient's condition and treatment, (2) clear instructions regarding post‐appointment activities, (3) knowing the patient as a person, and (4) the patient's self‐rated health. In terms of the secondary objective, those who answered very good/excellent regarding their self‐rated health had an 87% increased odds of better (very good/excellent) outcome of their pain clinic visit (or 1.87 times the odds of better outcome) compared with those who answered poor/fair/good.ConclusionsOur results suggest that pain physicians may positively impact patient perceived outcomes of clinic visits by explaining the patient's condition and treatment, providing instructions, and taking the time to understand the patient and their values.

Summary The defining characteristic of a profession – and especially a health‐care profession – is that the behaviour of its members is proscribed by a formal code of ethics. The main purpose of such codes is to guide practitioners' interactions with patients, assuring that patient interests are protected. In other words, the ethical code requires practitioners to place their patients' needs for proper diagnosis and appropriate treatment ahead of their own needs for income and advancement. The dental profession has a code of ethics that was developed by the American Dental Association many years ago; in most clinical situations, determination of proper behaviour is self‐evident. However, the field of temporoman‐dibular disorders ( TMD s) has been the subject of considerable controversy for over half a century, and many people have argued that this makes it impossible to evaluate various approaches to treatment of TMD s within an ethical framework. In this article, the authors argue that the large volume of scientific evidence in the contemporary TMD literature provides an ethical framework for the diagnosis and treatment of patients with TMD s within a biopsychosocial medical model. They present a summary of the research with contemporary scientific integrity, which has produced that information over a period of many years. Based on that research, they conclude that dentists may provide conservative and reversible treatments that will be successful for most TMD s and in doing so will comply with the profession's code of ethics. Conversely, the authors claim that those dentists who continue to follow the older mechanistic models of TMD aetiology and treatment are not only out of step scientifically, but are placing their patients' welfare at risk by providing unnecessary irreversible bite‐changing and jaw‐repositioning interventions. Therefore, debate of these issues should not be solely focused on scientific merit, but also upon the compelling ethical obligations that dentists have as a result of the contemporary scientific literature regarding TMD s.

Abstract Gleason score 7 (GS7) prostate cancer [tumors with both Gleason patterns 3 (GP3) and 4 (GP4)] portends a significantly more aggressive tumor than Gleason score 6 (GS6). It is, therefore, critical to understand the molecular relationship of adjacent GP3 and GP4 tumor cell populations and relate molecular abnormalities to disease progression. To decipher molecular relatedness, we used laser capture microdissection (LCM) and whole-genome amplification (WGA) to separately collect and amplify DNA from adjacent GP3 and GP4 cell populations from 14 cases of GS7 prostate cancer. We then carried out massively parallel mate-pair next generation sequencing (NGS) to examine the landscape of large chromosomal alterations. We identified four to 115 DNA breakpoints in GP3 and 17 to 480 in GP4. Our findings indicate that while GP3 and GP4 from the same tumor each possess unique breakpoints, they also share identical ones, indicating a common origin. Approximately 300 chromosomal breakpoints were localized to the regions affected in at least two tumors, whereas more than 3,000 were unique within the set of 14 tumors. TMPRSS2–ERG was the most recurrent rearrangement present in eight cases, in both GP3 and GP4. PTEN rearrangements were found in five of eight TMPRSS2–ERG fusion–positive cases in both GP3 and GP4. Hierarchical clustering analysis revealed that GP3 has greater breakpoint similarity to its partner GP4 compared with GP3 from different patients. We show evidence that LCM, WGA, and NGS of adjacent tumor regions provide an important tool in deciphering lineage relationships and discovering chromosomal alterations associated with tumor progression. Cancer Res; 73(11); 3275–84. ©2013 AACR.

Disease OverviewPolycythemia Vera (PV) and essential thrombocythemia (ET) are myeloproliferative neoplasms (MPN) primarily characterized by erythrocytosis and thrombocytosis, respectively. Other disease features include leukocytosis, splenomegaly, thrombohemorrhagic complications, vasomotor disturbances, pruritus and a small risk of disease progression into acute myeloid leukemia or myelofibrosis.DiagnosisAlmost all patients with PV harbor aJAK2mutation. When PV is suspected, the presence of aJAK2mutation highly suggests the diagnosis and its absence, combined with normal or increased serum erythropoietin level, excludes the diagnosis. Differential diagnosis of ET should include reactive thrombocytosis, chronic myeloid leukemia, prefibrotic myelofibrosis and RARS‐T (refractory anemia with ring sideroblasts associated with marked thrombocytosis). AJAK2mutation is found in 50–70% of patients with ET, myelofibrosis or RARS‐T and is capable of distinguishing reactive from clonal thrombocytosis.Risk StratificationCurrent risk stratification in PV and ET is designed to estimate the likelihood of thrombotic complications: high‐risk is defined by the presence of age >60 years or presence of thrombosis history; low‐risk is defined by the absence of both of these two risk factors. Recent data considersJAK2V617F and cardiovascular (CV) risk factors as additional risk factors for thrombosis. Presence of extreme thrombocytosis (platelet count >1,000 × 109/L) might be associated with acquired von Willebrand syndrome (AvWS) and, therefore, risk of bleeding. Risk factors for shortened survival in both PV and ET include advanced age, leukocytosis, and history of thrombosis.Risk‐Adapted TherapySurvival is near‐normal in ET and reasonably long in PV. The 10‐year risk of leukemic/fibrotic transformation is <1%/1% in ET and <3%/10% in PV. In contrast, the risk of thrombosis exceeds 20%. The main goal of therapy is therefore to prevent thrombohemorrhagic complications. In low risk patients, this is effectively and safely accomplished by the use of low‐dose aspirin in both PV and ET and phlebotomy (hematocrit target of <45%) in PV. In high risk patients, treatment with hydroxyurea is additionally recommended, although not mandated in older patients withoutJAK2V617F or CV risk factors. Treatment with busulfan or interferon‐α is usually effective in hydroxyurea failures. Screening for clinically significant AvWS is recommended before administrating aspirin in the presence of extreme thrombocytosis. Am. J. Hematol. 88:508–516, 2013. © 2013 Wiley Periodicals, Inc.

BACKGROUND: Four-meter gait speed (4MGS) has been associated with functional capacity and overall mortality in elderly patients, and may easily be translated to daily practice. We evaluated the association of 4MGS with meaningful outcomes. METHODS: In 70 subjects we conducted the 4MGS, 6-min walk test (6MWT), objectively measured physical activity, and assessed dyspnea, quality of life, and self-efficacy for walking and routine physical activity. 4MGS was measured in 3 separate time epochs during the 6MWT, to explore 4MGS variability. RESULTS: Diagnoses included COPD (51.4%), interstitial lung disease (38.6%), and other pulmonary conditions (10%). The mean ± SD values were: 4MGS 0.85 ± 0.21 m/s, 6-min walk distance (6MWD) 305 ± 115 m, and physical activity level 1.28 ± 0.17, which is consistent with severe physical inactivity. The gait speeds within the time epochs 1–2, 3–4, and 5–6 min during the 6MWT were not significantly different: 1.01 ± 0.29 m/s, 0.98 ± 0.31 m/s, and 1.00 ± 0.31 m/s, respectively. 4MGS had a significant correlation with 6MWD ( r = 0.70, P < .001). 6MWD was the dominant variable for predicting 4MGS. Other significant predictors of 4MGS included dyspnea, self-efficacy, quality of life, and objectively measured physical activity. CONCLUSIONS: 4MGS is significantly and independently associated with 6MWD, and may serve as a reasonable simple surrogate for 6MWD in subjects with chronic lung disease. Gait speed was remarkably stable throughout the 6MWT, which supports the validity of an abbreviated walk test such as 4MGS.