The purpose of this analysis was to revise the model for perioperative risk for esophagectomy for cancer utilizing The Society of Thoracic Surgeons General Thoracic Surgery Database to provide ...enhanced risk stratification and quality improvement measures for contributing centers.
The Society of Thoracic Surgeons General Thoracic Surgery Database was queried for all patients treated for esophageal cancer with esophagectomy between July 1, 2011, and June 30, 2014. Multivariable risk models for major morbidity, perioperative mortality, and combined morbidity and mortality were created with the inclusion of surgical approach as a risk factor.
In all, 4,321 esophagectomies were performed by 164 participating centers. The most common procedures included Ivor Lewis (32.5%), transhiatal (21.7%), minimally invasive esophagectomy, Ivor Lewis type (21.4%), and McKeown (10.0%). Sixty-nine percent of patients received induction therapy. Perioperative mortality (inpatient and 30-day) was 135 of 4,321 (3.4%). Major morbidity occurred in 1,429 patients (33.1%). Major morbidities include unexpected return to operating (15.6%), anastomotic leak (12.9%), reintubation (12.2%), initial ventilation beyond 48 hours (3.5%), pneumonia (12.2%), renal failure (2.0%), and recurrent laryngeal nerve paresis (2.0%). Statistically significant predictors of combined major morbidity or mortality included age more than 65 years, body mass index 35 kg/m(2) or greater, preoperative congestive heart failure, Zubrod score greater than 1, McKeown esophagectomy, current or former smoker, and squamous cell histology.
Thoracic surgeons participating in The Society of Thoracic Surgeons General Thoracic Surgery Database perform esophagectomy with low morbidity and mortality. McKeown esophagectomy is an independent predictor of combined postoperative morbidity or mortality. Revised predictors for perioperative outcome were identified to facilitate quality improvement processes and hospital comparisons.
Background The purpose of this study is to help define the indications for rotator cuff repair by identifying predictors of failure of nonoperative treatment. Methods A prospective, multicenter, ...cohort study design was used. All patients with full-thickness rotator cuff tears on magnetic resonance imaging were offered participation. Baseline data from this cohort were used to examine risk factors for failing a standard rehabilitation protocol. Patients who underwent surgery were defined as failing nonoperative treatment. A Cox proportional hazards model was fit to determinethe baseline factors that predicted failure. The dependent variable was time to surgery. The independent variables were tear severity and baseline patient factors: age, activity level, body mass index, sex, Single Assessment Numeric Evaluation score, visual analog scale score for pain, education, handedness, comorbidities, duration of symptoms, strength, employment, smoking status, and patient expectations. Results Of the 433 subjects in this study, 87 underwent surgery with 93% follow-up at 1 year and 88% follow-up at 2 years. The median age was 62 years, and 49% were female patients. Multivariate modeling, adjusted for the covariates listed previously, identified patient expectations regarding physical therapy ( P < .0001) as the strongest predictor of surgery. Higher activity level ( P = .011) and not smoking ( P = .023) were also significant predictors of surgery. Conclusion A patient's decision to undergo surgery is influenced more by low expectations regarding the effectiveness of physical therapy than by patient symptoms or anatomic features of the rotator cuff tear. As such, patient symptoms and anatomic features of the chronic rotator cuff tear may not be the best features to use when deciding on surgical intervention.
2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery Hillis, L. David, MD, FACC; Smith, Peter K., MD, FACC; Anderson, Jeffrey L., MD, FACC, FAHA ...
Journal of the American College of Cardiology,
12/2011, Letnik:
58, Številka:
24
Journal Article
Nanette K. Wenger, MD ACCF/AHA Task Force Members Jeffrey L. Anderson, MD, FACC, FAHA, Chair; Alice K. Jacobs, MD, FACC, FAHA, Immediate Past Chair; Jonathan L. Halperin, MD, FACC, FAHA, Chair-Elect; ...Nancy M. Albert, PhD, CCNS, CCRN; Mark A. Creager, MD, FACC, FAHA; David DeMets, PhD; Steven M. Ettinger, MD, FACC; Robert A. Guyton, MD, FACC; Judith S. Hochman, MD, FACC, FAHA; Frederick G. Kushner, MD, FACC, FAHA; E. Magnus Ohman, MD, FACC; William Stevenson, MD, FACC, FAHA; Clyde W. Yancy, MD, FACC, FAHA Table of Contents Developed in Collaboration With the American College of Emergency Physicians, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine Preamble (UPDATED)...e182 Introduction (UPDATED)...e184 Organization of Committee and Evidence Review (UPDATED)...e184 Document Review and Approval (UPDATED)...e185 Purpose of These Guidelines...e185 Overview of the Acute Coronary Syndromes...e186 Definition of Terms...e186 Pathogenesis of UA/NSTEMI...e186 Presentations of UA and NSTEMI...e189 Management Before UA/NSTEMI and Onset of UA/NSTEMI...e189 Identification of Patients at Risk of UA/NSTEMI...e189 Interventions to Reduce Risk of UA/NSTEMI...e190 Onset of UA/NSTEMI...e191 Recognition of Symptoms by Patient...e191 Silent and Unrecognized Events...e191 Initial Evaluation and Management...e191 Clinical Assessment...e191 Emergency Department or Outpatient Facility Presentation...e195 Questions to Be Addressed at the Initial Evaluation...e196 Early Risk Stratification...e196 Estimation of the Level of Risk...e198 Rationale for Risk Stratification...e198 History...e198 Anginal Symptoms and Anginal Equivalents...e198 Demographics and History in Diagnosis and Risk Stratification...e199 Estimation of Early Risk at Presentation...e200 Electrocardiogram...e202 Physical Examination...e203 Noncardiac Causes of Symptoms and Secondary Causes of Myocardial Ischemia...e204 Cardiac Biomarkers of Necrosis and the Redefinition of AMI...e204 Creatine Kinase-MB...e205 Cardiac Troponins...e205 Clinical Use...e205 Clinical Use of Marker Change Scores...e207 Bedside Testing for Cardiac Markers...e208 Myoglobin and CK-MB Subforms Compared With Troponins...e208 Summary Comparison of Biomarkers of Necrosis: Singly and in Combination...e208 Other Markers and Multimarker Approaches...e208 Ischemia...e208 Coagulation ...e209 Platelets...e209 Inflammation...e209 B-Type Natriuretic Peptides...e210 Immediate Management...e210 Chest Pain Units...e211 Discharge From ED or Chest Pain Unit...e212 Early Hospital Care...e213 Anti-Ischemic and Analgesic Therapy...e214 General Care...e215 Use of Anti-Ischemic Therapies...e215 Nitrates...e215 Morphine Sulfate...e217 Beta-Adrenergic Blockers...e217 Calcium Channel Blockers...e219 Inhibitors of the Renin-Angiotensin-Aldosterone System...e220 Other Anti-Ischemic Therapies...e221 Intra-Aortic Balloon Pump Counterpulsation...e221 Analgesic Therapy...e221 Recommendations for Antiplatelet/Anticoagulant Therapy in Patients for Whom Diagnosis of UA/NSTEMI Is Likely or Definite (UPDATED)...e221 Antiplatelet Therapy: Recommendations (UPDATED)...e221 Anticoagulant Therapy: Recommendations...e223 Additional Management Considerations for Antiplatelet and Anticoagulant Therapy: Recommendations (UPDATED)...e223 Antiplatelet/Anticoagulant Therapy in Patients for Whom Diagnosis of UA/NSTEMI Is Likely or Definite (NEW SECTION)...e224 Newer P2Y12 Receptor Inhibitors...e224 Choice of P2Y12 Receptor Inhibitors for PCI in UA/NSTEMI...e227 Timing of Discontinuation of P2Y12 Receptor Inhibitor Therapy for Surgical Procedures...e227 Interindividual Variability in Responsiveness to Clopidogrel...e228 Optimal Loading and Maintenance Dosages of Clopidogrel...e228 Proton Pump Inhibitors and Dual Antiplatelet Therapy for ACS...e229 Glycoprotein IIb/IIIa Receptor Antagonists (Updated to Incorporate Newer Trials and Evidence)...e230 Older Antiplatelet Agents and Trials (Aspirin, Ticlopidine, Clopidogrel)...e231 Aspirin...e231 Adenosine Diphosphate Receptor Antagonists and Other Antiplatelet Agents...e233 Anticoagulant Agents and Trials...e236 Unfractionated Heparin...e237 Low-Molecular-Weight Heparin...e238 LMWH Versus UFH...e238 Extended Therapy with LMWHs...e241 Direct Thrombin Inhibitors...e241 Factor Xa Inhibitors...e244 Long-Term Anticoagulation...e245 Platelet GP IIb/IIIa Receptor Antagonists...e246 Fibrinolysis...e251 Initial Conservative Versus Initial Invasive Strategies (UPDATED)...e251 General Principles...e252 Rationale for the Initial Conservative Strategy...e252 Rationale for the Invasive Strategy...e253 Timing of Invasive Therapy (NEW SECTION)...e253 Immediate Angiography...e254 Deferred Angiography...e254 Comparison of Early Invasive and Initial Conservative Strategies...e254 Subgroups...e257 Care Objectives...e258 Risk Stratification Before Discharge...e260 Care Objectives...e260 Noninvasive Test Selection...e262 Selection for Coronary Angiography...e263 Patient Counseling...e263 Coronary Revascularization...e263 Recommendations for Revascularization With PCI and CABG in Patients With UA/NSTEMI (UPDATED)...e263 Late Hospital Care, Hospital Discharge, and Post-Hospital Discharge Care...e263 Medical Regimen and Use of Medications...e263 Long-Term Medical Therapy and Secondary Prevention...e265 Convalescent and Long-Term Antiplatelet Therapy (UPDATED)...e266 Beta Blockers...e266 Inhibition of the Renin-Angiotensin-Aldosterone System...e267 Nitroglycerin...e267 Calcium Channel Blockers...e267 Warfarin Therapy (UPDATED)...e267 Lipid Management...e268 Blood Pressure Control...e270 Diabetes Mellitus...e270 Smoking Cessation...e270 Weight Management...e271 Physical Activity...e271 Patient Education...e272 Influenza...e272 Depression...e272 Nonsteroidal Anti-Inflammatory Drugs...e272 Hormone Therapy...e272 Antioxidant Vitamins and Folic Acid...e273 Postdischarge Follow-Up...e273 Cardiac Rehabilitation...e274 Return to Work and Disability...e275 Other Activities...e276 Patient Records and Other Information Systems...e277 Special Groups...e277 Women...e277 Profile of UA/NSTEMI in Women...e278 Management...e278 Pharmacological Therapy...e278 Coronary Artery Revascularization...e278 Initial Invasive Versus Initial Conservative Strategy...e279 Stress Testing...e281 Conclusions...e281 Diabetes Mellitus (UPDATED)...e281 Profile and Initial Management of Diabetic and Hyperglycemic Patients With UA/NSTEMI...e281 Intensive Glucose Control (NEW SECTION)...e282 Coronary Revascularization...e283 Conclusions...e284 Post-CABG Patients...e284 Pathological Findings...e285 Clinical Findings and Approach...e285 Conclusions...e285 Older Adults...e285 Pharmacological Management...e286 Functional Studies...e286 Percutaneous Coronary Intervention in Older Patients...e287 Contemporary Revascularization Strategies in Older Patients...e287 Conclusions...e287 Chronic Kidney Disease (UPDATED) ...e288 Angiography in Patients With CKD (NEW SECTION)...e288 Cocaine and Methamphetamine Users...e290 Coronary Artery Spasm With Cocaine Use...e290 Treatment...e291 Methamphetamine Use and UA/NSTEMI...e292 Variant (Prinzmetal's) Angina...e292 Clinical Picture...e292 Pathogenesis...e292 Diagnosis...e293 Treatment...e293 Prognosis...e293 Cardiovascular "Syndrome X"...e294 Definition and Clinical Picture...e294 Treatment...e295 Takotsubo Cardiomyopathy...e295 Conclusions and Future Directions...e295 Recommendations for Quality of Care and Outcomes for UA/NSTEMI (NEW SECTION)...e297 Quality Care and Outcomes (NEW SECTION)...e297 References...e297 Appendix 1.
Summary Background Treatment for patients with chronic lymphocytic leukaemia who are elderly or who have comorbidities is challenging because fludarabine-based chemoimmunotherapies are mostly not ...suitable. Chlorambucil remains the standard of care in many countries. We aimed to investigate whether the addition of ofatumumab to chlorambucil could lead to better clinical outcomes than does treatment with chlorambucil alone, while also being tolerable for patients who have few treatment options. Methods We carried out a randomised, open-label, phase 3 trial for treatment-naive patients with chronic lymphocytic leukaemia in 109 centres in 16 countries. We included patients who had active disease needing treatment, but in whom fludarabine-based treatment was not possible. We randomly assigned patients (1:1) to receive oral chlorambucil (10 mg/m2 ) on days 1–7 of a 28 day treatment course or to receive chlorambucil by this schedule plus intravenous ofatumumab (cycle 1: 300 mg on day 1 and 1000 mg on day 8; subsequent cycles: 1000 mg on day 1) for three to 12 cycles. Assignment was done with a randomisation list that was computer generated at GlaxoSmithKline, and was stratified, in a block size of two, by age, disease stage, and performance status. The primary endpoint was progression-free survival in the intention-to-treat population and assessment was done by an independent review committee that was masked to group assignment. The study is registered with ClinicalTrials.gov , number NCT00748189. Findings We enrolled 447 patients, median age 69 years (range 35–92). Between Dec 22, 2008, and May 26, 2011, we randomly assigned 221 patients to chlorambucil plus ofatumumab and 226 patients to chlorambucil alone. Median progression-free survival was 22·4 months (95% CI 19·0–25·2) in the group assigned to chlorambucil plus ofatumumab compared with 13·1 months (10·6–13·8) in the group assigned to chlorambucil only (hazard ratio 0·57, 95% CI 0·45–0·72; p<0·0001). Grade 3 or greater adverse events were more common in the chlorambucil plus ofatumumab group (109 50% patients; vs 98 43% given chlorambucil alone), with neutropenia being the most common event (56 26% vs 32 14%). Grade 3 or greater infections had similar frequency in both groups. Grade 3 or greater infusion-related adverse events were reported in 22 (10%) patients given chlorambucil plus ofatumumab. Five (2%) patients died during treatment in each group. Interpretation Addition of ofatumumab to chlorambucil led to clinically important improvements with a manageable side-effect profile in treatment-naive patients with chronic lymphocytic leukaemia who were elderly or had comorbidities. Chlorambucil plus ofatumumab is therefore an important treatment option for these patients who cannot tolerate more intensive therapy. Funding GlaxoSmithKline, Genmab A/S.
The Society of Thoracic Surgeons (STS) creates risk-adjustment models for common cardiothoracic operations for quality improvement purposes. Our aim was to update the lung cancer resection risk model ...utilizing the STS General Thoracic Surgery Database (GTSD) with a larger and more contemporary cohort.
We queried the STS GTSD for all surgical resections of lung cancers from January 1, 2012, through December 31, 2014. Logistic regression was used to create three risk models for adverse events: operative mortality, major morbidity, and composite mortality and major morbidity.
In all, 27,844 lung cancer resections were performed at 231 centers; 62% (n = 17,153) were performed by thoracoscopy. The mortality rate was 1.4% (n = 401), major morbidity rate was 9.1% (n = 2,545), and the composite rate was 9.5% (n = 2,654). Predictors of mortality included age, being male, forced expiratory volume in 1 second, body mass index, cerebrovascular disease, steroids, coronary artery disease, peripheral vascular disease, renal dysfunction, Zubrod score, American Society of Anesthesiologists rating, thoracotomy approach, induction therapy, reoperation, tumor stage, and greater extent of resection (all p < 0.05). For major morbidity and the composite measure, cigarette smoking becomes a risk factor whereas stage, renal dysfunction, congestive heart failure, and cerebrovascular disease lose significance.
Operative mortality and complication rates are low for lung cancer resection among surgeons participating in the GTSD. Risk factors from the prior lung cancer resection model are refined, and new risk factors such as prior thoracic surgery are identified. The GTSD risk models continue to evolve as more centers report and data are audited for quality assurance.
Background Chronic kidney disease is common and is associated with cardiovascular disease, cerebrovascular disease, and cognitive function, although the nature of this relationship remains uncertain. ...Study Design Cross-sectional cohort using baseline data from the Systolic Blood Pressure Intervention Trial (SPRINT). Setting & Participants Participants in SPRINT, a randomized clinical trial of blood pressure targets in older community-dwelling adults with cardiovascular disease, chronic kidney disease, or high cardiovascular disease risk and without diabetes or known stroke, who underwent detailed neurocognitive testing in the cognition substudy, SPRINT−Memory and Cognition in Decreased Hypertension (SPRINT-MIND). Predictors Urine albumin-creatinine ratio (ACR) and estimated glomerular filtration rate (eGFR). Outcomes Cognitive function, a priori defined as 5 cognitive domains based on 11 cognitive tests using z scores, and abnormal white matter volume quantified by brain magnetic resonance imaging. Results Of 9,361 SPRINT participants, 2,800 participated in SPRINT-MIND and 2,707 had complete data; 637 had brain imaging. Mean age was 68 years, 37% were women, 30% were black, and 20% had known cardiovascular disease. Mean eGFR was 70.8 ± 20.9 mL/min/1.73 m2 and median urine ACR was 9.7 (IQR, 5.7-22.5) mg/g. In adjusted analyses, higher ACR was associated with worse global cognitive function, executive function, memory, and attention, such that each doubling of urine ACR had the same association with cognitive performance as being 7, 10, 6, and 14 months older, respectively. Lower eGFR was independently associated with worse global cognitive function and memory. In adjusted models, higher ACR, but not eGFR, was associated with larger abnormal white matter volume. Limitations Cross-sectional only, no patients with diabetes were included. Conclusions In older adults, higher urine ACR and lower eGFR have independent associations with global cognitive performance with different affected domains. Albuminuria concurrently identifies a higher burden of abnormal brain white matter disease, suggesting that vascular disease may mediate these relationships.
Summary Background Ankylosing spondylitis is a chronic immune-mediated inflammatory disease characterised by spinal inflammation, progressive spinal rigidity, and peripheral arthritis. Interleukin 17 ...(IL-17) is thought to be a key inflammatory cytokine in the development of ankylosing spondylitis, the prototypical form of spondyloarthritis. We assessed the efficacy and safety of the anti-IL-17A monoclonal antibody secukinumab in treating patients with active ankylosing spondylitis. Methods We did a randomised double-blind proof-of-concept study at eight centres in Europe (four in Germany, two in the Netherlands, and two in the UK). Patients aged 18–65 years were randomly assigned (in a 4:1 ratio) to either intravenous secukinumab (2×10 mg/kg) or placebo, given 3 weeks apart. Randomisation was done with a computer-generated block randomisation list without a stratification process. The primary efficacy endpoint was the percentage of patients with a 20% response according to the Assessment of SpondyloArthritis international Society criteria for improvement (ASAS20) at week 6 (Bayesian analysis). Safety was assessed up to week 28. This study is registered with ClinicalTrials.gov , number NCT00809159. Findings 37 patients with moderate-to-severe ankylosing spondylitis were screened, and 30 were randomly assigned to receive either intravenous secukinumab (n=24) or placebo (n=6). The final efficacy analysis included 23 patients receiving secukinumab and six patients receiving placebo, and the safety analysis included all 30 patients. At week 6, ASAS20 response estimates were 59% on secukinumab versus 24% on placebo (99·8% probability that secukinumab is superior to placebo). One serious adverse event (subcutaneous abscess caused by Staphylococcus aureus ) occurred in the secukinumab-treated group. Interpretation Secukinumab rapidly reduced clinical or biological signs of active ankylosing spondylitis and was well tolerated. It is the first targeted therapy that we know of that is an alternative to tumour necrosis factor inhibition to reach its primary endpoint in a phase 2 trial. Funding Novartis.
Purpose To assess the effectiveness of a specific nonoperative physical therapy program in treating atraumatic full-thickness rotator cuff tears using a multicenter prospective cohort study design. ...Materials and methods Patients with atraumatic full-thickness rotator cuff tears who consented to enroll provided data via questionnaire on demographics, symptom characteristics, comorbidities, willingness to undergo surgery, and patient-related outcome assessments (Short Form 12 score, American Shoulder and Elbow Surgeons score, Western Ontario Rotator Cuff score, Single Assessment Numeric Evaluation score, and Shoulder Activity Scale). Physicians recorded physical examination and imaging data. Patients began a physical therapy program developed from a systematic review of the literature and returned for evaluation at 6 and 12 weeks. At those visits, patients could choose 1 of 3 courses: (1) cured (no formal follow-up scheduled), (2) improved (continue therapy with scheduled reassessment in 6 weeks), or (3) no better (surgery offered). Patients were contacted by telephone at 1 and 2 years to determine whether they had undergone surgery since their last visit. A Wilcoxon signed rank test with continuity correction was used to compare initial, 6-week, and 12-week outcome scores. Results The cohort consists of 452 patients. Patient-reported outcomes improved significantly at 6 and 12 weeks. Patients elected to undergo surgery less than 25% of the time. Patients who decided to have surgery generally did so between 6 and 12 weeks, and few had surgery between 3 and 24 months. Conclusion Nonoperative treatment using this physical therapy protocol is effective for treating atraumatic full-thickness rotator cuff tears in approximately 75% of patients followed up for 2 years.
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