Background: Medical school faculty are less enthusiastic about their academic careers than ever before. In this study, we measured the prevalence and determinants of intent to leave academic medicine.

Although statins are remarkably effective, they are still underprescribed because of concerns about muscle toxicity. We review the aspects of statin myopathy that are important to the primary care physician and provide a guide for evaluating patients on statins who present with muscle complaints. We outline the differential diagnosis, the risks and benefits of statin therapy in patients with possible toxicity, and the subsequent treatment options.

Introduction Transesophageal echocardiography (TEE) is used to evaluate for left atrial appendage (LAA) thrombi prior to restoration of sinus rhythm in atrial fibrillation (AF). We examined the relationship of atrial fibrosis quantified using late gadolinium enhancement MRI (LGE-MRI) with TEE findings. Methods and Results We included 178 patients with AF, undergoing TEE and LGE-MRI prior to ablation or cardioversion. LGE-MRI and subsequent image processing was used to quantify atrial fibrosis based on signal intensity analysis. The mean CHADS2 score was 1.24±1.08 and CHA2DS2-VASc was 2.08±1.33. The LAA was classified as normal, spontaneous echo contrast (SEC) present or thrombus present. LAA thrombus was found in 12 patients (6.7%) while SEC was identified in 19 patients (10.7%). Patients with thrombus had higher atrial fibrosis compared to patients without thrombus (26.9±17.4% vs 16.7±10.5%; p<0.01). Atrial fibrosis was also higher in patients with SEC (23.3±13.7%) compared to those without SEC (16.7±10.8%; p=0.01). Patients with high atrial fibrosis (>20%) were more likely to have a LAA thrombus (Odds Ratio 4.6; p=0.02) and SEC (Odds ratio 2.6; p=0.06). Multivariate logistic regression showed high fibrosis (Odds Ratio 3.6; p<0.01) and CHADS2≥2 (Odds Ratio 3.5; p<0.01) were significant predictors of TEE abnormalities (LAA thrombus or SEC). The area under the curve for the model including high fibrosis, AF type and CHADS2≥2 or CHA2DS2-VASc≥2 was 0.73 compared to 0.63 and 0.65 for CHADS2 and CHA2DS2-VASc alone. Conclusions Atrial fibrosis is independently associated with appendage thrombus and spontaneous contrast. It provides additional risk stratification not captured by clinical parameters.

The study provides further evidence that public reporting of physician-specific outcome data influences physician behavior and indicates that significant discrepancies exist in how scorecards are perceived by physicians versus patients.

It is assumed that platelets in diseased conditions share similar properties to platelets in healthy conditions, although this has never been examined in detail for myocardial infarction (MI). We examined platelets from patients with ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) compared with platelets from healthy volunteers to evaluate for differences in platelet phenotype and function. Platelet activation was examined and postreceptor signal transduction pathways were assessed. Platelet-derived plasma biomarkers were evaluated by receiver operator characteristic curve analysis. Maximum platelet activation through the thromboxane receptor was greater in STEMI than in NSTEMI but less through protease-activated receptor 1. Extracellular-signal related-kinase 5 activation, which can activate platelets, was increased in platelets from subjects with STEMI and especially in platelets from patients with NSTEMI. Matrix metalloproteinase 9 (MMP9) protein content and enzymatic activity were several-fold greater in platelets with MI than in control. Mean plasma MMP9 concentration in patients with MI distinguished between STEMI and NSTEMI (area under curve [AUC] 75% [confidence interval (CI) 60-91], P = 0.006) which was superior to troponin T (AUC 66% [CI 48-85, P = 0.08), predicting STEMI with 80% sensitivity (95% CI 56-94), 90% specificity (CI 68-99), 70% AUC (CI 54-86, P < 0.0001), and NSTEMI with 50% sensitivity (CI 27-70), 90% specificity (CI 68-99), 70% AUC (CI 54-86, P = 0.03). Platelets from patients with STEMI and NSTEMI show differences in platelet surface receptor activation and postreceptor signal transduction, suggesting the healthy platelet phenotype in which antiplatelet agents are often evaluated in preclinical studies is different from platelets in patients with MI.