IMPORTANCE Lymph node status is the primary determinant in treatment decision making in early gastric cancer (EGC). Current evaluation methods are not adequate for estimating lymph node metastasis (LNM) in EGC. OBJECTIVE To develop and validate a prediction model based on a fully quantitative collagen signature in the tumor microenvironment to estimate the individual risk of LNM in EGC. DESIGN, SETTING, AND PARTICIPANTS This retrospective study was conducted from August 1, 2016, to May 10, 2018, at 2 medical centers in China (Nanfang Hospital and Fujian Provincial Hospital). Participants included a primary cohort (n = 232) of consecutive patients with histologically confirmed gastric cancer who underwent radical gastrectomy and received a T1 gastric cancer diagnosis from January 1, 2008, to December 31, 2012. Patients with neoadjuvant radiotherapy, chemotherapy, or chemoradiotherapy were excluded. An additional consecutive cohort (n = 143) who received the same diagnosis from January 1, 2011, to December 31, 2013, was enrolled to provide validation. Baseline clinicopathologic data of each patient were collected. Collagen features were extracted in specimens using multiphoton imaging, and the collagen signature was constructed. An LNM prediction model based on the collagen signature was developed and was internally and externally validated. MAIN OUTCOMES AND MEASURES The area under the receiver operating characteristic curve (AUROC) of the prediction model and decision curve were analyzed for estimating LNM. RESULTS In total, 375 patients were included. The primary cohort comprised 232 consecutive patients, in whom the LNM rate was 16.4% (n = 38; 25 men [65.8%] with a mean [SD] age of 57.82 [10.17] years). The validation cohort consisted of 143 consecutive patients, in whom the LNM rate was 20.9% (n = 30; 20 men [66.7%] with a mean [SD] age of 54.10 [13.19] years). The collagen signature was statistically significantly associated with LNM (odds ratio, 5.470; 95% CI, 3.315-9.026; P < .001). Multivariate analysis revealed that the depth of tumor invasion, tumor differentiation, and the collagen signature were independent predictors of LNM. These 3 predictors were incorporated into the new prediction model, and a nomogram was established. The model showed good discrimination in the primary cohort (AUROC, 0.955; 95% CI, 0.919-0.991) and validation cohort (AUROC, 0.938; 95% CI, 0.897-0.981). An optimal cutoff value was selected in the primary cohort, which had a sensitivity of 86.8%, a specificity of 93.3%, an accuracy of 92.2%, a positive predictive value of 71.7%, and a negative predictive value of 97.3%. The validation cohort had a sensitivity of 90.0%, a specificity of 90.3%, an accuracy of 90.2%, a positive predictive value of 71.1%, and a negative predictive value of 97.1%. Among the 375 patients, a sensitivity of 87.3%, a specificity of 92.1%, an accuracy of 91.2%, a positive predictive value of 72.1%, and a negative predictive value of 96.9% were found. CONCLUSIONS AND RELEVANCE This study's findings suggest th...

SummaryAtrial fibrillation (AF) is one of the most common postoperative arrhythmias in patients who undergo coronary artery bypass grafting (CABG). The aim of this study was to evaluate the effect of preoperative atorvastatin on postoperative atrial fibrillation following coronary artery bypass grafting with cardiopulmonary bypass (CCABG). One hundred consecutive patients undergoing elective CCABG, without history of AF or previous statin treatment, were enrolled and randomly assigned to a statin group (atorvastatin 20 mg/d, n = 49) or a control group (placebo, n = 51) starting 7 days preoperatively. The primary endpoint was the occurrence of postoperative AF. C-reactive protein (CRP) levels were assessed in all selected patients before surgery and every 24 hours postoperatively until discharge from hospital. Atorvastatin significantly reduced the incidence of postoperative AF and postoperative peak CRP level versus placebo (18% versus 41%, P = 0.017; 129.3 ± 24.3 mg/L versus 149.3 ± 32.5 mg/L, P < 0.0001). Kaplan-Meier curves confirmed a significantly better postoperative atrial fibrillation-free survival in the statin group (χ 2 = 7.466, P = 0.006). Logistic regression analysis showed preoperative atorvastatin treatment was an independent factor associated with a significant reduction in postoperative AF (OR = 0.235, P = 0.007), whereas high postoperative CRP levels were associated with increased risk (OR = 2.421, P = 0.015). Preoperative atorvastatin administration may inhibit inflammatory reactions to prevent atrial fibrillation following coronary artery bypass grafting with cardiopulmonary bypass. (Int Heart J 2011; 52: 7-11) Key words: Coronary artery bypass grafting, Cardiopulmonary bypass, Atorvastatin, Atrial fibrillation A trial fibrillation (AF) is one of the most important complications after coronary artery bypass grafting (CABG) and has an incidence of approximately 30%.1,2) Atrial fibrillation can severely influence hemodynamic stability; it can induce loss of atrial pump function resulting in impairment of ventricular filling with a decrease in cardiac output and an increase in incidence of stroke, thus contributing to the rise of postoperative disability and mortality.3) For patients with atrial fibrillation, especially in those after CABG, a rapid ventricular rate significantly increases myocardial oxygen consumption, induces cardiac insufficiency, and aggravates myocardial ischemia; it can even lead to tachycardiomyopathy, which can severely threaten the life of the patient. Therefore, it is very important to prevent atrial fibrillation following CABG. Recent studies found that atrial fibrillation after CABG may be associated with inflammatory response, and statins have been shown to inhibit such inflammatory response, and reduce the incidence of AF after CABG. [4][5][6][7][8] Nevertheless, since atrial fibrillation has a significant genetic heterogeneity and the effects of the drugs used to treat the latter are different among different races, exploring the effects of statins on postoperative...