Risk factors predictive of atrial fibrillation after lung cancer surgery

Postoperative atrial fibrillation (POAF), the most frequent arrhythmia after pulmonary resection, is a cause of both morbidity and mortality. Being able to predict the risk of POAF before surgery would help us evaluate the surgical risk and plan prophylaxis. We investigated the reported preoperative risk factors associated with the incidence of POAF and found that the recommended predictive factors were quite variable. Therefore, we evaluated the previously reported preoperative risk factors for POAF using our institutional data. We discuss our findings in this short review. Male gender, resected lung volume, brain natriuretic peptide (BNP), and left ventricular early transmitral velocity/mitral annular early diastolic velocity (E/e′) calculated by echocardiography were suggested as independent predictors for POAF, but the predictive values of each individual parameter were not high. The lack of definitive predictors for POAF warrants further investigations by gathering the reported knowledge, to establish an effective preoperative examination strategy.     

Is left upper lobectomy for lung cancer a risk factor for cerebral infarction?

Purpose

Cerebral infarction is a rare complication of lung resection that can result in severe sequelae. Our aim was to investigate the characteristics of patients who suffer from cerebral infarction after surgery for lung cancer.

Methods

We retrospectively reviewed all patients who underwent resection of at least a single lobe for lung cancer at our institution between January 2008 and October 2013. We compared the patients who presented with cerebral infarction with those patients who did not within 30 days of surgery.

Results

A total of 562 patients underwent surgery, with five males and one female subsequently experiencing cerebral infarction. Five patients underwent left upper lobectomy and one underwent left lower lobectomy. Patient age, sex, body mass index, smoking index, and operative time were not significantly different between the six patients with postoperative cerebral infarction and the other 556 patients; only the type of operative procedure was significantly different (p < 0.001). Contrast-enhanced computed tomography revealed thrombosis in the stump of the left superior pulmonary vein in patients with postoperative cerebral infarction.

Conclusions

Cerebral infarction occurs at a high frequency in patients who undergo left upper lobectomy for lung cancer. Thrombosis in the left superior pulmonary-vein stump might cause cerebral infarction.

     

Bcl10 is phosphorylated on Ser138 by Ca2+/calmodulin-dependent protein kinase II

Ordered assembly of scaffold proteins Carma1-Bcl10-Malt1 determines NF-kappaB activation following T cell receptor (TCR) engagement. Carma1-Bcl10 interaction and the signaling pathway are controlled by Carma1 phosphorylation, which are induced by PKCtheta and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII). In addition to Carma1 phosphorylation, previous studies have demonstrated that Bcl10 is phosphorylated in the C-terminal Ser/Thr rich region following TCR engagement. However the kinases that phosphorylate Bcl10 are incompletely understood. Here we show that CaMKII phosphorylates Bcl10 on Ser138. Furthermore, a CaMKII inhibitor, KN93, and CaMKII siRNA substantially reduce Bcl10 phosphorylation induced by phorbol myristate acetate/ionomycin. S138A mutation prolongs Bcl10-induced NF-kappaB activation, suggesting that Bcl10 phosphorylation is involved in attenuation of NF-kappaB activation. These findings suggest that CaMKII modulates NF-kappaB activation via phosphorylating Bcl10 as well as Carma1.     

Spirometric and radiological evaluation of the remnant lung long after major pulmonary resection: can compensatory phenomena be recognized in clinical cases?

Purposes

The purpose of this study was to investigate the compensatory phenomena after lung resection in clinical cases by evaluating the spirometric and radiological parameters.

Methods

Forty patients undergoing lobectomy for stage IA lung cancer were divided into the following groups: (A) patients with <10 (n = 20) and (B) patients with ≥10 resected subsegments (n = 20). Comparisons were made of the predicted and observed postoperative values of spirometry and radiological parameters, such as lung volumetry and the “estimated lung weight”. Predicted values were based on the number of resected subsegments. The postoperative time to re-evaluation was at least 1 year for both groups.

Results

The predicted postoperative values of spirometry underestimated the actual values, and the differences were more significant in group B (forced vital capacity, p = 0.006, forced expiratory volume in 1 s, p = 0.011). Focusing on the remnant lungs on the surgical side, group B had significantly larger % postoperative lung volumes (161 ± 6.0 %) and % estimated lung weight (124 ± 5.4 %) than did group A (114 ± 3.8 %, p < 0.0001; 89.5 ± 4.4 %, p < 0.0001, respectively).

Conclusions

Major lung resection in clinical cases causes a compensatory restoration of the pulmonary function and tissue.     

Impact of Right Atrial Remodeling in Heart Failure With Preserved Ejection Fraction

BackgroundFew studies have investigated right atrial (RA) remodeling in heart failure (HF) with preserved ejection fraction (HFpEF). This study sought to characterize the RA remodeling in HFpEF and to determine its prognostic significance.Methods and ResultsPatients with HFpEF were classified based on the presence of RA enlargement (RA volume index >39 mL/m² in men and >33 mL/m² in women). Compared with patients with normal RA size (n = 234), patients with RA dilation (n = 67) showed a higher prevalence of atrial fibrillation (AF), worse right ventricular systolic function, more severe pulmonary hypertension, and a greater prevalence of mild tricuspid regurgitation, as well as impaired RA reservoir function, with increased hepatobiliary enzyme levels. AF was strongly associated with the presence of RA dilation (odds ratio [OR] 10.2, 95% confidence interval [CI] 4.00–26.1 in current AF vs no AF and odds ratio 3.38, 95% CI 1.26–9.07, earlier AF vs no AF). Patients with RA dilation had more than a two-fold increased risk of composite outcomes of all-cause mortality or HF hospitalization (adjusted hazard ratio 2.01, 95% CI 1.09–3.70, P = .02). The presence of RA dilation also displayed an additive prognostic value over left atrial dilation alone.ConclusionsThese data demonstrate that HFpEF with RA remodeling is associated with distinct echocardiographic features characterizing advanced right heart dysfunction with an increased risk of adverse outcomes.     

Increased thrombogenesity in patients with cyanotic congenital heart disease.

BACKGROUND: The basic mechanisms of thromboembolism in cyanotic congenital heart disease (CCHD) have not been well clarified. P-selectin on the platelets reflects platelet activation. Thrombomodulin is a critical cofactor for thrombin-mediated activation of protein C and reflects the anticoagulant activity of the endothelium. The present study was performed to evaluate whether platelet activation exists in patients with CCHD. METHODS AND RESULTS: Platelet P-selectin as a marker of platelet activation, plasma thrombomodulin level and protein C activity as markers of anticoagulant activity of the endothelium and thrombin - antithrombin complex III (TAT) were examined in 35 patients with CCHD. Plasma thrombomodulin level (1.1+/-0.9 vs 2.2+/-0.3 FU/ml) and protein C activity (71.1+/-29.8 vs 117.8+/-24.8%) were significantly lower in patients with CCHD as compared with the control subjects. The levels of plasma TAT (255+/-811 vs 1.9+/-0.9 ng/ml) and P-selectin on platelets (6.3 +/-4.5 vs 3.3+/-0.3 mean fluorescence intensity) were significantly higher in the patients with CCHD than in the controls. Four of the CCHD patients who experienced thromboembolic events had elevated levels of platelet P-selectin (p=0.02) compared with CCHD patients without thromboembolic events. CONCLUSION: Platelet activation exists in patients with CCHD and it may play an important role in the thromboembolic events in CCHD.     

Morphological and Immunohistochemical Changes in Intestinal Mucosa and PYY Release Following Total Colectomy with Ileal Pouch-Anal Anastomosis in Dogs

Other studies have shown that both morphologicaland functional adaptation occur in the ileal mucosaafter total colectomy and may be mediated by humoralfactors. To elucidate the participation of peptide YY (PYY) in intestinal adaptation after totalproctocolectomy with ileal pouch-anal anastomosis(IPAA), changes in the number of PYY-containing cellsand in histological appearance in the intestinal mucosa, especially in the mucosa of ileal pouch, wereinvestigated in dogs. We further examined changes inpostprandial PYY release in relation to those inPYY-containing cells. Ten adult beagle dogs underwent IPAA. Before and 2, 6, and 12 months aftersurgery, a test meal was given, and blood samples weretaken from a foreleg vein at intervals for 3 hr formeasurements of plasma PYY concentration byradioimmunoassay. Before and one year after surgery,morphological studies of the intestinal mucosa wereperformed using parameters such as villous height (VH),mucosal thickness (MT), and villous index (VI).Immunohistochemical studies of PYY were also done in the intestinalmucosa. Both fasting and postprandial plasma PYY levelswere reduced to half of the preoperative levels at twomonths after surgery. Thereafter, postprandial levels approached preoperative concentrations,while fasting levels remained unchanged. VH, MT, and VIwere significantly smaller in the ileal pouch than inthe ileal end of the controls. The MT of the ileal pouch was similar to that of the colon.PYY-containing cells in the mucosa of the ileal pouchwere distributed more densely than those in the ilealend, similar to those in the colon of the controls. It was concluded that after IPAA, the pouchmucosa gradually changed to resemble the colonic mucosanot only in histological appearance but also in thepopulation of PYY-containing cells. It is therefore considered that colonic transformation of theilealpouch mucosa is closely related to the increase inthe number of PYY-containing cells and the steadyrecovery of postprandial PYY secretion.     

Intracellular VacA Is a Valuable Marker to Predict Whether Helicobacter pylori Induces Progressive Atrophic Gastritis That Is Associated with the Development of Gastric Cancer

VacA was histochemically stained in biopsy specimen and was intracellularly and mainly located in fundic gland area. It is recognized gastric atrophy was observed in the H. pylori-positive patients with intracellular VacA compared with others. The aim of study is to understand the relationship between intracellular VacA and the progression of gastric atrophy that is associated with gastric cancer. Biopsy specimens and sera were obtained from 364 people in their 50s and 60s without gastric cancer diagnosed at first endoscopy undergoing diagnostic endoscopy, for H. pylori infection, histology, and the histochemical status of intracellular VacA using anti-VacA Ab during the follow-up period (mean, 7.3 years). Three hundred eleven of 364 enrolled patients were H. pylori positive and 53 patients were H. pylori negative at first endoscopy. VacA was intracellularly stained with vacuolation and cell destruction in the fundic gland in 98 of 311 H. pylori-positive patients and not stained in another 213 H. pylori-positive patients plus 53 H. pylori-negative patients at first endoscopy. Gastric atrophy has significantly progressed in the H. pylori-positive patints with intracellular VacA with gastric ulcers compared with the others and six gastric cancers have developed in this group during the follow-up period (mean, 7.3 years). Intracellular VacA is a valuable marker to predict whether Helicobacter pylori induces progressive atrophic gastritis that is associated with the development of gastric cancer.