ObjectiveWe aimed to identify predictors of left atrial appendage (LAA) thrombus in patients with atrial fibrillation (AF) and to enhance the prognostic value of the CHA2DS2-VASc score.MethodsDerivation cohort included 1033 consecutive AF patients referred for catheter ablation or direct current cardioversion, in whom transoesophageal echocardiography (TOE) was performed prior to the procedure. Logistic regression analysis was used to identify predictors of LAA thrombus on TOE. Receiver operating characteristic (ROC) curves were constructed to compare the newly developed score with the CHA2DS2 and CHA2DS2-VASc scores in the derivation and the validation (n=320) cohort.ResultsOn TOE, LAA thrombus was present in 59 (5.7%) patients in the derivation cohort. Aside from variables encompassed by the CHA2DS2-VASc score, LAA thrombus predictors included AF type (persistent/’permanent’ vs paroxysmal) and renal dysfunction. These predictors were incorporated into the CHA2DS2-VASc score. In ROC analysis, area under the curve (AUC) for the new score (CHA2DS2-VASc-RAF score) was significantly higher (0.81) than those for the CHA2DS2 and CHA2DS2-VASc scores (0.71 and 0.70, respectively). In the validation cohort, the CHA2DS2-VASc-RAF score also performed significantly better (AUC of 0.88) than the CHA2DS2 and CHA2DS2-VASc scores (AUC of 0.63 and 0.60, respectively).ConclusionIn real-world AF patients with majority on oral anticoagulation, LAA thrombus was found in approximately 6%. Two variables not included in the CHA2DS2-VASc score (AF type and renal dysfunction) proved strong, independent predictors of LAA thrombus and might improve thromboembolic risk stratification.

INTRODUCTION    Non-vitamin K antagonist oral anticoagulants (NOACs) are an alternative to vitamin K antagonists (VKAs) for stroke prevention in atrial fibrillation (AF). OBJECTIVES    The aim of the study was to assess the incidence of left atrial appendage (LAA) thrombus and dense spontaneous echo contrast (SEC), as well as to compare the clinical characteristics of patients with AF treated with different anticoagulant regimens. PATIENTS AND METHODS    We studied 1033 consecutive patients with AF, who underwent transesophageal echocardiography (TEE) before AF ablation or cardioversion. We excluded 174 patients without any prior oral anticoagulation or who underwent bridging with heparin before TEE. RESULTS    In the study group of 859 patients (median age, 61 years; men, 66%), 437 patients (50.9%) received VKAs; 191 (22.2%), dabigatran; 230 (26.8%), rivaroxaban; and 1 patient (0.1%), apixaban. There were no differences in baseline characteristics or the incidence of LAA thrombus (VKAs, 6.9%; NOACs, 5.5%; P = 0.40) and dense SEC (VKAs, 5.3%; NOACs, 3.3%; P = 0.18) between patients on VKAs and those on NOACs. Compared with patients treated with dabigatran, those on rivaroxaban more often had paroxysmal AF, higher ejection fraction, LAA emptying velocity, and platelet count, as well as lower left ventricular end‑diastolic dimension and hematocrit. The frequency of LAA thrombus in patients receiving dabigatran and those receiving rivaroxaban was comparable (6.8% vs 4.4%; P = 0.29), while dense SEC occurred more often in patients treated with dabigatran (5.2% vs 1.7%; P = 0.06). In a logistic regression analysis, none of the oral anticoagulation regimens predicted LAA thrombus in TEE, whereas maximal LAA emptying velocity was the only parameter independently associated with the presence of thrombus. CONCLUSIONS    In the studied group of patients with AF, the choice of anticoagulation did not depend on thromboembolic or bleeding risk.

Tobacco smoking remains the main cause of tobacco-dependent diseases like lung cancer, chronic obstructive pulmonary disease (COPD), in addition to cardiovascular diseases and other cancers. Whilst the majority of smokers will not develop either COPD or lung cancer, they are closely related diseases, occurring as co-morbidities at a higher rate than if they were independently triggered by smoking. A patient with COPD has a four- to six-fold greater risk of developing lung cancer independent of smoking exposure, when compared to matched smokers with normal lung function. The 10 year risk is about 8.8% in the COPD group and only 2% in patients with normal lung function. COPD is not a uniform disorder: there are different phenotypes. One of them is manifested by the prevalence of emphysema and this is complicated by malignant processes most often. Here, we present and discuss the clinical problems of COPD in patients with lung cancer and against lung cancer in the course of COPD. There are common pathological pathways in both diseases. These are inflammation with participation of macrophages and neutrophils and proteases. It is known that anticancer immune regulation is distorted towards immunosuppression, while in COPD the elements of autoimmunity are described. Cytotoxic T cells, lymphocytes B and regulatory T cells with the important role of check point molecules are involved in both processes. A growing number of lung cancer patients are treated with immune check point inhibitors (ICIs), and it was found that COPD patients may have benefits from this treatment. Altogether, the data point to the necessity for deeper analysis and intensive research studies to limit the burden of these serious diseases by prevention and by elaboration of specific therapeutic options.