Association of CHADS2 and CHA2DS2-VASc Scores with Left Atrial Thrombus with Nonvalvular Atrial Fibrillation: A Single Center Based Retrospective Study in a Cohort of 2695 Chinese Subjects.

The main mechanism of the CHADS2 and CHA2DS2-VASc scores to predict stroke in nonvalvular atrial fibrillation (NVAF) is still controversial. We evaluated the association of the CHADS2 and CHA2DS2-VASc scores with left atrial thrombus (LAT) as detected by transesophageal echocardiographic (TEE) and compared the predictive ability of these risk stratification schemes with nonvalvular atrial fibrillation (NVAF). Data from 2,695 consecutive NVAF patients in whom TEE was performed for screening LAT from July 2007 to February 2014 were analyzed. Only 3% of the subjects had LAT. Presence of LAT was not significantly associated with either CHADS2 (P = 0.07) or CHA2DS2-VASc score (P = 0.12). The area under the curve (AUC) concerning LAT prediction using CHADS2 and CHA2DS2-VASc was 0.574 and 0.569, respectively. A composition model includes previous stroke or transient ischemic attack, nonparoxysmal AF, moderate to severe left ventricular systolic dysfunction, left atrial enlargement, and cardiomyopathy which improved the discrimination significantly (AUC = 0.743). In our cohort, both CHADS2 and CHA2DS2-VASc scores were of limited value for predicting LAT in patients with NVAF. This questions the CHADS2/CHA2DS2-VASc score predicting stroke mainly through the mechanism of cardiogenic embolism. A scoring scheme combining clinical and echocardiographic parameters may better predict LAT as a surrogate for cardioembolic risk in NVAF patients.

A novel rat model of chronic heart failure following myocardial infarction.

In this report, we describe an improved method for the establishment of reproducible congestive heart failure (CHF) in a rat model. The area of myocardial infarction (MI) after ligation of the left anterior descending (LAD) coronary artery was quantified. Histological changes, heart function detected by echocardiography and isolated Langendorff perfusion, and selected biochemical factors were monitored after ligation of the LAD. Contrary to previous beliefs, thoracotomy in the second intercostal space provided a much better visualization of and easier access to the LAD and significantly reduced the mortality rate. Surface electrocardiogram (ECG) showed that the S-T interval was arched raised upward immediately after ligation. Typical morphological and functional changes of CHF were observed after LAD ligation. Cardiomyocytes in the infarcted zone were depleted and deranged. Biochemical analysis and enzyme-linked immunosorbent assay (ELISA) showed that superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and nitric oxide (NO) levels were significantly lowered in rats with MI than in the normal and sham groups, whereas serum malondialdehyde (MDA), MB isoenzyme of creatine kinase (CK-MB), cardiac troponin (cTnT) and C-reactive protein (CRP) levels were elevated. After MI, N-terminal pro-brain natriuretic peptide (NT-proBNP) was increased but insulin-like growth factor I (IGF-I) and vascular endothelial growth factor (VEGF) in culture supernatant were lower than in the normal and sham groups. We present an improved model for maximal reproducibility of experimental CHF in rats which allows the study of molecular and physiological variables in relation to CHF.