Background: The 2016 guidelines for left ventricular diastolic dysfunction diagnosis has been simplified from previous versions; however, multiparametric diagnosis approach still exists indeterminate left ventricular diastolic dysfunction category. Left atrial (LA) strain was recently found useful to predict elevated left ventricular (LV) filling pressures noninvasively. This study aimed to (1) analyze the diagnostic value of LA strain for noninvasive assessment of LV filling pressures in patients with stable coronary artery disease (CAD) with preserved LV ejection fraction (LVEF), using invasive hemodynamic assessment as the gold standard, and (2) explore whether LA strain combined with conventional diastolic parameters could detect elevated LV filling pressures alone. Methods: Sixty-four patients with stable CAD having LVEF > 50% and 30 healthy controls were enrolled. Twodimensional speckle-tracking echocardiography was used to measure LA strain during the reservoir (LASr), conduit, and contraction phases. LV end-diastolic pressure (LVEDP), as a surrogate for LV filling pressures, was invasively obtained by left heart catheterization. Logistic regression was used to calculate the odds ratio to predict LV filling pressures. Pearson's correlation was used to analyze associations between echocardiographic parameters and LVEDP. The area under the receiver-operating characteristic curve was calculated to determine the capability of the echocardiographic parameters to detect elevated LVEDP. Inter-technique agreement was analyzed by contingency tables and tested by kappa statistics.

Elevated plasma Hcy increases the risk of LA/LAA thrombus in non-valvular AF patients with low CHA2DS2-VASc score, thus it should be taken into account in prediction of thromboembolism.

The aberrant expression of fat mass and obesity-associated protein (FTO) has been confirmed to be associated with a variety of cancers and participates in the regulation of multiple biological behaviours. FTO plays an oncogenic role in bladder cancer, but few studies have focused on how FTO promotes bladder cancer progression by regulating miRNA synthesis. Here, we confirmed that FTO expression was significantly increased in bladder cancer and was associated with a poor prognosis. FTO overexpression promoted bladder cancer cell proliferation, whereas FTO knockdown inhibited bladder cancer cell proliferation. We also demonstrated that FTO promoted bladder cancer cell proliferation via the FTO/miR-576/CDK6 pathways. Taken together, our work revealed that FTO plays a critical role in bladder cancer and could be a potential diagnostic or prognostic biomarker for this disease.