Functional LA parameters are progressively altered in AL patients according to the MC stage. A decrease in 3D-PALS is associated with worse outcome, independently of LA volume.

BackgroundMyocardial infarction (MI) has been shown to induce fibrotic remodelling of the mitral and tricuspid valves. It is unknown whether MI also induces pathological remodelling of the aortic valve and alters aortic stenosis (AS) progression. We thus compared AS progression after an acute MI and in patients with/without history of MI, and assessed post-MI pathobiological changes within the aortic valve leaflets in a sheep model.MethodsSerial echocardiograms in human patients with AS were retrospectively analysed and compared between 3 groups: (1) acute MI at baseline (n=68), (2) prior history of MI (n=45) and (3) controls without MI (n=101). Annualised progression rates of AS severity were compared between these 3 groups. In addition, aortic valves were harvested from 15 sheep: (1) induced inferior MI (n=10) and (2) controls without MI (n=5), for biological and histological analyses.ResultsIn humans, the acute MI, previous MI and control groups had comparable baseline AS severity. Indexed aortic valve area (AVAi) declined faster in the acute MI group compared with controls (−0.07±0.06 vs −0.04±0.04 cm2/m2/year; p=0.004). After adjustment, acute MI status was significantly associated with faster AVAi progression (mean difference: −0.013 (95% CI −0.023 to −0.003) cm2/m2/year, p=0.008). In the post-MI experimental animal model, aortic valve thickness and qualitative/quantitative expression of collagen were significantly increased compared with controls.ConclusionsThe results of this study suggest that AS progression is accelerated following acute MI, which could be caused by increased collagen production and thickening of the aortic valve after the ischaemic event.

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Multiple lines of Anaplastic Lymphoma Kinase (ALK) Tyrosine Kinase Inhibitors (TKIs) are recommended for the treatment of ALK-positive Non-Small Cell Lung Cancer (NSCLC). This article provides an unusual case report of a 33-year-old male patient with a 91-month Progression-Free Survival (PFS) on a first-generation TKI, crizotinib.

Introduction: Residual mitral regurgitation (MR) is associated with worse outcomes after transcatheter edge to edge mitral valve repair (TEER) but is difficult to assess by echocardiography. Shear-stress induced by MR leads to altered Von Willebrand factor activity (vWF:Act), also reflected by increased closure time with adenosine diphosphate (CT-ADP), representing potential ways to screen for residual MR. CT-ADP can be assessed easily during TEER and is known to normalize swiftly after the correction of turbulent flow. Hypothesis: The improvement of CT-ADP is quick enough to allow real-time procedural guidance. Methods: We enrolled 39 patients undergoing TEER. MR severity was assessed by echocardiography during the procedure, 24-hours and 1-month post-TEER. CT-ADP was measured before TEER, 8 minutes after each clip deployment, 1 hour and 24 hours after the procedure. CT-ADP values were related with vWF:Act and MR severity at each time point. Results: Of 39 patients after TEER, 6 (15%) and 8 (21%) patients had residual MR ≥ moderate at 24-hours and 1-month respectively. There was no significant change in CT-ADP values during the procedure. The decrease of CT-ADP was however significant 1-hour post-TEER with stable values at 24-hours (last clip deployment: 136 [110-193]; 1 hour: 99 [82-131] and 24 hours: 95 [82-121] seconds, p<0.001). Concomitant increase in vWF:Act was observed after the procedure (baseline: 1.76 [1.29-2.05]; 1 hour: 1.84 [1.79-1.85] and 24 hours: 2.32 [1.84-2.5] IU/ml, p=0.002). Patients were stratified into 3 groups according to the residual MR grade at 1 month (≤ mild vs. moderate vs. >moderate). CT-ADP was not different among the groups (p=0.74). However, the difference in CT-ADP (1 month vs baseline values) was associated with MR improvement at the same time points (r=0.50; p=0.007). Conclusions: Although CT-ADP decreases after TEER and correlates with vWF:Act and MR improvement at 1 month, this decrease is first observed 1 hour after the procedure and does not seem to be quick enough to provide real-time monitoring of MR severity during TEER.