Telemedicine-guided very low-dose INR self-control is comparable with low-dose INR in thrombotic risk, and is superior in bleeding risk. Weekly testing is sufficient. Given the small number of MVR and DVR patients, results are only valid for AVR patients.
Calcific aortic stenosis (CAS) is the most common valvular disease in Western countries. Histological findings in patients with CAS extremely resemble those of atherosclerosis and include accumulation and modification of lipoproteins, inflammation, extracellular matrix remodeling, and calcification. Angiogenesis is another prominent feature of CAS; however, there is only a limited amount of data available regarding the mechanisms behind the pathological neovascularization of a structure that is originally avascular. The present study aims to identify the molecular basis that regulates blood vessel growth in stenotic aortic valves, focusing on the role of HIF-1α and VEGF pathway. A total of 19 native degenerating aortic valves obtained at valve replacement surgery have been processed for Western blot, immunohistochemical, morphometric, and ultrastructural analyses. First, we have demonstrated the adverse ECM remodeling and the significant thickening of the leaflet also showing that HIF-1α and VEGF are significantly upregulated in the stenotic valves, are locally produced and colocalize with angiogenesis and areas of calcification. Next, we have characterized, for the first time to the best of our knowledge, the morphological features of the neovasculature evidencing the presence of intact blood vessels in close proximity to the mineralized zones. These results suggest that the complex structural remodeling of the matrix might reduce oxygen availability in the valve cusp contributing to the stabilization of HIF-1α that in turn induces a metabolic adaptation through the upregulation of VEGF and the formation of new blood vessels not only to overcome the hypoxic state but also to sustain the calcification process.
Background:There are few comparative reports on the overall accuracy of neural networks (NN), assessed only versus multiple logistic regression (LR), to predict events in cardiovascular surgery studies and none has been performed among acute aortic dissection (AAD) Type A patients.Objectives:We aimed at investigating the predictive potential of 30-day mortality by a large series of risk factors in AAD Type A patients comparing the overall performance of NN versus LR.Methods:We investigated 121 plus 87 AAD Type A patients consecutively operated during 7 years in two Centres. Forced and stepwise NN and LR solutions were obtained and compared, using receiver operating characteristic area under the curve (AUC) and their 95% confidence intervals (CI) and Gini’s coefficients. Both NN and LR models were re-applied to data from the second Centre to adhere to a methodological imperative with NN.Results:Forced LR solutions provided AUC 87.9±4.1% (CI: 80.7 to 93.2%) and 85.7±5.2% (CI: 78.5 to 91.1%) in the first and second Centre, respectively. Stepwise NN solution of the first Centre had AUC 90.5±3.7% (CI: 83.8 to 95.1%). The Gini’s coefficients for LR and NN stepwise solutions of the first Centre were 0.712 and 0.816, respectively. When the LR and NN stepwise solutions were re-applied to the second Centre data, Gini’s coefficients were, respectively, 0.761 and 0.850. Few predictors were selected in common by LR and NN models: the presence of pre-operative shock, intubation and neurological symptoms, immediate post-operative presence of dialysis in continuous and the quantity of post-operative bleeding in the first 24 h. The length of extracorporeal circulation, post-operative chronic renal failure and the year of surgery were specifically detected by NN.Conclusions:Different from the International Registry of AAD, operative and immediate post-operative factors were seen as potential predictors of short-term mortality. We report a higher overall predictive accuracy with NN than with LR. However, the list of potential risk factors to predict 30-day mortality after AAD Type A by NN model is not enlarged significantly.
A postoperative serum PCT concentration of >0.5 ng/mL is highly suggestive of a postoperative complication. CRP changes do not contribute to predictive information.
The major finding of our study is that patient-prosthesis mismatch does not affect left ventricular mass regression in patients older than 65 with pure aortic stenosis who underwent mechanical aortic valve replacement. In older patients with low cardiac output requirements, even a small change in the valve effective orifice area after aortic valve replacement with modern efficient mechanical prosthesis, will result in a marked reduction of pressure gradient and this will be associated with a significant regression of left ventricular mass.
BackgroundThere are few long-term mortality prediction studies after acute aortic dissection (AAD) Type A and none were performed using new models such as neural networks (NN) or support vector machines (SVM) which may show a higher discriminatory potency than standard multivariable models.MethodsWe used 32 risk factors identified by Literature search and previously assessed in short-term outcome investigations. Models were trained (50%) and validated (50%) on 2 random samples from a consecutive 235-patient cohort. NN were run only on patients with complete data for all included variables (N = 211); SVM on the overall group. Discrimination was assessed by receiver operating characteristic area under the curve (AUC) and Gini's coefficients along with classification performance.ResultsThere were 84 deaths (36%) occurring at 564 ± 48 days (95%CI from 470 to 658 days). Patients with complete variables had a slightly lower death rate (60 of 211, 28%). NN classified 44 of 60 (73%) dead patients and 147 of 151 (97%) long-term survivors using 5 covariates: immediate post-operative chronic renal failure, circulatory arrest time, the type of surgery on ascending aorta plus hemi-arch, extracorporeal circulation time and the presence of Marfan habitus. Global accuracies of training and validation NN were excellent with AUC respectively 0.871 and 0.870 but classification errors were high among patients who died. Training SVM, using a larger number of covariates, showed no false negative or false positive cases among 118 randomly selected patients (error = 0%, AUC 1.0) whereas validation SVM, among 117 patients, provided 5 false negative and 11 false positive cases (error = 22%, AUC 0.821, p < 0.01 versus NN results). An html file was produced to adopt and manipulate the selected parameters for practical predictive purposes.ConclusionsBoth NN and SVM accurately selected a few operative and immediate post-operative factors and the Marfan habitus as long-term mortality predictors in AAD Type A. Although these factors were not new per se, their combination may be used in practice to index death risk post-operatively with good accuracy.
The hallmarks of calcific aortic valve disease (CAVD) are the significant quantitative and qualitative changes that occur in the extracellular matrix (ECM), which ultimately lead to increased leaflet stiffness and obstruction of left ventricular outflow. Mounting evidence suggests that ECM remodeling not only contribute to valve cell dysfunction but also alter certain cell signaling pathways responsible for the initiation and progression of the disease state. Matrix metalloproteinases (MMPs), collectively called matrixins, are a family of enzymes known to participate in numerous ECM remodeling events during embryonic development and in disease. The aim of the present study was to evaluate whether changes in MMP-9 expression might be involved in the pathophysiology of CAVD. For this purpose, we have analyzed a total of 19 pathologic valves from patients who underwent aortic valve replacement for calcific aortic stenosis. Microscopically, the cusp tissue showed diffuse fibrosis, neovascularization, and abnormal ECM remodeling with collagen disorganization and mineralization. Western blot and immunohistochemical analyses have been performed on both the areas overlying and remote from the mineral deposits. Protein expression data evidenced a significant upregulation of MMP-9 in the calcified lesion area. Consistent with these observations, immunohistochemistry demonstrated that MMP-9 protein was almost exclusively localized near or around the mineralized nodules, whereas was generally quite weak or absent in areas devoid of any calcification. Our data suggest that MMP-9 may play a key role in CAVD probably by promoting the fibrotic and procalcific remodeling of the ECM.
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