Device-related thrombus (DRT) is a known complication occurring in up to 7% of patients undergoing percutaneous left atrial appendage closure (LAAC). Since the target population of LAAC is generally ineligible for oral anticoagulant therapies, DRT raises important concerns. The aim of this review will be to summarize available evidence on DRT after LAAC focusing on its possible impact on outcomes. Recent findings showed a tighter association between DRT and neurological ischemic events. Antithrombotic regimen adopted after LAAC may have a protective effect against DRT. Many patient-related and procedural factors have been identified as possible predictors of DRT. A tailored approach, which takes into account DRT, is needed in the patient selection for LAAC and in the postprocedural follow-up.
Emerging evidences prove that the ongoing pandemic of coronavirus disease 2019 is strictly linked to coagulopathy even if pneumonia appears as the major clinical manifestation. The exact incidence of thromboembolic events is largely unknown, so that a relative significant number of studies have been performed in order to explore thrombotic risk in COVID-19 patients. Cytokine storm, mediated by pro-in lammatory interleukins, tumor necrosis factor α and elevated acute phase reactants, is primarily responsible for COVID-19-associated hypercoagulopathy. Also comorbidities, promoting endothelial dysfunction, contribute to a higher thromboembolic risk. In this review we aim to investigate epidemiology and clarify the pathophysiological pathways underlying hypercoagulability in COVID-19 patients, providing indications on the prevention of thromboembolic events in COVID-19. Furthermore we aim to reassume the pathophysiological paths involved in COVID-19 infection.
Aims It has already been demonstrated the efficacy of sacubitril/valsartan in the treatment of heart failure with reduced ejection fraction, but many of its properties are still unknown especially regarding its effects on endothelial dysfunction and arterial stiffness. Methods and results To this purpose, a longitudinal study involving 15 patients with dilated cardiomyopathy with reduced left ventricular ejection fraction (LVEF) was started; the purpose was collecting at the beginning and at the end of the study blood pressure measurements, transthoracic echocardiography images, parameters of endothelial function with peripheral arterial tonometry (EndoPAT®), and non-invasive evaluation of the aortic stiffness parameters by using applanation tonometry (SphygmoCor® Px system). Aortic stiffness parameters weren’t different at 6 months, compared to baseline. There was a slight, not significant increase in augmentation pressure (P = 0.889), augmentation index (P = 0.906), and sphygmic wave velocity (P = 0.263). Systolic, diastolic, and differential central arterial pressure didn’t change. RHI (reactive hyperaemia index) increased significantly after 6 months (P = 0.001) as well as augmentation index corrected for 75 b.p.m. Ejection fraction (32.21% ± 5.7 to 38.43% ± 8.4; P = 0.010) and diastolic dysfunction degree (P = 0.021) improved significantly. Mitral regurgitation improvement wasn’t statistically significant (P = 0.116). Tricuspid annular plane systolic excursion didn’t change while pulmonary systolic arterial pressure increased, although not significantly (22.83 mmHg ± 4 to 27.33 mmHg ± 6; P = 0.068) and within the normal range values. Conclusions Sacubitril/valsartan can improve endothelial function significantly in patients with dilated cardiomyopathy and reduced LVEF. It can also improve left ventricular function, mitral regurgitation, and diastolic function. Conversely, this drug seems to have no effects on vascular stiffness.
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