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.
Coeliac disease (CD) is an autoimmune condition with a high prevalence among general population and multisystemic involvement: a more complex scene than a merely gastrointestinal disease. Therefore, an early diagnosis and treatment with a gluten-free diet is mainly important to reduce mortality and comorbidities. Together with autoimmune diseases (as Hashimoto thyroiditis, insulin-dependent diabetes mellitus, autoimmune liver disease and connective tissue diseases), also an accelerated progression of atherosclerosis and a higher prevalence of heart disease have been reported in coeliacs. In the present paper we tried to collect from literature the emergent data on the probable relationship between coeliac and cardiovascular disease, focusing on pathophysiological bases of vascular injury. Data and opinions on the development of cardiovascular risk in patients with CD are conflicting. However, the major evidence supports the theory of an increased cardiovascular risk in CD, due to many mechanisms of myocardial injury, such as chronic malabsorption, abnormalities of intestinal permeability, and direct immune response against self-proteins. The conclusions that come from these data suggest the utility of a careful cardiovascular follow up in coeliac patients.
Mitral annular disjunction (MAD) is a structural abnormality of the mitral annulus, defined by a detachment of the atrial wall-mitral valvular junction from the left ventricular (LV) free wall. This structural abnormality in mitral annulus fibrosus is significantly associated with the presence of mitral valve prolapse (MVP) [1], but it can be also detected in normal cases as an anatomical variation of the mitral annulus fibrosus [2]. The main tools to detect MAD are echocardiography and cardiac magnetic resonance. Prevalence of MAD in the general population ranges from 7% [1] to 9% [2]. Several studies proved an association between MAD and arrhythmic events, independently of concomitant mitral valve abnormalities, suggesting the existence of a novel entity: MAD arrhythmic syndrome [3]. Herein we describe a case report of a middle age man with MAD who experienced ventricular arrhythmias and placement of an implantable cardioverter-defibrillator (ICD).
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