Aetiologic diagnosis of coronary artery aneurysm in a patient with pancreatitis, dacryoadenitis, and sialadenitis

No abstract available

Pre-existing Psychiatric Morbidity Is Strongly Associated to Takotsubo Syndrome. A Case-Control Study

BackgroundTakotsubo syndrome (TTS) is an emerging disease characterized by an acute and reversible myocardial dysfunction which may have an influence on clinical status and prognosis. Despite extensive research, its pathophysiology has not been completely elucidated; among other hypothesis, a heart-brain interaction has been proposed. MethodsThe aim of this study was to assess the impact of psychiatric disorders and of some personality types on the pathogenesis of TTS. We conducted a retrospective observational case-control study. We enrolled a total of 50 patients, 25 with a previous diagnosis of TTS and 25 patients with a history of acute coronary syndrome (ACS), that underwent a comprehensive lifetime psychiatric assessment. ResultsWe found no significant difference between TTS and ACS patients in cardiovascular risk profile. The frequency of lifetime psychiatric disorders was significantly greater in TTS. In particular, in the univariate analysis, TTS group showed a higher prevalence of mood disorders (Major Depressive Disorder, Bipolar Disorder, Dysthymia; 16 vs. 2, P < 0.001) and anxiety disorder (Generalized Anxiety Disorder, Panic Disorder, Agoraphobia; 20 vs. 8, P = 0.001) compared with ACS group. There was also a significant tendency in TTS patients to psychotropic medication use, substance abuse, and psychologist or psychiatrist consulting. However, there was no difference between the groups in previous stressful events and Type D personality. Moreover, the multivariate analysis showed that mood disorders were independently associated with TTS (OR 16.9, 95% CI, 2.2-127). ConclusionOur study demonstrated that pre-existing anxiety disorders and mostly mood disorders were significantly higher in TTS patients than in ACS group, suggesting the role of psychiatric disorders as possible pathophysiological substrate of TTS

Circulating sST2 and catestatin levels in patients with acute worsening of heart failure: a report from the CATSTAT‐HF study

n/

Do We Need to Define Therapeutic Ranges for Edoxaban Plasma Concentration?

Do We Need to Define Therapeutic Ranges for Edoxaban Plasma Concentration

Erratum to: Pan-azole-Resistant Candida guilliermondii from a Leukemia Patient's Silent Funguria

n/

SGLT2 inhibitors and the risk of urinary tract infections in patients with heart failure: A pooled analysis examining safety endpoints

n/

Targeting prolyl-isomerase Pin1 prevents mitochondrial oxidative stress and vascular dysfunction: insights in patients with diabetes

The present study demonstrates that Pin1 is a common activator of key pathways involved in diabetic vascular disease in different experimental settings including primary human endothelial cells, knockout mice, and diabetic patients. Gene silencing and genetic disruption of Pin1 prevent hyperglycaemia-induced mitochondrial oxidative stress, endothelial dysfunction, and vascular inflammation. Moreover, we have translated our findings to diabetic patients. In line with our experimental observations, Pin1 up-regulation is associated with impaired flow-mediated dilation, increased oxidative stress, and plasma levels of adhesion molecules. In perspective, these findings may provide the rationale for mechanism-based therapeutic strategies in patients with diabete

ORal anticoagulants In fraGile patients with percutAneous endoscopic gastrostoMy and atrIal fibrillation: the (ORIGAMI) study

BACKGROUND: Randomized trials support the safety and efficacy of direct oral anticoagulants (DOACs) versus vitamin K antagonists (VKAs) in patients with nonvalvular atrial fibrillation, leading to increased use of these compounds. Crushed forms of DOACs have been shown to be reliable, but evidence supporting percutaneous endoscopic gastrostomy (PEG) delivery is lacking. PEG is a long-term option for enteral food and drug delivery in patients unable to maintain oral intake, bypassing the risks and disadvantages of parenteral nutrition.AIMS: The ORal anticoagulants In fraGile patients with percutAneous endoscopic gastrostoMy and atrIal fibrillation (ORIGAMI) study investigates the safety and efficacy of Edoxaban administered via PEG in patients with atrial fibrillation and a clinical indication for a long-term anticoagulation.DESIGN: In this prospective, single-centre observational study, 12 PEG-treated patients with indication to anticoagulation will receive edoxaban via PEG and will be followed up to 6 months. Plasma antifactor Xa activity and edoxaban concentrations will be assessed. Thromboembolic (ischaemic stroke, systemic embolism, venous thromboembolism) and bleeding events (Bleeding Academic Research Consortium and Thrombolysis in Myocardial Infarction) will be recorded at 1 and 6 months.PRELIMINARY CASES: A retrospective analysis of five atrial fibrillation cases undergoing PEG implantation at our Institution who received edoxaban via PEG showed plasma anti-FXa levels at a steady state of 146 ± 15 ng/ml, without major adverse event at a mean follow-up of 6 months.CONCLUSION: ORIGAMI prospectively investigates PEG-administration of edoxaban in PEG-treated patients requiring long-term anticoagulation. Our preliminary retrospective data support this route of DOAC administration. CLINICALTRIALS.GOV IDENTIFIER: NCT04271293

The nuclear pore protein Nup153 associates with chromatin and regulates cardiac gene expression in dystrophic mdx hearts.

Aims Beyond the control of nuclear-cytoplasmic trafficking nucleoporins regulate gene expression and are involved in cardiac diseases. Notably, a number of cardiovascular disorders have been linked to alterations in epigenetic mechanisms. Here we aimed to determine the contribution of Nup153 to the epigenetic alterations occurring in cardiomyopathy of dystrophin-deficient mdx mice (C57BL/10ScSn-Dmdmdx/J). Methods and results Nup153 was lysine-acetylated and its expression was significantly increased at protein level in mdx hearts compared with controls. Accordingly, lysine acetyl transferase (KAT) activity associated with Nup153 was higher in mdx hearts paralleling increased binding with the lysine acetylases P300/CBP-associated factor (PCAF) and p300. Interestingly, Nup153 silencing in mdx organotypic heart tissue slices caused a reduction in PCAF- and p300-specific activities. Remarkably, the level of nitric oxide (NO), which is reduced in mdx mice, was important for KAT-dependent regulation of Nup153. In fact, treatment of mdx heart tissue with an NO donor or the KAT inhibitor anacardic acid normalized Nup153 protein expression. Nup153 was recruited to chromatin and regulated the transcription of genes involved in cardiac remodelling, including the actin-binding protein nexilin. Accordingly, nexilin protein expression was abrogated by Nup153 silencing in mdx organotypic cultures. Electrophysiological and molecular experiments revealed that Nup153 overexpression in normal cardiomyocytes increases Cav1.2 calcium channel expression and function. Alterations in Nup153 protein expression and intracellular localization were also found in dystrophic cardiomyocytes derived from patient-specific induced pluripotent stem cells. Importantly, Nup153 up-regulation and increased acetylation were also found in the heart of Duchenne muscular dystrophy patients. Conclusions Our data indicate that Nup153 is an epigenetic regulator which, upon altered NO signalling, mediates the activation of genes potentially associated with early dystrophic cardiac remodelling