Incidence and predictors of thrombotic complications in 4742 patients with COVID-19 or other acute infectious respiratory diseases: A propensity score-matched study

Background. A prothrombotic state, attributable to excessive inflammation, cytokine storm, hypoxia, and immobilization, is a feature of SARS-CoV-2 infection. Up to 30% of patients with severe COVID-19 remain at high risk of thromboembolic events despite anticoagulant administration, with adverse impact on in-hospital prognosis. Methods. We retrospectively studied 4742 patients with acute infectious respiratory disease (AIRD); 2579 were diagnosed to have COVID-19 and treated with heparin, whereas 2163 had other causes of AIRD. We compared the incidence and predictors of total, arterial, and venous thrombosis, both in the whole population and in a propensity score-matched subpopulation of 3036 patients (1518 in each group). Results. 271 thrombotic events occurred in the whole population: 121 (4.7%) in the COVID-19 group and 150 (6.9%) in the no-COVID-19 group (p < 0.001). No differences in the incidence of total (p = 0.11), arterial (p = 0.26), and venous (p = 0.38) thrombosis were found between the two groups after adjustment for confounding clinical variables and in the propensity score-matched subpopulation. Likewise, there were no significant differences in bleeding rates between the two groups. Clinical predictors of arterial thrombosis included age (p = 0.006), diabetes mellitus (p = 0.034), peripheral artery disease (p < 0.001), and previous stroke (p < 0.001), whereas history of solid cancer (p < 0.001) and previous deep vein thrombosis (p = 0.007) were associated with higher incidence of venous thrombosis. Conclusions. Hospitalized patients with COVID-19 treated with heparin do not seem to show significant differences in the cumulative incidence of thromboembolic events as well as in the incidence of arterial and venous thrombosis separately, compared with AIRD patients with different etiological diagnosis

Restricted T-Cell Repertoire in the Epicardial Adipose Tissue of Non-ST Segment Elevation Myocardial Infarction Patients

Aims: Human epicardial adipose tissue, a dynamic source of multiple bioactive factors, holds a close functional and anatomic relationship with the epicardial coronary arteries and communicates with the coronary artery wall through paracrine and vasocrine secretions. We explored the hypothesis that T-cell recruitment into epicardial adipose tissue (EAT) in patients with non-ST segment elevation myocardial infarction (NSTEMI) could be part of a specific antigen-driven response implicated in acute coronary syndrome onset and progression. Methods and Results: We enrolled 32 NSTEMI patients and 34 chronic coronary syndrome (CCS) patients undergoing coronary artery bypass grafting (CABG) and 12 mitral valve disease (MVD) patients undergoing surgery. We performed EAT proteome profiling on pooled specimens from three NSTEMI and three CCS patients. We performed T-cell receptor (TCR) spectratyping and CDR3 sequencing in EAT and peripheral blood mononuclear cells of 29 NSTEMI, 31 CCS, and 12 MVD patients. We then used computational modeling studies to predict interactions of the TCR beta chain variable region (TRBV) and explore sequence alignments. The EAT proteome profiling displayed a higher content of pro-inflammatory molecules (CD31, CHI3L1, CRP, EMPRINN, ENG, IL-17, IL-33, MMP-9, MPO, NGAL, RBP-4, RETN, VDB) in NSTEMI as compared to CCS (P < 0.0001). CDR3-beta spectratyping showed a TRBV21 enrichment in EAT of NSTEMI (12/29 patients; 41%) as compared with CCS (1/31 patients; 3%) and MVD (none) (ANOVA for trend P < 0.001). Of note, 11/12 (92%) NSTEMI patients with TRBV21 perturbation were at their first manifestation of ACS. Four patients with the first event shared a distinctive TRBV21-CDR3 sequence of 178 bp length and 2/4 were carriers of the human leukocyte antigen (HLA)-A*03:01 allele. A 3D analysis predicted the most likely epitope able to bind HLA-A3*01 and interact with the TRBV21-CDR3 sequence of 178 bp length, while the alignment results were consistent with microbial DNA sequences. Conclusions: Our study revealed a unique immune signature of the epicardial adipose tissue, which led to a 3D modeling of the TCRBV/peptide/HLA-A3 complex, in acute coronary syndrome patients at their first event, paving the way for epitope-driven therapeutic strategies

Single-center experience in percutaneous closure of arterial duct with Amplatzer duct Occluder II additional sizes

Objectives: This study aimed to report a large, single-center experience of percutaneous arterial duct (AD) closure using Amplatzer Duct Occluder II Additional Sizes device (ADO II-AS)(St. Jude Medical Corp, St. Paul, MN, USA). Background: Transcatheter closure of AD remains challenging in low body weight patients and those who have a persisting shunt following a previous attempt at interventional closure. Recent technical advances in device design may address these issues. Methods: From May 2011 to April 2016, 109 patients underwent attempted percutaneous closure of AD with ADO II-AS at our Institution. Mean age and weight were 4.8 ± 8.1 years (range 0-48) and 21.4 ± 20.6 kg (range 3-93), respectively. Fifteen patients (13.8%) were ≤6 kg (age 3.5 ± 2.0 months; weight 4.7 ± 1.1 kg). Arterial duct morphology was type A in 62 (57%), type B in 1 (1%), type C in 32 (29%), type D in 7 (6%) and type E in 6 patients (6%), respectively. Arterial approach was used to negotiate and deploy the occluding device in 103 patients (94.5%). Results: AD diameter was 2.2 ± 0.6 (range 1.5–4.5) resulting in QP/QS of 1.9 ± 0.7 (range 1-3.3). Mean pulmonary artery pressure and PA/aortic pressure ratio were 19.3 ± 5.0 mm Hg (range 12-38) and 0.34 ± 0.14 (range 0.14-0.95), respectively. Successful device deployment was achieved in 107 patients (98.2%). Neither procedural morbidity nor mortality was recorded. Immediate, 24h and mid-term (30 ± 17 months) complete occlusion was recorded in 71%, 98.1%, and 100% of patients, respectively. Conclusion: In our experience, trans-catheter closure of AD of different sizes and morphologies using ADO II-AS is highly feasible, safe and effective also in challenging anatomic/clinical settings. © 2016 Wiley Periodicals, Inc