bluuebunny/crossref_metadata_2025_split huggingface dataset:
701 ECMO assistance during TAVI in high-risk patient with recent COVID-19 pneumonia
Authors: Vizzari Giampiero , Ceresa Fabrizio , Mancini Nastasia , Colarusso Luigi , Perna Alessia , Paola Federico Di , Mobilia Gianni , Iannello Pietro , Patanè Francesco , Micari Antonio 
Published: December 2021

Abstract

Methods and results
A 87 years old woman, with history of dyslipidemia and permanent Atrial Fibrillation, already undergone full SARS-CoV2 vaccination few months before, referred to our E.R. with complain of dyspnoea and chest pain. COVID-19 molecular test resulted positive and CT Scan of the chest confirmed the presence of several areas of ground-glass opacity and consolidation together with bilateral pleural effusion (right 6 cm with pulmonary atelectasis; left 2 cm), not requiring drainage. Moreover, it showed severe calcification of both the aortic valve and root. Transthoracic echocardiogram showed eccentric LV hypertrophy with diffuse hypokinesia (EF 20–25%), ectatic ascending aorta (45 mm) with severe LF-LG aortic stenosis (AVAi 0.19 cm2) and moderate regurgitation, moderate-severe mitral regurgitation. During hospitalization in the COVID-19 Unit, despite O2 therapy she experienced worsening of the respiratory status with concomitant pulmonary oedema, hypotension and acute kidney injury, requiring administration of i.v. dobutamine and high dose diuretics. After gradual stabilization and COVID-19 negativization on 10th molecular test, she was transferred to our Coronary Care Unit. Coronary angiography showed absence of significant stenoses in the main vessels. In the following days the patient underwent a new clinical deterioration with dyspnoea, hypotension (BP 85/50 mmHg), oliguria and ankle swelling, requiring Ventimask O2 therapy and Dobutamine infusion. Transtoracic echocardiogram confirmed EF of 25% with PASP 30 mmHg. We decided to perform a ‘Rescue’ TAVI procedure, facilitated by extra-corporeal cardiac and respiratory support. CT Angiography of the chest, performed with low-dose contrast injection under amines infusion, showed severly calcific aortic valve with large sizes of the ring (Virtual Basal Ring area 620 mm2, perimeter 91 mm), measures compatible with the largest sizes of TAVI prostheses. After Veno-Arterial Extracorporeal Membrane Oxygenation (ECMO) cannulation, we performed the implantation of a 34 mm Evolut R (Medtronic) TAVI prosthesis, post-dilated with 24 mm balloon for under-expansion due to massive calcification. During both self-expandable TAVI delivery and balloon inflation the patient underwent two phases of cardiac arrest, during which the ECMO flow provided a proper circulatory support.

Conclusions
Since percutaneous valve replacement the patient’s recovery was fast with rapid ECMO removal and discontinuation of inotropic therapy. Few weeks after discharge, at first follow-up examination, the patient appeared asymptomatic, in excellent clinical conditions. 701 Figure
780 Appearing and disappearing right-heart thrombus: a case reporto in COVID-19 patient
Authors: Campi Giacomo , Finocchi Martina , Palagano Nicolas , Calcagno Emanuela , Pesci Alessandra , Vinci Costanza , Aspite Silvia , Cimolato Barbara , Vannucchi Vieri , Landini Giancarlo 
Published: December 2021

Abstract

Aims
Venous thromboembolism represents frequent complication of patients with severe COVID-19 disease. Several reports about atypical thrombosis are described, rarely it has been described a right venticular thrombus during the course of infection. We report a case of right endoventricular thrombosis in a patient with SARS-Cov-2 pneumonia.

Methods and results
A 58-year-old man was admitted to our ward for severe respiratory failure in interstitial pneumonia. The nasopharyngeal swab for COVID-19 resulted positive. Steroids and prophylaxis with LMWH were started, associated to CPAP to maintain good gas exchange. During hospitalization a venous ECD was performed with evidence of left popliteal thrombosis despite the therapy. d-Dimer was 4463  ng/ml. A new onset AF was documented at the telemetry, without troponin elevation. A cardiac ultrasound was performed showing a right endoventricular lesion of 1.8  cm adhering to the free wall of the right ventricle. A CT-pulmonary angiogram (CTPA) resulted negative for pulmonary embolism and confirmed suspected right ventricular thrombus. Treatment with fondaparinux 7.5 mg was started. After 10 days, cardiac ultrasound shown complete resolution of thrombosis, and CT confirmed the disappearing of the mass. Dabigatran 150  mg twice/day was started. Patient clinically improved and he was discharged after 20 days of hospitalization.

Conclusions
SARS-CoV-2 infection may cause inflammation with cytokine storm and hypercoagulability leading to venous thromboembolism. Atypical thrombus formation was reported, including right-ventricle free wall. Early caridac ultrasound was critical to make diagnosis and starting prompt treatment, therefore routine cardiac ultrasound is mandatory in severe COVID-19 patients.
260 Impact of ‘atherosclerotic pabulum’ on in hospital mortality for SARS-CoV-2 infection. Is calcium score alone enough to identify at risk patients?
Authors: Dellino Carlo Maria , Cabrelle Giulio , Previtero Marco , Continisio Saverio , Montonati Carolina , Marra Martina Perazzolo , De Conti Giorgio , Motta Raffaella , Iliceto Sabino , Pergola Valeria 
Published: December 2021

Abstract
Although the primary cause of death in COVID-19 infection is respiratory failure, there are evidences that cardiac manifestations may contribute to overall mortality and can even be the primary cause of death. More importantly, it is recognized that COVID-19 is associated with a high incidence of thrombotic complications. Two-hundred-eighty-four patients with proven SARS-CoV-2 infection who had a non-contrast Chest CT at our facility were analysed for coronary calcium score. Clinical and radiological data were retrieved. Patients with coronary calcium had higher inflammatory burden at admission (d-dimer, CRP, Procalcitonin) and higher Troponin at admission and at zenith. While there was no correlation with presence of consolidation and ground glass opacities, patients with coronary calcium had higher incidence of bilateral infiltration and higher in-hospital mortality. Peak troponin was associated with higher mortality, intensive care unit admission and mechanical ventilation in both univariable at multivariate analysis. Calcium score has demonstrated to be a good prognostic indicator for in-hospital mortality in patients with SARS-CoV-2 infection. Patients with higher atherosclerotic burden are at higher risk of fatality and complications. Our findings could have significant clinical implications in selecting at risk patients for allocation of resources especially in those with ‘atherosclerotic pabulum’, where inflammation activated by SARS-CoV-2 may play a role in fatal and non-fatal events.
405 Myopericarditis after SARS-CoV-2 MRNA vaccination: casual or causal relationship?
Authors: Golino Michele , Licciardello Claudio , Matteo Federica , Giovenzana Fulvio Lorenzo Francesco , Franzosi Cinzia , Blasi Federico , Genoni Paola , Seganfreddo Fancesca , Cadonati Cristina , Morello Matteo , Di Martino Sara Elena , Marazzato Jacopo , Angeli Fabio , De Ponti Roberto 
Published: December 2021

Abstract

Aims
Myopericarditis have been reported as rare event after SARS-CoV-2 vaccination with mRNA-1273 and BNT162b2. However, these data referred to the month of May 2021, when only a few people under the age of 30 had been vaccinated. The aim was to report cases diagnosed with myopericarditis short after vaccination admitted to our hospital.

Methods and results
An observational study was performed recording all cases of patients (pts) hospitalized for myopericarditis which occurred within 14 days of SARS-CoV-2 mRNA vaccination. From June to August 2021, 12 pts were hospitalized for myopericarditis; four of them (33%) were young male pts (29 ± 12 years old) with no history of CVDs or SARS-CoV-2 infection but with a recent second dose of Covid-19 mRNA-1273 vaccine (mean interval from the injection 3 ± 2 days). ECG showed diffuse ST-segment elevation without specularity (Figure 1). SARS-CoV-2 molecular swab tested negative; laboratory (lab) test showed a slight increase of white blood cells (11 267 ± 1047 108/l) and a marked increase of C-reactive protein (78 ± 79 mg/l), troponin T (179 ± 179 ng/l), and Nt-proBNP (876 ± 198 ng/l); transthoracic echocardiogram showed normal left ventricle ejection fraction (mean 55 ± 3%) and in one case only mild pericardial effusion; chest X-ray showed pleural effusion in one case only. Pts were then hospitalized for an average of 7 ± 2 days and an anti-inflammatory therapy based on acetylsalicylic acid and colchicine (in one case also with cortisone) was established. In the following days, pts gradually recovered and were discharged home. After 10 days, two pts underwent a cardiac magnetic resonance imaging (cMRI) revealing myocardial oedema and late gadolinium enhancement in the subepicardial and midmyocardium, along the basal and mid-apical lateral wall; due to relative contraindications, the same examination was scheduled later for the other two pts. These cases deserve specific considerations on the causal relationship between heart inflammation and SARS-CoV-2 mRNA vaccines. Among the various pathophysiological hypothesis there is the high levels of antibodies that mRNA vaccines can generate in young male subjects or the consideration of mRNA as a natural adjuvant capable of activating disproportionately the innate immune system; in both cases, the result is an immune overreaction that can affect various organs including the heart.

Conclusions
Although the number of our cases is small and all pts recovered in a short time, the timing of symptoms and the similarities in clinical findings and lab characteristics call for further investigations.
308 Sex-related differences in long COVID-19 syndrome
Authors: Pelà Giovanna , Aiello Marina , Solinas Emilia , Mantovanelli Luca , Cavalli Chiara , Tagliaferri Sara , Ranzieri Silvia , Frizzelli Annalisa , Marchi Laura , Corradi Massimo , Mori Pier Anselmo , Majori Maria , Goldoni Matteo , Chetta Alfredo 
Published: December 2021

Abstract

Aims
Sex-differences have been demonstrated in the acute phase of COVID-19 infection; females (f) were found to be less prone to develop a severe disease than males (M), but few studies have assessed sex-differences in Long-COVID-19 syndrome.

Methods and results
The aim of this prospective/retrospective study was to characterize the long-term consequences of this infection from a sex-perspective. For this purpose, we enrolled 223 patients (89 F and 134 M) who experienced a SARS-CoV-2 infection. In the acute phase of the illness, females reported more frequently than males: weakness, dysgeusia, anosmia, thoracic pain, palpitations, diarrhoea, and myalgia without significant differences in breathlessness, cough, and sleep disturbance. After a mean follow-up time of 5 months after the acute phase, females were significantly more likely than males to report weakness, thoracic pain, palpitations, and sleep disturbance but not myalgia and cough. At the multivariate logistic regression, women were statistically significantly likely to experience persistent symptoms such as dyspnoea, fatigue, chest pain, and palpitations. On the contrary, myalgia, cough and sleep disturbance were not influenced by sex.

Conclusions
We demonstrated that females were more symptomatic than males not only in the acute phase but also at follow-up. Sex was found to be an important determinant of Long-COVID syndrome because it is a significant predictor of persistent symptoms in females, such as dyspnoea, fatigue, chest pain, and palpitations. Our results suggest the need for long-term follow-up of these patients from a sex-perspective in order to implement early preventive and personalized therapeutic strategies.
724 Cardiovascular morbidity and mortality related to non-alcoholic fatty liver disease: a systematic review and meta-analysis of prospective studies
Authors: Bisaccia Giandomenico , Ricci Fabrizio , Melchiorre Eugenia , Tana Claudio , Renda Giulia , Khanji Mohammed , Fedorowski Artur , De Caterina Raffaele , Gallina Sabina 
Published: December 2021

Abstract

Aims
Whether non-alcoholic fatty liver disease (NAFLD) is a risk factor for cardiovascular (CV) events is still debated. Currently available evidence derives from non-homogeneous studies yielding conflicting results. We set out to assess the relationship between NAFLD and CV morbidity and mortality by pooling results of previous studies.

Methods
We performed a systematic review and meta-analysis of prospective observational studies published from 1966 through 2021 reporting summary-level outcome data in subjects with and without NAFLD. Adjusted risk ratios (RRs) and 95% confidence intervals (CIs) for all-cause mortality, CV mortality, myocardial infarction (MI), stroke, major adverse cerebrocardiovascular events (MACCE) and atrial fibrillation (AF) were pooled through inverse variance random-effect meta-analysis to compute the summary effect size. We performed post hoc subgroup analysis stratified by geographical region and univariate mixed-effect model meta-regression analysis to address statistical heterogeneity.

Results
We identified a total of 29 studies pooling an overall population of 5 626 573 middle-aged individuals (mean age 56 ± 8; male sex 53%; NAFLD 5.8%, n = 326 389). Mean follow-up was 10 ± 6 years. Compared with control population, presence of NAFLD was associated with similar risk of all-cause death (RR 1.17; 95% CI 0.89–1.52) and CV death (RR 0.84; 95% CI 0.64–1.10). When analysed by geographic location, pooled estimates of RR (95% CI) for all-cause death were 1.57 (1.00–2.48) for Western countries, and 0.81 (0.52–1.1.26) for Eastern countries (test for subgroup difference, P = 0.04). Meta-regression analysis showed a stronger relationship between NAFLD and all-cause mortality proportional to increasing body mass index (P = 0.048). NAFLD was associated with increased risk of myocardial infarction (RR 1.35; 95% CI 1.09–1.68), stroke (RR 1.20; 95% CI 1.06–1.35), MACCE (RR 2.09; 95% CI 1.57–2.78), and atrial fibrillation (RR 1.37; 95% CI 1.05–1.78).

Conclusion
NAFLD portends excess all-cause mortality but only in Western countries. CV mortality was similar in NAFLD and non-NAFLD groups. NAFLD is associated with increased risk of incident MI, stroke, MACCE, and AF.
738 Role of non-coding RNA uc.194 and uc.443+A in the intrastent restenosis
Authors: Boccuto Fabiola , Tammè Laura , Iaconetti Claudio , Sabatino Jolanda , Polimeni Alberto , Sorrentino Sabato , Carbone Andrea , Gareri Clarice , Mancuso Teresa , De Rosa Salvatore , Indolfi Ciro 
Published: December 2021

Abstract

Aims
Vascular smooth muscle cells (VSMCs) play a key role in the vessel wall, being active partaker in vascular remodelling and influencing multiple pathophysiological phenomena, such as progression of atherosclerosis, in-stent restenosis and vascular reactivity. Recently antisense oligonucleotides have shown promising results as a therapeutic option. The aim of this study was to analyse the expression profile and function of T-UCRs in vascular smooth muscle cells (VSMCs)—both in vitro and in vivo—and to evaluate the effects of their inhibition by the use of specific antisense oligonucleotides.

Methods
After obtaining cell cultures of vascular smooth muscle cells, we modified their phenotype varying growth conditions. A microarray and qRT-PCR expression profile analysis and a cell cycle analysis with cell proliferation/apoptosis/migration assay were performed. In vivo studies were performed on rat carotids after cell damage and administration of specific antisense oligonucleotides.

Results
There were significant differences in the expression of T-UCRs in VSMCs with a proliferating and quiescent phenotype. In particular, 5 T-UCRs were found to be upregulated in VSMCs. These types of cells were subsequently transfected with specific antisense oligonucleotides obtaining a reduction in their proliferative activity in particular with the inhibition of the T-UCRs uc.194 and uc.443 + A. MiR-10A and miR-34b-5p were identified with complementary sequences respectively to uc.194 and uc.443 + A. The increase of these miRs following the inhibition of the T-UCRs were closely related to the inhibition of the proliferative signals of VSMCs. Similarly, the same results were obtained in vivo.

Conclusions
The expression levels of non-coding RNAs uc.194 and uc. 443 + A increase in proliferating smooth muscle cells in vitro and in the vascular wall following damage, suggesting an important role of these molecules in the phenomenon of intra-stent restenosis. Through the inhibition of uc.194 and uc.443 + A using an antisense strategy, we demonstrated a reduction in cell proliferation and migration processes and, consequently, in the formation of neointima. A possible relationship was also highlighted between the aforementioned non-coding RNAs and some micro-RNAs (miR-10A and miR-34b-5p), negative regulators of the proliferative phenotype of VSMCs. The inhibition of the analysed T-UCRs would allow the maintenance of the contractile phenotype thanks to the activity of the miRs analysed in this study. Our results might pave the way for the identification of new therapeutic targets in order to prevent and reduce the incidence of intra-stent restenosis.
25 Atrial remodelling in patients affected by chronic heart failure in therapy with sacubitril/valsartan
Authors: Magnesa Michele , Mazzeo Pietro , Fortunato Martino , Mennella Raffaele , Tricarico Lucia , Correale Michele , Croella Francesca , Mallardi Adriana , Leopizzi Alessandra , Ceci Vincenzo , Alfieri Simona , Iacoviello Massimo , Biase Matteo Di , Brunetti Natale Daniele 
Published: December 2021

Abstract

Aims
Left atrial (LA) enlargement has been demonstrated to be a predictor of adverse cardiovascular outcomes, such as atrial fibrillation (AF), heart failure (HF), and cardiovascular death. Previous studies showed left ventricle ejection fraction (LVEF) improvement and reverse remodelling can be achieved after therapy with sacubitril/valsartan in real-world settings. We sought to investigate the association between left atrial (LA) structural and functional remodelling in patients with chronic HF after therapy with sacubitril/valsartan.

Methods and results
Patients affected by chronic HF with LV dysfunction (LVEF &lt; 35%), NYHA functional class II–III were followed up between September 2019 and March 2020. All patients underwent clinical and echocardiography Follow-up at baseline and after 6 months of therapy with sacubitril/valsartan. Measures of LA structure [LA end-systolic volume (LAESV)] and function [left atrial emptying fraction (LAEF), peak atrial longitudinal strain (PALS), LA conduit strain and peak atrial contraction strain (PACS)] were calculated. A total of 47 patients (median age 66 ± 7.97, male gender 85%, mean LVEF 28.33 ± 5.61%) were enrolled. The left atrial strain parameters (PALS and LA conduit) resulted higher at 6 months follow-up respect to baseline values, (14.68 ± 7.16 vs. 18.67 ± 8.03, P &lt; 0.001, and −7.61 ± 4.07 vs. −9.71 ± 5.23, P = 0.007, respectively).

Conclusions
Treatment with sacubitril/valsartan in patients with HFrEF is associated with an improvement in LA functional remodelling in a real-world scenario.
488 Candidacy for heart transplantation in adult congenital heart disease patients: a single-centre, retrospective, cohort study
Authors: D’Angelo Emanuela Concetta , Angeli Emanuela , Ragni Luca , Gargiulo Gaetano Domenico , Donti Andrea , Potena Luciano , Tonoli Federica , Bartolacelli Ylenia , Bulgarelli Ambra , Careddu Lucio , Ciuca Cristina , Zanoni Rossana , Assenza Gabriele Egidy 
Published: December 2021

Abstract

Aims
End-stage heart failure (HF) is the leading cause of death in adult congenital heart disease (ACHD) population. Heart transplantation (HTx) improves prognosis in ACHD end-stage HF but candidacy evaluation, referral pattern, and correct listing timing are not fully elucidated in this population. To evaluate factors associated to refusal from Htx in ACHD patients with end-stage HF referred for HTx evaluation.

Methods and results
This retrospective cohort study enrolled consecutive ACHD patients considered for HTx in our institution between 2014 and 2020 and patients undergone HTx between 2000 and 2013. Refusal from HTx served as primary study endpoint. Between 2014 and 2020, 46 ACHD patients were evaluated for HTx, 14 ACHD patients underwent HTx between 2001 and 2013. The main indication to HTx in patients with single ventricle physiology was Fontan failure, while in patients with systemic left ventricle and systemic right ventricle physiology, it was systemic ventricular dysfunction. We compared clinical, anatomical and demographic data of 41 patients accepted for transplantation with 15 patients refused after screening. Risk factors for refusal were: coexistence of multiple high risk features [odds ratio (OR): 3.6; 95% confidence interval (CI): 1.1–12.9; P 0.048]; anatomical factors (OR: 14.5; 95% CI: 3.1–68.4; P 0.001), out-of-centre ACHD/HTx program referral (OR: 5.3; 95% CI: 1.5 to 19.0; p 0.01). Survival in patients accepted for HTx was significantly higher than survival in patients declined from HTx with landmark comparison at 20, 40 and 60 months of 87%, 78%, and 72% vs. 70%, 59%, and 20%, respectively. HTx refusal identifies a high risk ACHD patient subgroup (hazard ratio for overall mortality: 3.1; 95% CI: 1.1–8.3; P 0.02).

Conclusions
In our study risk factors for refusal from HTx are adverse anatomical features, coexistence of multiple conventional HTx high risk factors and out-of-centre referral. ACHD patients refused from HTx present shorter time to death. Efforts to increase HTx candidacy and to reduce referral delay in tertiary centre are strongly necessary for this growing population.