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4 results on '"Debora, D'Elia"'

1. Lipoprotein(a) Genotype Influences the Clinical Diagnosis of Familial Hypercholesterolemia

Author

Olmastroni, Elena, Gazzotti, Marta, Averna, Maurizio, Arca, Marcello, Tarugi, Patrizia, Calandra, Sebastiano, Bertolini, Stefano, Catapano, Alberico L, Casula, Manuela, Laura D'Erasmo, Angelo Baldassare Cefalu, Andrea Bartuli, Paola Sabrina Buonuomo, Andrea Benso, Guglielmo Beccuti, Giacomo Biasucci, Maria Elena Capra, Gianni Biolo, Pierandrea Vinci, Luca Bonanni, Claudio Borghi, Sergio D'Addato, Antonio Carlo Bossi, Giancarla Meregalli, Adriana Branchi, Paolo Calabrò, Francesca Carubbi, Fabio Nascimbeni, Francesco Cipollone, Marco Bucci, Nadia Citroni, Maria Del Ben, Francesco Baratta, Massimo Federici, Martina Montagna, Claudio Ferri, Serena Notargiacomo, Anna Maria Fiorenza, Emanuela Colombo, Giuliana Fortunato, Maria Donata Di Taranto, Andrea Giaccari, Simona Moffa, Francesco Giorgino, Sergio Di Molfetta, Ornella Guardamagna, Luisa De Sanctis, Arcangelo Iannuzzi, Raimondo Cavallaro, Gabriella Iannuzzo, Marco Gentile, Lorenzo Iughetti, Patrizia Bruzzi, Salvatore Lia, Alessandro Lupi, Giuseppe Mandraffino, Arianna Toscano, Rossella Marcucci, Martina Berteotti, Lorenzo Maroni, Fabiana Locatelli, Tiziana Montalcini, Giuliana Mombelli, Sandro Muntoni, Davide Baldera, Gianfranco Parati, Angelina Passaro, Valerio Pecchioli, Cristina Pederiva, Giuseppe Banderali, Antonio Pipolo, Debora D'Elia, Matteo Pirro, Vanessa Bianconi, Livia Pisciotta, Elena Formisano, Francesco Purrello, Roberto Scicali, Elena Repetti, Elena Cantino, Elisabetta Rinaldi, Elena Sani, Riccardo Sarzani, Francesco Spannella, Francesco Sbrana, Beatrice Dal Pino, Patrizia Suppressa, Veronica Cocco, Chiara Trenti, Emanuele Alberto Negri, Josè Pablo Werba, Alessandra Romandini, Sabina Zambon, Alberto Zambon, Maria Grazia Zenti, Giulia Fainelli, Fabio Pellegatta, Liliana Grigore, Katia Bonomo, Eleonora Capatti, Ada Cutolo, Fabio Fimiani, Simonetta Genovesi, Sandro Inchiostro, Chiara Pavanello, Roberta Pujia, Alon Schaffer, Olmastroni, Elena, Gazzotti, Marta, Averna, Maurizio, Arca, Marcello, Tarugi, Patrizia, Calandra, Sebastiano, Bertolini, Stefano, Catapano, Alberico L, Casula, Manuela, and Laura D'Erasmo, Angelo Baldassare Cefalu, Andrea Bartuli, Paola Sabrina Buonuomo, Andrea Benso, Guglielmo Beccuti, Giacomo Biasucci, Maria Elena Capra, Gianni Biolo, Pierandrea Vinci, Luca Bonanni, Claudio Borghi, Sergio D'Addato, Antonio Carlo Bossi, Giancarla Meregalli, Adriana Branchi, Paolo Calabrò, Francesca Carubbi, Fabio Nascimbeni, Francesco Cipollone, Marco Bucci, Nadia Citroni, Maria Del Ben, Francesco Baratta, Massimo Federici, Martina Montagna, Claudio Ferri, Serena Notargiacomo, Anna Maria Fiorenza, Emanuela Colombo, Giuliana Fortunato, Maria Donata Di Taranto, Andrea Giaccari, Simona Moffa, Francesco Giorgino, Sergio Di Molfetta, Ornella Guardamagna, Luisa De Sanctis, Arcangelo Iannuzzi, Raimondo Cavallaro, Gabriella Iannuzzo, Marco Gentile, Lorenzo Iughetti, Patrizia Bruzzi, Salvatore Lia, Alessandro Lupi, Giuseppe Mandraffino, Arianna Toscano, Rossella Marcucci, Martina Berteotti, Lorenzo Maroni, Fabiana Locatelli, Tiziana Montalcini, Giuliana Mombelli, Sandro Muntoni, Davide Baldera, Gianfranco Parati, Angelina Passaro, Valerio Pecchioli, Cristina Pederiva, Giuseppe Banderali, Antonio Pipolo, Debora D'Elia, Matteo Pirro, Vanessa Bianconi, Livia Pisciotta, Elena Formisano, Francesco Purrello, Roberto Scicali, Elena Repetti, Elena Cantino, Elisabetta Rinaldi, Elena Sani, Riccardo Sarzani, Francesco Spannella, Francesco Sbrana, Beatrice Dal Pino, Patrizia Suppressa, Veronica Cocco, Chiara Trenti, Emanuele Alberto Negri, Josè Pablo Werba, Alessandra Romandini, Sabina Zambon, Alberto Zambon, Maria Grazia Zenti, Giulia Fainelli, Fabio Pellegatta, Liliana Grigore, Katia Bonomo, Eleonora Capatti, Ada Cutolo, Fabio Fimiani, Simonetta Genovesi, Sandro Inchiostro, Chiara Pavanello, Roberta Pujia, Alon Schaffer

Subjects
cardiovascular risk, lipoprotein(a), familial hypercholesterolemia
Abstract

Background Evidence suggests that LPA risk genotypes are a possible contributor to the clinical diagnosis of familial hypercholesterolemia (FH). This study aimed at determining the prevalence of LPA risk variants in adult individuals with FH enrolled in the Italian LIPIGEN (Lipid Transport Disorders Italian Genetic Network) study, with (FH/M+) or without (FH/M-) a causative genetic variant. Methods and Results An lp(a) [lipoprotein(a)] genetic score was calculated by summing the number risk-increasing alleles inherited at rs3798220 and rs10455872 variants. Overall, in the 4.6% of 1695 patients with clinically diagnosed FH, the phenotype was not explained by a monogenic or polygenic cause but by genotype associated with high lp(a) levels. Among 765 subjects with FH/M- and 930 subjects with FH/M+, 133 (17.4%) and 95 (10.2%) were characterized by 1 copy of either rs10455872 or rs3798220 or 2 copies of either rs10455872 or rs3798220 (lp(a) score ≥1). Subjects with FH/M- also had lower mean levels of pretreatment low-density lipoprotein cholesterol than individuals with FH/M+ (t test for difference in means between FH/M- and FH/M+ groups

Published
2023

2. Lipoprotein(a) Genotype Influences the Clinical Diagnosis of Familial Hypercholesterolemia

Author

Olmastroni, Elena, Gazzotti, Marta, Averna, Maurizio, Arca, Marcello, Tarugi, Patrizia, Calandra, Sebastiano, Bertolini, Stefano, Catapano, Alberico L, Casula, Manuela, Laura, D'Erasmo, Angelo Baldassare Cefalù, Andrea, Bartuli, Paola Sabrina Buonuomo, Andrea, Benso, Guglielmo, Beccuti, Giacomo, Biasucci, Maria Elena Capra, Gianni, Biolo, Pierandrea, Vinci, Luca, Bonanni, Claudio, Borghi, Sergio, D'Addato, Antonio Carlo Bossi, Giancarla, Meregalli, Adriana, Branchi, Paolo, Calabrò, Francesca, Carubbi, Fabio, Nascimbeni, Francesco, Cipollone, Marco, Bucci, Nadia, Citroni, Maria Del Ben, Francesco, Baratta, Massimo, Federici, Martina, Montagna, Claudio, Ferri, Serena, Notargiacomo, Anna Maria Fiorenza, Emanuela, Colombo, Giuliana, Fortunato, Maria Donata Di Taranto, Andrea, Giaccari, Simona, Moffa, Francesco, Giorgino, Sergio Di Molfetta, Ornella, Guardamagna, Luisa De Sanctis, Arcangelo, Iannuzzi, Raimondo, Cavallaro, Gabriella, Iannuzzo, Gentile, MARCO PAOLO, Lorenzo, Iughetti, Patrizia, Bruzzi, Lia, Salvatore, Alessandro, Lupi, Giuseppe, Mandraffino, Arianna, Toscano, Rossella, Marcucci, Martina, Berteotti, Lorenzo, Maroni, Fabiana, Locatelli, Tiziana, Montalcini, Giuliana, Mombelli, Sandro, Muntoni, Davide, Baldera, Gianfranco, Parati, Angelina, Passaro, Valerio, Pecchioli, Cristina, Pederiva, Giuseppe, Banderali, Antonio, Pipolo, Debora, D'Elia, Matteo, Pirro, Vanessa, Bianconi, Livia, Pisciotta, Elena, Formisano, Purrello, Francesco, Scicali, Roberto, Elena, Repetti, Elena, Cantino, Elisabetta, Rinaldi, Elena, Sani, Riccardo, Sarzani, Francesco, Spannella, Francesco, Sbrana, Beatrice Dal Pino, Patrizia, Suppressa, Veronica, Cocco, Chiara, Trenti, Emanuele Alberto Negri, Josè Pablo Werba, Alessandra, Romandini, Sabina, Zambon, Alberto, Zambon, Maria Grazia Zenti, Giulia, Fainelli, Fabio, Pellegatta, Liliana, Grigore, Katia, Bonomo, Eleonora, Capatti, Ada, Cutolo, Fabio, Fimiani, Simonetta, Genovesi, Sandro, Inchiostro, Chiara, Pavanello, Pujia, Roberta, Alon, Schaffer, Stefano, Bertolini, Sebastiano, Calandra, Alberico Luigi Catapano, Manuela, Casula, Elena, Olmastroni, Patrizia, Tarugi, Marta, Gazzotti, and Federica, Galimberti

Subjects
cardiovascular risk, clinical diagnosis, familial hypercholesterolemia, lipoprotein(a)
Published
2023

3. Secondary Cardiovascular Prevention after Acute Coronary Syndrome: Emerging Risk Factors and Novel Therapeutic Targets

Author

Angelo Silverio, Francesco Paolo Cancro, Luca Esposito, Michele Bellino, Debora D’Elia, Monica Verdoia, Maria Giovanna Vassallo, Michele Ciccarelli, Carmine Vecchione, Gennaro Galasso, and Giuseppe De Luca

Subjects
acute coronary syndrome, coronary artery disease, emerging therapies, inflammasome, inflammation, lipoprotein(a), microbiota, secondary prevention, General Medicine
Abstract

The control of cardiovascular risk factors, the promotion of a healthy lifestyle, and antithrombotic therapy are the cornerstones of secondary prevention after acute coronary syndrome (ACS). However, many patients have recurrent ischemic events despite the optimal control of traditional modifiable risk factors and the use of tailored pharmacological therapy, including new-generation antiplatelet and lipid-lowering agents. This evidence emphasizes the importance of identifying novel risk factors and targets to optimize secondary preventive strategies. Lipoprotein(a) (Lp(a)) has emerged as an independent predictor of adverse events after ACS. New molecules such as anti-PCSK9 monoclonal antibodies, small interfering RNAs, and antisense oligonucleotides can reduce plasma Lp(a) levels and are associated with a long-term outcome benefit after the index event. The inflammatory stimulus and the inflammasome, pivotal elements in the development and progression of atherosclerosis, have been widely investigated in patients with coronary artery disease. More recently, randomized clinical trials including post-ACS patients treated with colchicine and monoclonal antibodies targeting cytokines yielded promising results in the reduction in major cardiovascular events after an ACS. Gut dysbiosis has also raised great interest for its potential pathophysiological role in cardiovascular disease. This evidence, albeit preliminary and needing confirmation by larger population-based studies, suggests the possibility of targeting the gut microbiome in particularly high-risk populations. The risk of recurrent ischemic events after ACS is related to the complex interaction between intrinsic predisposing factors and environmental triggers. The identification of novel risk factors and targets is fundamental to customizing patient clinical management with a precision medicine perspective.

Published
2023

4. Acute Coronary Syndrome in patients with SARS-CoV-2 infection: Pathophysiology and Translational Perspectives

Author

Francesco Paolo Cancro, Michele Bellino, Luca Esposito, Stefano Romei, Mario Centore, Debora D’Elia, Mario Cristiano, Angelantonio Maglio, Albino Carrizzo, Barbara Rasile, Carmine Alfano, Carmine Vecchione, and Gennaro Galasso

Subjects
General Earth and Planetary Sciences, General Environmental Science
Abstract

Acute coronary syndromes (ACS) may complicate the clinical course of patients with Coronavirus Disease 2019 (COVID-19). It is still unclear whether this condition is a direct consequence of the primary disease. However, several mechanisms including direct cellular damage, endothelial dysfunction, in-situ thrombosis, systemic inflammatory response, and oxygen supply-demand imbalance have been described in patients with COVID-19. The onset of a prothrombotic state may also be facilitated by the endothelial dysfunction secondary to the systemic inflammatory response and to the direct viral cell damage. Moreover, dysfunctional endothelial cells may enhance vasospasm and platelet aggregation. The combination of these factors promotes atherosclerotic plaque instability, thrombosis and, consequently, type 1 myocardial infarction. Furthermore, severe hypoxia due to extensive pulmonary involvement, in association with other conditions described in COVID-19 such as sepsis, tachyarrhythmias, anemia, hypotension, and shock, may lead to mismatch between oxygen supply and demand, and cause type 2 myocardial infarction. A deeper understanding of the potential pathophysiological mechanisms underlying ACS in patients with COVID-19 could help the therapeutic management of these very high-risk patients.

Published
2022

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