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3. Rationale and design of the CV-PREVITAL study: an Italian multiple cohort randomised controlled trial investigating innovative digital strategies in primary cardiovascular prevention

Author

Baldassarre, D, Iacoviello, L, Baetta, R, Roncaglioni, M, Condorelli, G, Remuzzi, G, Gensini, G, Frati, L, Ricciardi, W, Conaldi, P, Uccelli, A, Blandini, F, Bosari, S, Scambia, G, Fini, M, Di Malta, A, Amato, M, Veglia, F, Bonomi, A, Klersy, C, Colazzo, F, Pengo, M, Gorini, F, Auteri, L, Ferrante, G, Baviera, M, Ambrosio, G, Catapano, A, Gialluisi, A, Malavazos, A, Castelvecchio, S, Corsi-Romanelli, M, Cardani, R, La Rovere, M, Agnese, V, Pane, B, Prati, D, Spinardi, L, Liuzzo, G, Arbustini, E, Volterrani, M, Visconti, M, Werba, J, Genovese, S, Bilo, G, Invitti, C, Di Blasio, A, Lombardi, C, Faini, A, Rosa, D, Ojeda-Fernandez, L, Foresta, A, De Curtis, A, Di Castelnuovo, A, Scalvini, S, Pierobon, A, Gorini, A, Valenti, L, Luzi, L, Racca, A, Bandi, M, Tremoli, E, Menicanti, L, Parati, G, Pompilio, G, Colombo, G, Vavassori, C, Biondi, M, Frigerio, B, Ravani, A, Sansaro, D, Coggi, D, Romandini, A, Giroli, M, Giuliani, M, Bonmi, A, Rondinelli, M, Trudu, C, Cinieri, C, Monturano, M, Colazo, F, Inviti, C, Di Blasi, A, Torlasco, C, Gilardini, L, Soranna, D, Zambon, A, Perger, E, Zanotti, L, Badano, L, Cova, L, Gentilini, D, Grappiolo, L, Condoreli, G, Ferante, G, Papa, L, Savevski, V, Ieva, F, Romano, I, Remzzi, G, Ojeda, L, Clerici, F, Palumbo, A, Genini, G, Catpano, A, Mattioli, R, Longhi, E, Mantovani, L, Madotto, F, Bonaccio, M, Gianfagna, F, Ghulam, A, Magnacca, S, Noro, F, Costanzo, S, Esposito, S, Orlandi, S, Persichillo, M, Bracone, F, Panzera, T, Ruggiero, E, Parisi, R, Franciosa, S, Morelli, M, De Rita, F, Cerletti, C, de Gaetano, G, Donati, M, Mencanti, L, Romanelli, M, Cerri, A, Dubini, C, Trevisan, M, Renna, L, Milani, V, Boveri, S, Giubbilini, P, Ramputi, L, Baroni, I, De Angeli, G, Riciardi, W, Olmetti, F, Bussotti, M, Gaetano, C, Baiardi, P, Bachetti, T, Balbi, M, Comini, L, Lorenzoni, M, Olivares, A, Traversi, E, Garre, C, Sideri, R, Clemenza, F, Gentile, G, Caruana, G, Cuscino, N, Di Gesaro, G, Greco, A, Loddo, I, Tuzzolino, F, Ucelli, A, Palombo, D, Spinella, G, Mozzetta, G, Ameri, P, Zoppoli, G, Finotello, A, Porto, I, Pratesi, G, Bladini, F, Spnardi, L, Clerici, M, Pelusi, S, Bianco, C, Carpani, R, Periti, G, Margarita, S, Lanza, G, Severino, A, Pedicino, D, D'Amario, D, D'Aiello, A, Vinci, R, Bonanni, A, Brecciaroli, M, Filomia, S, Pastorino, R, Boccia, S, Urbani, A, Sanguinetti, M, Santoliquido, A, Proto, L, Tarquini, D, Grimaldi, M, Leonardi, S, Elia, A, Currao, A, Urtis, M, Di Toro, A, Giuliani, L, Caminiti, G, Marcolongo, F, Sposato, B, Guadagni, F, Morsella, V, Marziale, A, Protti, G, Baldassarre D., Iacoviello L., Baetta R., Roncaglioni M. C., Condorelli G., Remuzzi G., Gensini G., Frati L., Ricciardi W., Conaldi P. G., Uccelli A., Blandini F., Bosari S., Scambia G., Fini M., Di Malta A., Amato M., Veglia F., Bonomi A., Klersy C., Colazzo F., Pengo M., Gorini F., Auteri L., Ferrante G., Baviera M., Ambrosio G., Catapano A., Gialluisi A., Malavazos A. E., Castelvecchio S., Corsi-Romanelli M. M., Cardani R., La Rovere M. T., Agnese V., Pane B., Prati D., Spinardi L., Liuzzo G., Arbustini E., Volterrani M., Visconti M., Werba J. P., Genovese S., Bilo G., Invitti C., Di Blasio A., Lombardi C., Faini A., Rosa D., Ojeda-Fernandez L., Foresta A., De Curtis A., Di Castelnuovo A., Scalvini S., Pierobon A., Gorini A., Valenti L., Luzi L., Racca A., Bandi M., Tremoli E., Menicanti L., Parati G., Pompilio G., Colombo G., Vavassori C., Biondi M. L., Frigerio B., Ravani A., Sansaro D., Coggi D., Romandini A., Giroli M., Giuliani M., Bonmi A., Rondinelli M., Trudu C., Cinieri C., Monturano M., Colazo F., Inviti C., Di Blasi A., Torlasco C., Gilardini L., Soranna D., Zambon A., Perger E., Zanotti L., Badano L., Cova L., Gentilini D., Grappiolo L., Condoreli G., Ferante G., Papa L., Savevski V., Ieva F., Romano I., Remzzi G., Ojeda L., Clerici F., Palumbo A., Genini G. F., Catpano A., Mattioli R., Longhi E., Mantovani L. G., Madotto F., Bonaccio M., Gianfagna F., Ghulam A., Magnacca S., Noro F., Costanzo S., Esposito S., Orlandi S., Persichillo M., Bracone F., Panzera T., Ruggiero E., Parisi R., Franciosa S., Morelli M., De Rita F., Cerletti C., de Gaetano G., Donati M. B., Mencanti L., Romanelli M. M. C., Cerri A., Dubini C., Trevisan M. B., Renna L. V., Milani V., Boveri S., Giubbilini P., Ramputi L., Baroni I., De Angeli G., Riciardi W., Olmetti F., Bussotti M., Gaetano C., Baiardi P., Bachetti T., Balbi M., Comini L., Lorenzoni M., Olivares A., Traversi E., Garre C., Sideri R., Clemenza F., Gentile G., Caruana G., Cuscino N., Di Gesaro G., Greco A., Loddo I., Tuzzolino F., Ucelli A., Palombo D., Spinella G., Mozzetta G., Ameri P., Zoppoli G., Finotello A., Porto I., Pratesi G., Bladini F., Spnardi L., Clerici M., Pelusi S., Bianco C., Carpani R., Periti G., Margarita S., Lanza G. A., Severino A., Pedicino D., D'Amario D., D'Aiello A., Vinci R., Bonanni A., Brecciaroli M., Filomia S., Pastorino R., Boccia S., Urbani A., Sanguinetti M., Santoliquido A., Proto L., Tarquini D., Grimaldi M. C., Leonardi S., Elia A., Currao A., Urtis M., Di Toro A., Giuliani L., Caminiti G., Marcolongo F., Sposato B., Guadagni F., Morsella V., Marziale A., Protti G., Baldassarre, D, Iacoviello, L, Baetta, R, Roncaglioni, M, Condorelli, G, Remuzzi, G, Gensini, G, Frati, L, Ricciardi, W, Conaldi, P, Uccelli, A, Blandini, F, Bosari, S, Scambia, G, Fini, M, Di Malta, A, Amato, M, Veglia, F, Bonomi, A, Klersy, C, Colazzo, F, Pengo, M, Gorini, F, Auteri, L, Ferrante, G, Baviera, M, Ambrosio, G, Catapano, A, Gialluisi, A, Malavazos, A, Castelvecchio, S, Corsi-Romanelli, M, Cardani, R, La Rovere, M, Agnese, V, Pane, B, Prati, D, Spinardi, L, Liuzzo, G, Arbustini, E, Volterrani, M, Visconti, M, Werba, J, Genovese, S, Bilo, G, Invitti, C, Di Blasio, A, Lombardi, C, Faini, A, Rosa, D, Ojeda-Fernandez, L, Foresta, A, De Curtis, A, Di Castelnuovo, A, Scalvini, S, Pierobon, A, Gorini, A, Valenti, L, Luzi, L, Racca, A, Bandi, M, Tremoli, E, Menicanti, L, Parati, G, Pompilio, G, Colombo, G, Vavassori, C, Biondi, M, Frigerio, B, Ravani, A, Sansaro, D, Coggi, D, Romandini, A, Giroli, M, Giuliani, M, Bonmi, A, Rondinelli, M, Trudu, C, Cinieri, C, Monturano, M, Colazo, F, Inviti, C, Di Blasi, A, Torlasco, C, Gilardini, L, Soranna, D, Zambon, A, Perger, E, Zanotti, L, Badano, L, Cova, L, Gentilini, D, Grappiolo, L, Condoreli, G, Ferante, G, Papa, L, Savevski, V, Ieva, F, Romano, I, Remzzi, G, Ojeda, L, Clerici, F, Palumbo, A, Genini, G, Catpano, A, Mattioli, R, Longhi, E, Mantovani, L, Madotto, F, Bonaccio, M, Gianfagna, F, Ghulam, A, Magnacca, S, Noro, F, Costanzo, S, Esposito, S, Orlandi, S, Persichillo, M, Bracone, F, Panzera, T, Ruggiero, E, Parisi, R, Franciosa, S, Morelli, M, De Rita, F, Cerletti, C, de Gaetano, G, Donati, M, Mencanti, L, Romanelli, M, Cerri, A, Dubini, C, Trevisan, M, Renna, L, Milani, V, Boveri, S, Giubbilini, P, Ramputi, L, Baroni, I, De Angeli, G, Riciardi, W, Olmetti, F, Bussotti, M, Gaetano, C, Baiardi, P, Bachetti, T, Balbi, M, Comini, L, Lorenzoni, M, Olivares, A, Traversi, E, Garre, C, Sideri, R, Clemenza, F, Gentile, G, Caruana, G, Cuscino, N, Di Gesaro, G, Greco, A, Loddo, I, Tuzzolino, F, Ucelli, A, Palombo, D, Spinella, G, Mozzetta, G, Ameri, P, Zoppoli, G, Finotello, A, Porto, I, Pratesi, G, Bladini, F, Spnardi, L, Clerici, M, Pelusi, S, Bianco, C, Carpani, R, Periti, G, Margarita, S, Lanza, G, Severino, A, Pedicino, D, D'Amario, D, D'Aiello, A, Vinci, R, Bonanni, A, Brecciaroli, M, Filomia, S, Pastorino, R, Boccia, S, Urbani, A, Sanguinetti, M, Santoliquido, A, Proto, L, Tarquini, D, Grimaldi, M, Leonardi, S, Elia, A, Currao, A, Urtis, M, Di Toro, A, Giuliani, L, Caminiti, G, Marcolongo, F, Sposato, B, Guadagni, F, Morsella, V, Marziale, A, Protti, G, Baldassarre D., Iacoviello L., Baetta R., Roncaglioni M. C., Condorelli G., Remuzzi G., Gensini G., Frati L., Ricciardi W., Conaldi P. G., Uccelli A., Blandini F., Bosari S., Scambia G., Fini M., Di Malta A., Amato M., Veglia F., Bonomi A., Klersy C., Colazzo F., Pengo M., Gorini F., Auteri L., Ferrante G., Baviera M., Ambrosio G., Catapano A., Gialluisi A., Malavazos A. E., Castelvecchio S., Corsi-Romanelli M. M., Cardani R., La Rovere M. T., Agnese V., Pane B., Prati D., Spinardi L., Liuzzo G., Arbustini E., Volterrani M., Visconti M., Werba J. P., Genovese S., Bilo G., Invitti C., Di Blasio A., Lombardi C., Faini A., Rosa D., Ojeda-Fernandez L., Foresta A., De Curtis A., Di Castelnuovo A., Scalvini S., Pierobon A., Gorini A., Valenti L., Luzi L., Racca A., Bandi M., Tremoli E., Menicanti L., Parati G., Pompilio G., Colombo G., Vavassori C., Biondi M. L., Frigerio B., Ravani A., Sansaro D., Coggi D., Romandini A., Giroli M., Giuliani M., Bonmi A., Rondinelli M., Trudu C., Cinieri C., Monturano M., Colazo F., Inviti C., Di Blasi A., Torlasco C., Gilardini L., Soranna D., Zambon A., Perger E., Zanotti L., Badano L., Cova L., Gentilini D., Grappiolo L., Condoreli G., Ferante G., Papa L., Savevski V., Ieva F., Romano I., Remzzi G., Ojeda L., Clerici F., Palumbo A., Genini G. F., Catpano A., Mattioli R., Longhi E., Mantovani L. G., Madotto F., Bonaccio M., Gianfagna F., Ghulam A., Magnacca S., Noro F., Costanzo S., Esposito S., Orlandi S., Persichillo M., Bracone F., Panzera T., Ruggiero E., Parisi R., Franciosa S., Morelli M., De Rita F., Cerletti C., de Gaetano G., Donati M. B., Mencanti L., Romanelli M. M. C., Cerri A., Dubini C., Trevisan M. B., Renna L. V., Milani V., Boveri S., Giubbilini P., Ramputi L., Baroni I., De Angeli G., Riciardi W., Olmetti F., Bussotti M., Gaetano C., Baiardi P., Bachetti T., Balbi M., Comini L., Lorenzoni M., Olivares A., Traversi E., Garre C., Sideri R., Clemenza F., Gentile G., Caruana G., Cuscino N., Di Gesaro G., Greco A., Loddo I., Tuzzolino F., Ucelli A., Palombo D., Spinella G., Mozzetta G., Ameri P., Zoppoli G., Finotello A., Porto I., Pratesi G., Bladini F., Spnardi L., Clerici M., Pelusi S., Bianco C., Carpani R., Periti G., Margarita S., Lanza G. A., Severino A., Pedicino D., D'Amario D., D'Aiello A., Vinci R., Bonanni A., Brecciaroli M., Filomia S., Pastorino R., Boccia S., Urbani A., Sanguinetti M., Santoliquido A., Proto L., Tarquini D., Grimaldi M. C., Leonardi S., Elia A., Currao A., Urtis M., Di Toro A., Giuliani L., Caminiti G., Marcolongo F., Sposato B., Guadagni F., Morsella V., Marziale A., and Protti G.

Abstract

Introduction Prevention of cardiovascular disease (CVD) is of key importance in reducing morbidity, disability and mortality worldwide. Observational studies suggest that digital health interventions can be an effective strategy to reduce cardiovascular (CV) risk. However, evidence from large randomised clinical trials is lacking. Methods and analysis The CV-PREVITAL study is a multicentre, prospective, randomised, controlled, open-label interventional trial designed to compare the effectiveness of an educational and motivational mobile health (mHealth) intervention versus usual care in reducing CV risk. The intervention aims at improving diet, physical activity, sleep quality, psycho-behavioural aspects, as well as promoting smoking cessation and adherence to pharmacological treatment for CV risk factors. The trial aims to enrol approximately 80 000 subjects without overt CVDs referring to general practitioners' offices, community pharmacies or clinics of Scientific Institute for Research, Hospitalization and Health Care (Italian acronym IRCCS) affiliated with the Italian Cardiology Network. All participants are evaluated at baseline and after 12 months to assess the effectiveness of the intervention on short-term endpoints, namely improvement in CV risk score and reduction of major CV risk factors. Beyond the funded life of the study, a long-term (7 years) follow-up is also planned to assess the effectiveness of the intervention on the incidence of major adverse CV events. A series of ancillary studies designed to evaluate the effect of the mHealth intervention on additional risk biomarkers are also performed. Ethics and dissemination This study received ethics approval from the ethics committee of the coordinating centre (Monzino Cardiology Center; R1256/20-CCM 1319) and from all other relevant IRBs and ethics committees. Findings are disseminated through scientific meetings and peer-reviewed journals and via social media. Partners are informed about the study's

Published
2023

4. Biological profiling in the spectrum of acute coronary syndrome: characterizing patients from MINOCA to NSTEMI with different features of the culprit plaque

Author

D'aiello, A, primary, Pedicino, D, additional, Bonanni, A, additional, Vinci, R, additional, Severino, A, additional, Ponzo, M, additional, Conte, C, additional, Cribari, F, additional, Filomia, S, additional, Brecciaroli, M, additional, Grimaldi, M C, additional, Montone, R A, additional, Massetti, M, additional, Crea, F, additional, and Liuzzo, G, additional

Published
2023
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5. Transcatheter versus surgical aortic valve replacement in patients with aortic stenosis: molecular pathways and correlation with clinical and echocardiographic parameters

Author

Pedicino, D, primary, D'aiello, A, additional, Bonanni, A, additional, Vinci, R, additional, Severino, A, additional, Pasquini, A, additional, Burzotta, F, additional, Trani, C, additional, Ciampi, P, additional, Aurigemma, C, additional, Bruno, P, additional, Russo, G, additional, Massetti, M, additional, Crea, F, additional, and Liuzzo, G, additional

Published
2023
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6. Relation between high-sensitivity troponin i serum levels and myocardial ischemia in patients with suspected chronic coronary syndrome: the RESET-MI study

Author

De Vita, A, primary, Bruno, I, additional, Baroni, S, additional, Moretti, G, additional, Tempestini, F, additional, Telesca, A, additional, Tremamunno, S, additional, Felici, T, additional, Verrillo, A, additional, Lamendola, P, additional, Cambise, N, additional, Liuzzo, G, additional, Crea, F, additional, Giordano, A, additional, and Lanza, G A, additional

Published
2023
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7. Molecular Hallmarks of Ischemia with Non-Obstructive Coronary Arteries: The “INOCA versus Obstructive CCS” Challenge

Author

Bonanni, A., D'aiello, A., Pedicino, D., Di Sario, M., Vinci, R., Ponzo, M., Ciampi, P., Curto, D. L., Conte, C., Cribari, F., Canonico, F., Russo, G., Montone, R. A., Trani, C., Severino, A., Crea, F., Liuzzo, G., Bonanni A., Pedicino D., Di Sario M., Vinci R., Ponzo M., Ciampi P., Conte C., Cribari F., Canonico F. (ORCID:0000-0001-6936-4548), Montone R. A., Trani C. (ORCID:0000-0001-9777-013X), Severino A., Crea F. (ORCID:0000-0001-9404-8846), Liuzzo G. (ORCID:0000-0002-5714-0907), Bonanni, A., D'aiello, A., Pedicino, D., Di Sario, M., Vinci, R., Ponzo, M., Ciampi, P., Curto, D. L., Conte, C., Cribari, F., Canonico, F., Russo, G., Montone, R. A., Trani, C., Severino, A., Crea, F., Liuzzo, G., Bonanni A., Pedicino D., Di Sario M., Vinci R., Ponzo M., Ciampi P., Conte C., Cribari F., Canonico F. (ORCID:0000-0001-6936-4548), Montone R. A., Trani C. (ORCID:0000-0001-9777-013X), Severino A., Crea F. (ORCID:0000-0001-9404-8846), and Liuzzo G. (ORCID:0000-0002-5714-0907)

Abstract

Up to 4 million patients with signs of myocardial ischemia have no obstructive coronary artery disease (CAD). The absence of precise guidelines for diagnosis and treatment in non-obstructive CAD encourages the scientific community to fill the gap knowledge, to provide non-invasive and less expensive diagnostic tools. The aim of our study was to explore the biological profile of Ischemia with Non-Obstructive Coronary Arteries (INOCA) patients with microvascular dysfunction compared to patients presenting with obstructive chronic coronary syndrome (ObCCS) in order to find specific hallmarks of each clinical condition. We performed a gene expression array from peripheral blood mononuclear cells (PBMCs) isolated from INOCA (n = 18) and ObCCS (n = 20) patients. Our results showed a significantly reduced gene expression of molecules involved in cell adhesion, signaling, vascular motion, and inflammation in INOCA as compared to the ObCCS group. In detail, we found lower expression of Platelet and Endothelial Cell Adhesion Molecule 1 (CD31, p < 0.0001), Intercellular Adhesion Molecule-1 (ICAM1, p = 0.0004), Tumor Necrosis Factor (TNF p = 0.0003), Transferrin Receptor (TFRC, p = 0.002), and Vascular Endothelial Growth Factor A (VEGFA, p = 0.0006) in the INOCA group compared with ObCCS. Meanwhile, we observed an increased expression of Hyaluronidase (HYAL2, p < 0.0001) in INOCA patients in comparison to ObCCS. The distinct expression of molecular biomarkers might allow an early and non-invasive differential diagnosis between ObCCS and INOCA, improving clinical management and treatment options, in the era of personalized medicine.

Published
2022

8. Air Pollution and Coronary Plaque Vulnerability and Instability: An Optical Coherence Tomography Study

Author

Montone, R. A., Camilli, M., Russo, M., Termite, C., La Vecchia, G., Iannaccone, G., Rinaldi, R., Gurgoglione, F., Del Buono, M. G., Sanna, T., Trani, C., Liuzzo, G., Crea, F., Niccoli, G., Montone R. A., Camilli M., Russo M., La Vecchia G., Iannaccone G., Rinaldi R., Gurgoglione F., Del Buono M. G., Sanna T. (ORCID:0000-0002-5760-6885), Trani C. (ORCID:0000-0001-9777-013X), Liuzzo G. (ORCID:0000-0002-5714-0907), Crea F. (ORCID:0000-0001-9404-8846), Niccoli G. (ORCID:0000-0002-3187-6262), Montone, R. A., Camilli, M., Russo, M., Termite, C., La Vecchia, G., Iannaccone, G., Rinaldi, R., Gurgoglione, F., Del Buono, M. G., Sanna, T., Trani, C., Liuzzo, G., Crea, F., Niccoli, G., Montone R. A., Camilli M., Russo M., La Vecchia G., Iannaccone G., Rinaldi R., Gurgoglione F., Del Buono M. G., Sanna T. (ORCID:0000-0002-5760-6885), Trani C. (ORCID:0000-0001-9777-013X), Liuzzo G. (ORCID:0000-0002-5714-0907), Crea F. (ORCID:0000-0001-9404-8846), and Niccoli G. (ORCID:0000-0002-3187-6262)

Abstract

Objectives: We assessed the relationship between exposure to air pollutants and mechanisms of coronary instability evaluated by optical coherence tomography (OCT) in patients with acute coronary syndrome (ACS). Background: Air pollution is an emerging key player in determining the residual risk of coronary events. However, pathophysiological mechanisms linking air pollution and coronary events have been not adequately investigated. Methods: Patients with ACS undergoing OCT imaging were retrospectively selected. Mechanism of culprit lesion instability was classified as plaque rupture (PR) or intact fibrous cap (IFC) by OCT, and the presence of macrophage infiltrates (MØI) and thin-cap fibroatheroma (TCFA) at the culprit site was also assessed. Based on each case's home address, exposure to several pollutants was evaluated, including particulate matter 2.5 (PM2.5), PM10, and carbon monoxide (CO). Only patients with >2 years of available data on air pollution exposure prior to ACS were enrolled. Results: We included 126 patients (median age: 67.0 years of age; IQR: 55.5-76.0; 97 male patients [77.0%]). Sixty-six patients (52.4%) had PR as the mechanism of plaque instability. Patients with PR were exposed to significantly higher PM2.5 levels than to IFC, and PM2.5 was independently associated with PR (odds ratio: 1.194; 95% CI: 1.036 to 1.377; P = 0.015). Moreover, exposure to higher levels of PM2.5 was independently associated with the presence of TCFA and of MØI at the culprit site. Interestingly, PM2.5, PM10, and CO levels were positively and significantly correlated with serum levels of C-reactive protein. Conclusions: We provide novel insights into the missing link between air pollution and increased risk of coronary events. In particular, exposure to higher concentrations of air pollutants is associated with the presence of vulnerable plaque features and with plaque rupture as a mechanism of coronary instability. An enhanced systemic and plaque inflammatory act

Published
2022

9. Inflammation across the spectrum of hypertrophic cardiac phenotypes

Author

Lillo, Rosa, Graziani, Francesca, Franceschi, Francesco, Iannaccone, Giulia, Massetti, Massimo, Olivotto, I, Crea, Filippo, Liuzzo, Giovanna, Lillo R, Graziani F (ORCID:0000-0002-4520-5689), Franceschi F (ORCID:0000-0001-6266-445X), Iannaccone G, Massetti M (ORCID:0000-0002-7100-8478), Crea F (ORCID:0000-0001-9404-8846), Liuzzo G. (ORCID:0000-0002-5714-0907), Lillo, Rosa, Graziani, Francesca, Franceschi, Francesco, Iannaccone, Giulia, Massetti, Massimo, Olivotto, I, Crea, Filippo, Liuzzo, Giovanna, Lillo R, Graziani F (ORCID:0000-0002-4520-5689), Franceschi F (ORCID:0000-0001-6266-445X), Iannaccone G, Massetti M (ORCID:0000-0002-7100-8478), Crea F (ORCID:0000-0001-9404-8846), and Liuzzo G. (ORCID:0000-0002-5714-0907)

Abstract

The hypertrophic cardiomyopathy phenotype encompasses a heterogeneous spectrum of genetic and acquired diseases characterized by the presence of left ventricular hypertrophy in the absence of abnormal cardiac loading conditions. This "umbrella diagnosis" includes the "classic" hypertrophic cardiomyopathy (HCM), due to sarcomere protein gene mutations, and its phenocopies caused by intra- or extracellular deposits, such as Fabry disease (FD) and cardiac amyloidosis (CA). All these conditions share a wide phenotypic variability which results from the combination of genetic and environmental factors and whose pathogenic mediators are poorly understood so far. Accumulating evidence suggests that inflammation plays a critical role in a broad spectrum of cardiovascular conditions, including cardiomyopathies. Indeed, inflammation can trigger molecular pathways which contribute to cardiomyocyte hypertrophy and dysfunction, extracellular matrix accumulation, and microvascular dysfunction. Growing evidence suggests that systemic inflammation is a possible key pathophysiologic process potentially involved in the pathogenesis of cardiac disease progression, influencing the severity of the phenotype and clinical outcome, including heart failure. In this review, we summarize current knowledge regarding the prevalence, clinical significance, and potential therapeutic implications of inflammation in HCM and two of its most important phenocopies, FD and CA.

Published
2023

10. Device-based remote monitoring strategies for guided management of patients with heart failure: a systematic review and meta-analysis

Author

Zito, A, primary, Princi, G, additional, Romiti, G F, additional, Basili, S, additional, Liuzzo, G, additional, Sanna, T, additional, Restivo, A, additional, Ciliberti, G, additional, Trani, C, additional, Burzotta, F, additional, Cesario, A, additional, Savarese, G, additional, Crea, F, additional, and D'Amario, D, additional

Published
2022
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13. Personalized clinical phenotyping through systems medicine and artificial intelligence

Author

Cesario, A, D'Oria, M, Bove, F, Privitera, G, Boskoski, I, Pedicino, D, Boldrini, L, Erra, C, Loreti, C, Liuzzo, G, Crea, F, Armuzzi, A, Gasbarrini, A, Calabresi, P, Padua, L, Costamagna, G, Antonelli, M, Valentini, V, Auffray, C, Scambia, G, Cesario A., D'oria M., Bove F., Privitera G., Boskoski I., Pedicino D., Boldrini L., Erra C., Loreti C., Liuzzo G., Crea F., Armuzzi A., Gasbarrini A., Calabresi P., Padua L., Costamagna G., Antonelli M., Valentini V., Auffray C., Scambia G., Cesario, A, D'Oria, M, Bove, F, Privitera, G, Boskoski, I, Pedicino, D, Boldrini, L, Erra, C, Loreti, C, Liuzzo, G, Crea, F, Armuzzi, A, Gasbarrini, A, Calabresi, P, Padua, L, Costamagna, G, Antonelli, M, Valentini, V, Auffray, C, Scambia, G, Cesario A., D'oria M., Bove F., Privitera G., Boskoski I., Pedicino D., Boldrini L., Erra C., Loreti C., Liuzzo G., Crea F., Armuzzi A., Gasbarrini A., Calabresi P., Padua L., Costamagna G., Antonelli M., Valentini V., Auffray C., and Scambia G.

Abstract

Personalized Medicine (PM) has shifted the traditional top-down approach to medicine based on the identification of single etiological factors to explain diseases, which was not suitable for explaining complex conditions. The concept of PM assumes several interpretations in the literature, with particular regards to Genetic and Genomic Medicine. Despite the fact that some disease-modifying genes affect disease expression and progression, many complex conditions cannot be understood through only this lens, especially when other lifestyle factors can play a crucial role (such as the environment, emotions, nutrition, etc.). Personalizing clinical phenotyping becomes a challenge when different pathophysiological mechanisms underlie the same manifestation. Brain disorders, cardiovascular and gastroentero-logical diseases can be paradigmatic examples. Experiences on the field of Fondazione Policlinico Gemelli in Rome (a research hospital recognized by the Italian Ministry of Health as national leader in “Personalized Medicine” and “Innovative Biomedical Technologies”) could help understanding which techniques and tools are the most performing to develop potential clinical phenotypes person-alization. The connection between practical experiences and scientific literature highlights how this potential can be reached towards Systems Medicine using Artificial Intelligence tools.

Published
2021

14. Use of Levosimendan as bridge therapy to surgical correction of post-infarction ventricular septal defect: a case report

Author

Camilli, M., Ciampi, P., Pedicino, D., D'Aiello, A., Mazza, A., Montone, R. A., Sanna, T., Rebuzzi, A. G., Massetti, M., Crea, F., Liuzzo, G., Camilli M., Ciampi P., Pedicino D., Montone R. A., Sanna T. (ORCID:0000-0002-5760-6885), Rebuzzi A. G. (ORCID:0000-0002-9873-957X), Massetti M. (ORCID:0000-0002-7100-8478), Crea F. (ORCID:0000-0001-9404-8846), Liuzzo G. (ORCID:0000-0002-5714-0907), Camilli, M., Ciampi, P., Pedicino, D., D'Aiello, A., Mazza, A., Montone, R. A., Sanna, T., Rebuzzi, A. G., Massetti, M., Crea, F., Liuzzo, G., Camilli M., Ciampi P., Pedicino D., Montone R. A., Sanna T. (ORCID:0000-0002-5760-6885), Rebuzzi A. G. (ORCID:0000-0002-9873-957X), Massetti M. (ORCID:0000-0002-7100-8478), Crea F. (ORCID:0000-0001-9404-8846), and Liuzzo G. (ORCID:0000-0002-5714-0907)

Abstract

– OBJECTIVE: Ventricular septal defect (VSD) is an uncommon but frequently fatal complication following acute myocardial infarction. In medically treated patients, mortality rates exceed 90%, while the surgical repair is associated with better outcomes, even though optimal surgical timing is still under debate. CASE REPORT: We present the case of a 78-years-old man with no previous remarkable cardiological history admitted to our Emergency Department with the diagnosis of anteri- or ST-elevation myocardial infarction and significant reduction of left ventricular ejection fraction. The emergency coronary angiography showed sub-occlusion of the left anterior descending coronary artery, treated with stent implantation. The post-procedural echocardiography unveiled the presence of an apical VSD with a large left-to-right shunt, significant right ventricular overload and dysfunction. An intra-aortic balloon pump (IABP) was positioned and, after Heart Team evaluation, a delayed surgical approach was planned. As a bridge to the intervention Levosimendan infusion was administered, on top of IABP support, and a significant improvement in bi-ventricular function and pressure profiles was obtained. Cardiac surgery was successfully performed 9 days after the admission without periprocedural complications. CONCLUSIONS: This unique case supports the use of Levosimendan as a valid pharmacological strategy for perioperative management of VSD.

Published
2021

15. From angiotensin-converting enzyme 2 disruption to thromboinflammatory microvascular disease: A paradigm drawn from COVID-19

Author

Vinci, R., Pedicino, D., Andreotti, F., Russo, G., D'Aiello, A., De Cristofaro, R., Crea, F., Liuzzo, G., Vinci R., Pedicino D., Andreotti F. (ORCID:0000-0002-1456-6430), Russo G., De Cristofaro R. (ORCID:0000-0002-8066-8849), Crea F. (ORCID:0000-0001-9404-8846), Liuzzo G. (ORCID:0000-0002-5714-0907), Vinci, R., Pedicino, D., Andreotti, F., Russo, G., D'Aiello, A., De Cristofaro, R., Crea, F., Liuzzo, G., Vinci R., Pedicino D., Andreotti F. (ORCID:0000-0002-1456-6430), Russo G., De Cristofaro R. (ORCID:0000-0002-8066-8849), Crea F. (ORCID:0000-0001-9404-8846), and Liuzzo G. (ORCID:0000-0002-5714-0907)

Abstract

We concisely review clinical, autopsy, experimental and molecular data of 2019 coronavirus disease (COVID-19). Angiotensin-converting enzyme 2 disruption and thromboinflammatory microangiopathy emerge as distinctive features. Briefly, entry of the virus into microvessels can profoundly disrupt the local renin-angiotensin system, cause endothelial injury, activate the complement cascade and induce powerful thromboinflammatory reactions, involving, in particular, von Willebrand factor, that, if widespread, may lead to microvascular plugging, ischemia and, ultimately, organ failure. We believe the current COVID-19 data consolidate a widely unrecognised paradigm of potentially fatal thromboinflammatory microvascular disease.

Published
2021

16. Transcatheter versus surgical aortic valve replacement in patients with aortic stenosis: characterization of molecular pathways before and after treatment

Author

Bonanni, A, primary, Pedicino, D, additional, D'aiello, A, additional, Vinci, R, additional, Severino, A, additional, Russo, G, additional, Cribari, F, additional, Conte, C, additional, Filomia, S, additional, Bruno, P, additional, Burzotta, F, additional, Trani, C, additional, Massetti, M, additional, Crea, F, additional, and Liuzzo, G, additional

Published
2022
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17. Restricted T-Cell Repertoire in the Epicardial Adipose Tissue of Non-ST Segment Elevation Myocardial Infarction Patients

Author

Pedicino, Daniela, Severino, Anna, Di Sante, Gabriele, De Rosa, Maria Cristina, Pirolli, Davide, Vinci, Ramona, Pazzano, V., Giglio, A. F., Trotta, F., Russo, G., Ruggio, A., Pisano, Eugenia, D'Aiello, Alessia, Canonico, Francesco, Ciampi, P., Cianflone, D., Cianfanelli, L., Grimaldi, Maria Chiara, Filomia, Simone, Luciani, Nicola, Glieca, Franco, Bruno, Piergiorgio, Massetti, Massimo, Ria, Francesco, Crea, Filippo, Liuzzo, Giovanna, Pedicino D., Severino A., Di Sante G. (ORCID:0000-0001-6608-3388), De Rosa M. C., Pirolli D. (ORCID:0000-0003-2303-2577), Vinci R., Pisano E., d'Aiello A., Canonico F. (ORCID:0000-0001-6936-4548), Grimaldi M. C., Filomia S., Luciani N. (ORCID:0000-0002-9407-0303), Glieca F. (ORCID:0000-0003-3645-7152), Bruno P. (ORCID:0000-0002-1075-5808), Massetti M. (ORCID:0000-0002-7100-8478), Ria F. (ORCID:0000-0002-8444-0307), Crea F. (ORCID:0000-0001-9404-8846), Liuzzo G. (ORCID:0000-0002-5714-0907), Pedicino, Daniela, Severino, Anna, Di Sante, Gabriele, De Rosa, Maria Cristina, Pirolli, Davide, Vinci, Ramona, Pazzano, V., Giglio, A. F., Trotta, F., Russo, G., Ruggio, A., Pisano, Eugenia, D'Aiello, Alessia, Canonico, Francesco, Ciampi, P., Cianflone, D., Cianfanelli, L., Grimaldi, Maria Chiara, Filomia, Simone, Luciani, Nicola, Glieca, Franco, Bruno, Piergiorgio, Massetti, Massimo, Ria, Francesco, Crea, Filippo, Liuzzo, Giovanna, Pedicino D., Severino A., Di Sante G. (ORCID:0000-0001-6608-3388), De Rosa M. C., Pirolli D. (ORCID:0000-0003-2303-2577), Vinci R., Pisano E., d'Aiello A., Canonico F. (ORCID:0000-0001-6936-4548), Grimaldi M. C., Filomia S., Luciani N. (ORCID:0000-0002-9407-0303), Glieca F. (ORCID:0000-0003-3645-7152), Bruno P. (ORCID:0000-0002-1075-5808), Massetti M. (ORCID:0000-0002-7100-8478), Ria F. (ORCID:0000-0002-8444-0307), Crea F. (ORCID:0000-0001-9404-8846), and Liuzzo G. (ORCID:0000-0002-5714-0907)

Abstract

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 wit

Published
2022

18. Monocyte-Platelet Aggregates Triggered by CD31 Molecule in Non-ST Elevation Myocardial Infarction: Clinical Implications in Plaque Rupture

Author

Vinci, Ramona, Pedicino, Daniela, Bonanni, Alice, D'Aiello, A., Pisano, Eugenia, Ponzo, Myriana, Severino, Anna, Ciampi, Pellegrino, Canonico, Francesco, Russo, Giulio, Di Sario, Marianna, Vergallo, Rocco, Filomia, Simone, Montone, Rocco Antonio, Flego, Davide, Stefanini, L., Piacentini, Roberto, Conte, C., Cribari, Francesco, Massetti, Massimo, Crea, Filippo, Liuzzo, Giovanna, Vinci R., Pedicino D., Bonanni A., Pisano E., Ponzo M., Severino A., Ciampi P., Canonico F. (ORCID:0000-0001-6936-4548), Russo G., Di Sario M., Vergallo R., Filomia S., Montone R. A., Flego D., Piacentini R. (ORCID:0000-0003-4215-1643), Cribari F., Massetti M. (ORCID:0000-0002-7100-8478), Crea F. (ORCID:0000-0001-9404-8846), Liuzzo G. (ORCID:0000-0002-5714-0907), Vinci, Ramona, Pedicino, Daniela, Bonanni, Alice, D'Aiello, A., Pisano, Eugenia, Ponzo, Myriana, Severino, Anna, Ciampi, Pellegrino, Canonico, Francesco, Russo, Giulio, Di Sario, Marianna, Vergallo, Rocco, Filomia, Simone, Montone, Rocco Antonio, Flego, Davide, Stefanini, L., Piacentini, Roberto, Conte, C., Cribari, Francesco, Massetti, Massimo, Crea, Filippo, Liuzzo, Giovanna, Vinci R., Pedicino D., Bonanni A., Pisano E., Ponzo M., Severino A., Ciampi P., Canonico F. (ORCID:0000-0001-6936-4548), Russo G., Di Sario M., Vergallo R., Filomia S., Montone R. A., Flego D., Piacentini R. (ORCID:0000-0003-4215-1643), Cribari F., Massetti M. (ORCID:0000-0002-7100-8478), Crea F. (ORCID:0000-0001-9404-8846), and Liuzzo G. (ORCID:0000-0002-5714-0907)

Abstract

Despite the recent innovations in cardiovascular care, atherothrombosis is still a major complication of acute coronary syndromes (ACS). We evaluated the involvement of the CD31 molecule in thrombotic risk through the formation of monocyte-platelet (Mo-Plt) aggregates in patients with ACS with no-ST-segment elevation myocardial infarction (NSTEMI) on top of dual anti-platelet therapy (DAPT). We enrolled 19 control (CTRL) subjects, 46 stable angina (SA), and 86 patients with NSTEMI, of which, 16 with Intact Fibrous Cap (IFC) and 19 with Ruptured Fibrous Cap (RFC) as assessed by the Optical Coherence Tomography (OCT). The expression of CD31 on monocytes and platelets was measured. Following the coronary angiography, 52 NSTEMIs were further stratified according to thrombus grade (TG) evaluation. Finally, a series of ex vivo experiments verified whether the CD31 participates in Mo-Plt aggregate formation. In patients with NSTEMI, CD31 was reduced on monocytes and was increased on platelets, especially in NSTEMI presented with RFC plaques compared to those with IFC lesions, and in patients with high TG compared to those with zero/low TG. Ex vivo experiments documented an increase in Mo-Plt aggregates among NSTEMI, which significantly decreased after the CD31 ligation, particularly in patients with RFC plaques. In NSTEMI, CD31 participates in Mo-Plt aggregate formation in spite of optimal therapy and DAPT, suggesting the existence of alternative thrombotic pathways, as predominantly displayed in patients with RFC.

Published
2022

20. Takotsubo syndrome: a way to reach a straightforward diagnosis

Author

Bonanni, A, primary, Pedicino, D, additional, Vinci, R, additional, D'Aiello, A, additional, Ponzo, M, additional, Ciampi, P, additional, Pisano, E, additional, Canonico, F, additional, Di Sario, M, additional, Conte, C, additional, Cribari, F, additional, Grimaldi, M C, additional, Severino, A, additional, Crea, F, additional, and Liuzzo, G, additional

Published
2021
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21. Colchicine in ischemic heart disease: the good, the bad and the ugly

Author

D'Amario, D., Cappetta, D., Cappannoli, Luigi, Princi, Giuseppe, Migliaro, Stefano, Diana, Giovanni, Chouchane, K., Borovac, J. A., Restivo, Attilio, Arcudi, Alessandra, De Angelis, Aniello, Vergallo, Rocco, Montone, Rocco Antonio, Galli, M., Liuzzo, Giovanna, Crea, Filippo, Cappannoli L., Princi G., Migliaro S., Diana G., Restivo A., Arcudi A., De Angelis A., Vergallo R., Montone R. A., Liuzzo G. (ORCID:0000-0002-5714-0907), Crea F. (ORCID:0000-0001-9404-8846), D'Amario, D., Cappetta, D., Cappannoli, Luigi, Princi, Giuseppe, Migliaro, Stefano, Diana, Giovanni, Chouchane, K., Borovac, J. A., Restivo, Attilio, Arcudi, Alessandra, De Angelis, Aniello, Vergallo, Rocco, Montone, Rocco Antonio, Galli, M., Liuzzo, Giovanna, Crea, Filippo, Cappannoli L., Princi G., Migliaro S., Diana G., Restivo A., Arcudi A., De Angelis A., Vergallo R., Montone R. A., Liuzzo G. (ORCID:0000-0002-5714-0907), and Crea F. (ORCID:0000-0001-9404-8846)

Abstract

Inflammation is the main pathophysiological process involved in atherosclerotic plaque formation, progression, instability, and healing during the evolution of coronary artery disease (CAD). The use of colchicine, a drug used for decades in non-ischemic cardiovascular (CV) diseases and/or systemic inflammatory conditions, stimulated new perspectives on its potential application in patients with CAD. Previous mechanistic and preclinical studies revealed anti-inflammatory and immunomodulatory effects of colchicine exerted through its principal mechanism of microtubule polymerization inhibition, however, other pleiotropic effects beneficial to the CV system were observed such as inhibition of platelet aggregation and suppression of endothelial proliferation. In randomized double-blinded clinical trials informing our clinical practice, low doses of colchicine were associated with the significant reduction of cardiovascular events in patients with stable CAD and chronic coronary syndrome (CCS) while in patients with a recent acute coronary syndrome (ACS), early initiation of colchicine treatment significantly reduced major adverse CV events (MACE). On the other hand, the safety profile of colchicine and its potential causal relationship to the observed increase in non-CV deaths warrants further investigation. For these reasons, postulates of precision medicine and patient-tailored approach with regards to benefits and harms of colchicine treatment should be employed at all times due to potential toxicity of colchicine as well as the currently unresolved signal of harm concerning non-CV mortality. The main goal of this review is to provide a balanced, critical, and comprehensive evaluation of currently available evidence with respect to colchicine use in the setting of CAD.

Published
2021

22. Brain-derived neurotrophic factor in patients with acute coronary syndrome

Author

Montone, Rocco Antonio, Camilli, Massimiliano, Del Buono, Marco Giuseppe, Russo, Michele, Rinaldi, R., Canonico, Francesco, Pedicino, Daniela, Severino, Anna, D'Amario, Domenico, Trani, Carlo, Liuzzo, Giovanna, Crea, Filippo, Niccoli, Giampaolo, Montone R. A., Camilli M., Del Buono M. G., Russo M., Canonico F. (ORCID:0000-0001-6936-4548), Pedicino D., Severino A., D'Amario D., Trani C. (ORCID:0000-0001-9777-013X), Liuzzo G. (ORCID:0000-0002-5714-0907), Crea F. (ORCID:0000-0001-9404-8846), Niccoli G. (ORCID:0000-0002-3187-6262), Montone, Rocco Antonio, Camilli, Massimiliano, Del Buono, Marco Giuseppe, Russo, Michele, Rinaldi, R., Canonico, Francesco, Pedicino, Daniela, Severino, Anna, D'Amario, Domenico, Trani, Carlo, Liuzzo, Giovanna, Crea, Filippo, Niccoli, Giampaolo, Montone R. A., Camilli M., Del Buono M. G., Russo M., Canonico F. (ORCID:0000-0001-6936-4548), Pedicino D., Severino A., D'Amario D., Trani C. (ORCID:0000-0001-9777-013X), Liuzzo G. (ORCID:0000-0002-5714-0907), Crea F. (ORCID:0000-0001-9404-8846), and Niccoli G. (ORCID:0000-0002-3187-6262)

Abstract

Brain-derived neurotrophic factor (BDNF) is a neurotrophic factor highly expressed in coronary plaques, particularly in macrophages, and in activated platelets. Thus, a possible role in the pathogenesis of acute coronary syndrome (ACS) has been suggested. We evaluated systemic BDNF levels according to the different clinical presentations of ACS. Moreover, we assessed the relationship between BDNF levels and the presence of optical coherence tomography (OCT)-defined macrophage infiltrates (MØI) and healed plaques along the culprit vessel. We enrolled consecutive patients presenting with ST-elevation myocardial infarction (STEMI) or non-ST-elevation (NSTE)-ACS. Serum BDNF levels were assessed by enzyme-linked immunosorbent assay. Plaque characteristics of the culprit vessel were assessed by OCT. Among 126 ACS patients (median age 68.00, interquartile range [IQR] 59.75–75.25 years, male 74.6%, 71 (56.3%) were NSTE-ACS and 55 (43.7%) were STEMI. BDNF levels were higher in STEMI patients compared to NSTE-ACS. OCT assessment was performed in 53 (42.1%) patients. Patients with MØI (n = 27) had higher BDNF levels compared to patients without MØI. Furthermore, patients with healed plaques (n = 13) had lower BDNF levels than patients without healed plaques. At multivariate regression analysis BDNF levels independently predicted the presence of MØI (odds ratio [OR] = 2.856; 95% confidence interval [CI] [1.151–7.090], P = 0.024) and the absence of healed plaques (OR = 0.438, 95% CI [0.185–0.992], P= 0.050). Among ACS patients, BDNF levels were higher in patients with STEMI. Moreover, BDNF levels were independently associated with MØI and with the absence of healed plaques along the culprit vessel, suggesting a possible role of BDNF in promoting plaque inflammation, destabilization and occlusive thrombosis.

Published
2021

23. Personalized clinical phenotyping through systems medicine and artificial intelligence

Author

Cesario, Alfredo, D'Oria, M., Bove, F., Privitera, G., Boskoski, Ivo, Pedicino, Daniela, Boldrini, Luca, Erra, Carmen, Loreti, Claudia, Liuzzo, Giovanna, Crea, Filippo, Armuzzi, Alessandro, Gasbarrini, Antonio, Calabresi, Paolo, Padua, Luca, Costamagna, Guido, Antonelli, Massimo, Valentini, Vincenzo, Auffray, C., Scambia, Giovanni, Cesario A. (ORCID:0000-0003-4687-0709), Boskoski I. (ORCID:0000-0001-8194-2670), Pedicino D., Boldrini L., Erra C., Loreti C., Liuzzo G. (ORCID:0000-0002-5714-0907), Crea F. (ORCID:0000-0001-9404-8846), Armuzzi A. (ORCID:0000-0003-1572-0118), Gasbarrini A. (ORCID:0000-0002-7278-4823), Calabresi P. (ORCID:0000-0003-0326-5509), Padua L. (ORCID:0000-0003-2570-9326), Costamagna G. (ORCID:0000-0002-8100-2731), Antonelli M. (ORCID:0000-0003-3007-1670), Valentini V. (ORCID:0000-0003-4637-6487), Scambia G. (ORCID:0000-0003-2758-1063), Cesario, Alfredo, D'Oria, M., Bove, F., Privitera, G., Boskoski, Ivo, Pedicino, Daniela, Boldrini, Luca, Erra, Carmen, Loreti, Claudia, Liuzzo, Giovanna, Crea, Filippo, Armuzzi, Alessandro, Gasbarrini, Antonio, Calabresi, Paolo, Padua, Luca, Costamagna, Guido, Antonelli, Massimo, Valentini, Vincenzo, Auffray, C., Scambia, Giovanni, Cesario A. (ORCID:0000-0003-4687-0709), Boskoski I. (ORCID:0000-0001-8194-2670), Pedicino D., Boldrini L., Erra C., Loreti C., Liuzzo G. (ORCID:0000-0002-5714-0907), Crea F. (ORCID:0000-0001-9404-8846), Armuzzi A. (ORCID:0000-0003-1572-0118), Gasbarrini A. (ORCID:0000-0002-7278-4823), Calabresi P. (ORCID:0000-0003-0326-5509), Padua L. (ORCID:0000-0003-2570-9326), Costamagna G. (ORCID:0000-0002-8100-2731), Antonelli M. (ORCID:0000-0003-3007-1670), Valentini V. (ORCID:0000-0003-4637-6487), and Scambia G. (ORCID:0000-0003-2758-1063)

Abstract

Personalized Medicine (PM) has shifted the traditional top-down approach to medicine based on the identification of single etiological factors to explain diseases, which was not suitable for explaining complex conditions. The concept of PM assumes several interpretations in the literature, with particular regards to Genetic and Genomic Medicine. Despite the fact that some disease-modifying genes affect disease expression and progression, many complex conditions cannot be understood through only this lens, especially when other lifestyle factors can play a crucial role (such as the environment, emotions, nutrition, etc.). Personalizing clinical phenotyping becomes a challenge when different pathophysiological mechanisms underlie the same manifestation. Brain disorders, cardiovascular and gastroentero-logical diseases can be paradigmatic examples. Experiences on the field of Fondazione Policlinico Gemelli in Rome (a research hospital recognized by the Italian Ministry of Health as national leader in “Personalized Medicine” and “Innovative Biomedical Technologies”) could help understanding which techniques and tools are the most performing to develop potential clinical phenotypes person-alization. The connection between practical experiences and scientific literature highlights how this potential can be reached towards Systems Medicine using Artificial Intelligence tools.

Published
2021

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

Author

De Vita, Antonio, De Matteis, Giuseppe, D'Aiello, A., Ravenna, S. E., Liuzzo, Giovanna, Lanza, Gaetano Antonio, Massetti, Massimo, Crea, Filippo, Gasbarrini, Antonio, Franceschi, Francesco, Covino, Marcello, De Vita A., De Matteis G., Liuzzo G. (ORCID:0000-0002-5714-0907), Lanza G. A. (ORCID:0000-0003-2187-6653), Massetti M. (ORCID:0000-0002-7100-8478), Crea F. (ORCID:0000-0001-9404-8846), Gasbarrini A. (ORCID:0000-0002-7278-4823), Franceschi F. (ORCID:0000-0001-6266-445X), Covino M. (ORCID:0000-0002-6709-2531), De Vita, Antonio, De Matteis, Giuseppe, D'Aiello, A., Ravenna, S. E., Liuzzo, Giovanna, Lanza, Gaetano Antonio, Massetti, Massimo, Crea, Filippo, Gasbarrini, Antonio, Franceschi, Francesco, Covino, Marcello, De Vita A., De Matteis G., Liuzzo G. (ORCID:0000-0002-5714-0907), Lanza G. A. (ORCID:0000-0003-2187-6653), Massetti M. (ORCID:0000-0002-7100-8478), Crea F. (ORCID:0000-0001-9404-8846), Gasbarrini A. (ORCID:0000-0002-7278-4823), Franceschi F. (ORCID:0000-0001-6266-445X), and Covino M. (ORCID:0000-0002-6709-2531)

Abstract

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.

Published
2021

25. Upregulated monocyte expression of PLIN2 is associated with early arterial injury in children with overweight/obesity

Author

Pisano, Eugenia, Pacifico, L., Perla, F. M., Liuzzo, Giovanna, Chiesa, C., Lavorato, M., Mingrone, Geltrude, Fabrizi, M., Fintini, D., Severino, Anna, Manco, M., Pisano E., Liuzzo G. (ORCID:0000-0002-5714-0907), Mingrone G. (ORCID:0000-0003-2021-528X), Severino A., Pisano, Eugenia, Pacifico, L., Perla, F. M., Liuzzo, Giovanna, Chiesa, C., Lavorato, M., Mingrone, Geltrude, Fabrizi, M., Fintini, D., Severino, Anna, Manco, M., Pisano E., Liuzzo G. (ORCID:0000-0002-5714-0907), Mingrone G. (ORCID:0000-0003-2021-528X), and Severino A.

Abstract

Background and aims: Perilipin 2 (PLIN2) regulates intracellular lipid metabolism in macrophages, and thus, plays a role in atherosclerosis. Aim of the study was to evaluate whether PLIN2 dysregulation is involved in the onset of preclinical atherosclerosis in children with overweight/obesity and to explore dysregulation mechanisms. Methods: Sixty-three children with overweight/obesity and 21 normal weight children (controls) of the same age and sex were enrolled. Carotid intima media thickness (cIMT) was evaluated; mRNA expression of PLIN2 and proteasome subunits (PSMD3, PSMC4) was determined by Real Time PCR, and protein expression of PLIN2, LAMP2A and Hsc70 by Western blot analysis; fluorimetric assay was used to measure proteasome chymotrypsin like activity. We performed transient LAMP2A downregulation by siRNA and quantified intracellular lipids in monocytes by Nile Red staining and flow cytometry analysis. Results: PLIN2 protein levels were significantly higher in children with overweight/obesity and correlated with cIMT after adjusting for confounders. Accordingly, monocytes of children with overweight/obesity showed a higher intracellular amount of lipids compared with controls. mRNA expression of the regulatory subunits PSMC4 and PSMD3 and proteasome activity were lower in children with overweight/obesity, while expression of LAMP2A and Hsc70 proteins, which belong to the chaperone-mediated autophagy (CMA) pathway, was not different, suggesting that PLIN2 dysregulation in monocytes was due to an impairment of proteasome efficiency and was not CMA related. Conclusion: PLIN2 was overexpressed in monocytes of children with overweight/obesity and could contribute to the onset of arteropathy. Our data suggest that proteasome impairment could contribute to PLIN2 overexpression.

Published
2021

26. A machine-learning parsimonious multivariable predictive model of mortality risk in patients with Covid-19

Author

Murri, Rita, Lenkowicz, Jacopo, Masciocchi, Carlotta, Iacomini, C., Fantoni, Massimo, Damiani, Andrea, Marchetti, A., Sergi, P. D. A., Arcuri, G., Cesario, Alfredo, Patarnello, S., Antonelli, Massimo, Bellantone, Rocco Domenico Alfonso, Bernabei, Roberto, Boccia, Stefania, Calabresi, Paolo, Cambieri, Andrea, Cauda, Roberto, Colosimo, Cesare, Crea, Filippo, De Maria Marchiano, Ruggero, De Stefano, Valerio, Franceschi, Francesco, Gasbarrini, Antonio, Parolini, Ornella, Richeldi, Luca, Sanguinetti, Maurizio, Urbani, Andrea, Zega, Maurizio, Scambia, Giovanni, Valentini, Vincenzo, Armuzzi, Alessandro, Barba, Marta, Baroni, Silvia, Bellesi, Silvia, Bentivoglio, Anna Rita, Biasucci, Luigi Marzio, Biscetti, Federico, Candelli, Marcello, Capalbo, Gennaro, Cattani Franchi, Paola, Chiusolo, Patrizia, Cingolani, Antonella, Corbo, Giuseppe Maria, Covino, Marcello, Cozzolino, A. M., D'Alfonso, Maria Elena, De Angelis, Giulia, De Pascale, Gennaro, Frisullo, Giovanni, Gabrielli, M., Gambassi, Giovanni, Garcovich, M., Gremese, Elisa, Grieco, D. L., Iaconelli, A., Iorio, Raffaele, Landi, Francesco, Larici, Anna Rita, Liuzzo, Giovanna, Maviglia, Riccardo, Miele, Luca, Montalto, Massimo, Natale, Luigi, Nicolotti, Nicola, Ojetti, Veronica, Pompili, Maurizio, Posteraro, Brunella, Rapaccini, Gian Ludovico, Rinaldi, R., Rossi, Elena, Santoliquido, Angelo, Sica, Simona, Tamburrini, Enrica, Teofili, Luciana, Testa, Antonia Carla, Tosoni, A., Trani, Carlo, Varone, Francesco, Verme, L. Z. D., Murri R. (ORCID:0000-0003-4263-7854), Lenkowicz J., Masciocchi C., Fantoni M. (ORCID:0000-0001-6913-8460), Damiani A., Cesario A. (ORCID:0000-0003-4687-0709), Antonelli M. (ORCID:0000-0003-3007-1670), Bellantone R. (ORCID:0000-0002-0844-3469), Bernabei R. (ORCID:0000-0002-9197-004X), Boccia S. (ORCID:0000-0002-1864-749X), Calabresi P. (ORCID:0000-0003-0326-5509), Cambieri A., Cauda R. (ORCID:0000-0002-1498-4229), Colosimo C. (ORCID:0000-0003-3800-3648), Crea F. (ORCID:0000-0001-9404-8846), De Maria R. (ORCID:0000-0003-2255-0583), De Stefano V. (ORCID:0000-0002-5178-5827), Franceschi F. (ORCID:0000-0001-6266-445X), Gasbarrini A. (ORCID:0000-0002-7278-4823), Parolini O. (ORCID:0000-0002-5211-6430), Richeldi L. (ORCID:0000-0001-8594-1448), Sanguinetti M. (ORCID:0000-0002-9780-7059), Urbani A. (ORCID:0000-0001-9168-3174), Zega M. (ORCID:0000-0002-7821-2615), Scambia G. (ORCID:0000-0003-2758-1063), Valentini V. (ORCID:0000-0003-4637-6487), Armuzzi A. (ORCID:0000-0003-1572-0118), Barba M. (ORCID:0000-0001-6084-7666), Baroni S. (ORCID:0000-0002-3410-2617), Bellesi S., Bentivoglio A. (ORCID:0000-0002-9663-095X), Biasucci L. M. (ORCID:0000-0002-6921-6497), Biscetti F. (ORCID:0000-0001-7449-657X), Candelli M. (ORCID:0000-0001-8443-7880), Capalbo G., Cattani P. (ORCID:0000-0003-4678-4763), Chiusolo P. (ORCID:0000-0002-1355-1587), Cingolani A. (ORCID:0000-0002-3793-2755), Corbo G. (ORCID:0000-0002-8104-4659), Covino M. (ORCID:0000-0002-6709-2531), D'Alfonso M., De Angelis G. (ORCID:0000-0002-7087-7399), De Pascale G. (ORCID:0000-0002-8255-0676), Frisullo G., Gambassi G. (ORCID:0000-0002-7030-9359), Gremese E. (ORCID:0000-0002-2248-1058), Iorio R. (ORCID:0000-0002-6270-0956), Landi F. (ORCID:0000-0002-3472-1389), Larici A. (ORCID:0000-0002-1882-6244), Liuzzo G. (ORCID:0000-0002-5714-0907), Maviglia R., Miele L. (ORCID:0000-0003-3464-0068), Montalto M. (ORCID:0000-0001-8819-3684), Natale L. (ORCID:0000-0002-7949-5119), Nicolotti N., Ojetti V. (ORCID:0000-0002-8953-0707), Pompili M. (ORCID:0000-0001-6699-7980), Posteraro B. (ORCID:0000-0002-1663-7546), Rapaccini G. (ORCID:0000-0002-6467-857X), Rossi E. (ORCID:0000-0002-7572-9379), Santoliquido A. (ORCID:0000-0003-1539-4017), Sica S. (ORCID:0000-0003-2426-3465), Tamburrini E. (ORCID:0000-0003-4930-426X), Teofili L. (ORCID:0000-0002-7214-1561), Testa A. (ORCID:0000-0003-2217-8726), Trani C. (ORCID:0000-0001-9777-013X), Varone F., Murri, Rita, Lenkowicz, Jacopo, Masciocchi, Carlotta, Iacomini, C., Fantoni, Massimo, Damiani, Andrea, Marchetti, A., Sergi, P. D. A., Arcuri, G., Cesario, Alfredo, Patarnello, S., Antonelli, Massimo, Bellantone, Rocco Domenico Alfonso, Bernabei, Roberto, Boccia, Stefania, Calabresi, Paolo, Cambieri, Andrea, Cauda, Roberto, Colosimo, Cesare, Crea, Filippo, De Maria Marchiano, Ruggero, De Stefano, Valerio, Franceschi, Francesco, Gasbarrini, Antonio, Parolini, Ornella, Richeldi, Luca, Sanguinetti, Maurizio, Urbani, Andrea, Zega, Maurizio, Scambia, Giovanni, Valentini, Vincenzo, Armuzzi, Alessandro, Barba, Marta, Baroni, Silvia, Bellesi, Silvia, Bentivoglio, Anna Rita, Biasucci, Luigi Marzio, Biscetti, Federico, Candelli, Marcello, Capalbo, Gennaro, Cattani Franchi, Paola, Chiusolo, Patrizia, Cingolani, Antonella, Corbo, Giuseppe Maria, Covino, Marcello, Cozzolino, A. M., D'Alfonso, Maria Elena, De Angelis, Giulia, De Pascale, Gennaro, Frisullo, Giovanni, Gabrielli, M., Gambassi, Giovanni, Garcovich, M., Gremese, Elisa, Grieco, D. L., Iaconelli, A., Iorio, Raffaele, Landi, Francesco, Larici, Anna Rita, Liuzzo, Giovanna, Maviglia, Riccardo, Miele, Luca, Montalto, Massimo, Natale, Luigi, Nicolotti, Nicola, Ojetti, Veronica, Pompili, Maurizio, Posteraro, Brunella, Rapaccini, Gian Ludovico, Rinaldi, R., Rossi, Elena, Santoliquido, Angelo, Sica, Simona, Tamburrini, Enrica, Teofili, Luciana, Testa, Antonia Carla, Tosoni, A., Trani, Carlo, Varone, Francesco, Verme, L. Z. D., Murri R. (ORCID:0000-0003-4263-7854), Lenkowicz J., Masciocchi C., Fantoni M. (ORCID:0000-0001-6913-8460), Damiani A., Cesario A. (ORCID:0000-0003-4687-0709), Antonelli M. (ORCID:0000-0003-3007-1670), Bellantone R. (ORCID:0000-0002-0844-3469), Bernabei R. (ORCID:0000-0002-9197-004X), Boccia S. (ORCID:0000-0002-1864-749X), Calabresi P. (ORCID:0000-0003-0326-5509), Cambieri A., Cauda R. (ORCID:0000-0002-1498-4229), Colosimo C. (ORCID:0000-0003-3800-3648), Crea F. (ORCID:0000-0001-9404-8846), De Maria R. (ORCID:0000-0003-2255-0583), De Stefano V. (ORCID:0000-0002-5178-5827), Franceschi F. (ORCID:0000-0001-6266-445X), Gasbarrini A. (ORCID:0000-0002-7278-4823), Parolini O. (ORCID:0000-0002-5211-6430), Richeldi L. (ORCID:0000-0001-8594-1448), Sanguinetti M. (ORCID:0000-0002-9780-7059), Urbani A. (ORCID:0000-0001-9168-3174), Zega M. (ORCID:0000-0002-7821-2615), Scambia G. (ORCID:0000-0003-2758-1063), Valentini V. (ORCID:0000-0003-4637-6487), Armuzzi A. (ORCID:0000-0003-1572-0118), Barba M. (ORCID:0000-0001-6084-7666), Baroni S. (ORCID:0000-0002-3410-2617), Bellesi S., Bentivoglio A. (ORCID:0000-0002-9663-095X), Biasucci L. M. (ORCID:0000-0002-6921-6497), Biscetti F. (ORCID:0000-0001-7449-657X), Candelli M. (ORCID:0000-0001-8443-7880), Capalbo G., Cattani P. (ORCID:0000-0003-4678-4763), Chiusolo P. (ORCID:0000-0002-1355-1587), Cingolani A. (ORCID:0000-0002-3793-2755), Corbo G. (ORCID:0000-0002-8104-4659), Covino M. (ORCID:0000-0002-6709-2531), D'Alfonso M., De Angelis G. (ORCID:0000-0002-7087-7399), De Pascale G. (ORCID:0000-0002-8255-0676), Frisullo G., Gambassi G. (ORCID:0000-0002-7030-9359), Gremese E. (ORCID:0000-0002-2248-1058), Iorio R. (ORCID:0000-0002-6270-0956), Landi F. (ORCID:0000-0002-3472-1389), Larici A. (ORCID:0000-0002-1882-6244), Liuzzo G. (ORCID:0000-0002-5714-0907), Maviglia R., Miele L. (ORCID:0000-0003-3464-0068), Montalto M. (ORCID:0000-0001-8819-3684), Natale L. (ORCID:0000-0002-7949-5119), Nicolotti N., Ojetti V. (ORCID:0000-0002-8953-0707), Pompili M. (ORCID:0000-0001-6699-7980), Posteraro B. (ORCID:0000-0002-1663-7546), Rapaccini G. (ORCID:0000-0002-6467-857X), Rossi E. (ORCID:0000-0002-7572-9379), Santoliquido A. (ORCID:0000-0003-1539-4017), Sica S. (ORCID:0000-0003-2426-3465), Tamburrini E. (ORCID:0000-0003-4930-426X), Teofili L. (ORCID:0000-0002-7214-1561), Testa A. (ORCID:0000-0003-2217-8726), Trani C. (ORCID:0000-0001-9777-013X), and Varone F.

Abstract

The COVID-19 pandemic is impressively challenging the healthcare system. Several prognostic models have been validated but few of them are implemented in daily practice. The objective of the study was to validate a machine-learning risk prediction model using easy-to-obtain parameters to help to identify patients with COVID-19 who are at higher risk of death. The training cohort included all patients admitted to Fondazione Policlinico Gemelli with COVID-19 from March 5, 2020, to November 5, 2020. Afterward, the model was tested on all patients admitted to the same hospital with COVID-19 from November 6, 2020, to February 5, 2021. The primary outcome was in-hospital case-fatality risk. The out-of-sample performance of the model was estimated from the training set in terms of Area under the Receiving Operator Curve (AUROC) and classification matrix statistics by averaging the results of fivefold cross validation repeated 3-times and comparing the results with those obtained on the test set. An explanation analysis of the model, based on the SHapley Additive exPlanations (SHAP), is also presented. To assess the subsequent time evolution, the change in paO2/FiO2 (P/F) at 48 h after the baseline measurement was plotted against its baseline value. Among the 921 patients included in the training cohort, 120 died (13%). Variables selected for the model were age, platelet count, SpO2, blood urea nitrogen (BUN), hemoglobin, C-reactive protein, neutrophil count, and sodium. The results of the fivefold cross-validation repeated 3-times gave AUROC of 0.87, and statistics of the classification matrix to the Youden index as follows: sensitivity 0.840, specificity 0.774, negative predictive value 0.971. Then, the model was tested on a new population (n = 1463) in which the case-fatality rate was 22.6%. The test model showed AUROC 0.818, sensitivity 0.813, specificity 0.650, negative predictive value 0.922. Considering the first quartile of the predicted risk score (low-risk sc

Published
2021

27. Platelet hyaluronidase 2 enrichment in acute coronary syndromes: a conceivable role in monocyte-platelet aggregate formation

Author

Vinci, Ramona, Pedicino, Daniela, D'Aiello, A., Ciampi, Pellegrino, Ponzo, Myriana, Bonanni, Alice, Russo, G., Montone, Rocco Antonio, Massetti, Massimo, Crea, Filippo, Liuzzo, Giovanna, Vinci R., Pedicino D., Ciampi P., Ponzo M., Bonanni A., Montone R. A., Massetti M. (ORCID:0000-0002-7100-8478), Crea F. (ORCID:0000-0001-9404-8846), Liuzzo G. (ORCID:0000-0002-5714-0907), Vinci, Ramona, Pedicino, Daniela, D'Aiello, A., Ciampi, Pellegrino, Ponzo, Myriana, Bonanni, Alice, Russo, G., Montone, Rocco Antonio, Massetti, Massimo, Crea, Filippo, Liuzzo, Giovanna, Vinci R., Pedicino D., Ciampi P., Ponzo M., Bonanni A., Montone R. A., Massetti M. (ORCID:0000-0002-7100-8478), Crea F. (ORCID:0000-0001-9404-8846), and Liuzzo G. (ORCID:0000-0002-5714-0907)

Abstract

Acute Coronary Syndromes (ACS) with plaque erosion display dysregulated hyaluronan metabolism, with increased hyaluronidase-2 (HYAL2) expression. However, the expression and the role of this enzyme on platelets has never been explored. We evaluated the platelet’s HYAL2 (pltHYAL2) levels on I) stable angina (SA) and II) ACS patients, furtherly sub-grouped in Intact-Fibrous-Cap (IFC) and Ruptured-Fibrous-Cap (RFC), according to Optical Coherence Tomography. We assessed the HYAL2 role through an in vitro model setting of co-cultured monocytes and platelets, before and after treatment with low-molecular-weight hyaluronic acid (HA) as pro-inflammatory stimulus and with or without HYAL2-antibody to inhibit HYAL2 activity. ACS patients exhibit higher pltHYAL2 levels comparing to SA, with the higher expression for IFC group. The addition of HYAL2-antibody significantly reduced the percentage of monocyte-platelet binding, suggesting that pltHYAL2 enrichment at the site of the culprit lesion is a key mediator in the systemic thrombo-inflammatory status of ACS presenting with plaque erosion.

Published
2021

28. No blossom for fractional flow reserve in FLOWER-MI

Author

Leone, Antonio Maria, Liuzzo, Giovanna, Leone A. M. (ORCID:0000-0002-1276-9883), Liuzzo G. (ORCID:0000-0002-5714-0907), Leone, Antonio Maria, Liuzzo, Giovanna, Leone A. M. (ORCID:0000-0002-1276-9883), and Liuzzo G. (ORCID:0000-0002-5714-0907)

Abstract

N/A

Published
2021

29. Levosimendan for acute right heart failure in COVID-19: another arrow in our quiver?

Author

CRIBARI, F., CONTE, C., RUGGIO, A., NARDUCCI, M. L., PEDICINO, D., BIASUCCI, L. M., and LIUZZO, G.

Abstract

OBJECTIVE: SARS-CoV-2 infection is associated with a higher risk of acute right heart failure (RHF) due to primary right ventricle (RV) dilation and systemic inflammatory response, which in turn lead to microvascular and cardiomyocytes dysfunction, local hypoxia and multi-organ failure. In this clinical setting, levosimendan could be a viable therapy thanks to its right-heart tropism and its additional pleiotropic properties. CASE REPORT: We present the case of a 72 years-old man with positive nasopharyngeal swab for SARS-CoV-2 infection, mild pulmonary involvement and clinical signs of new-onset RHF. We started a 12-hour levosimendan cycle to improve RV performance and reduce cardiac filling pressures. RESULTS: We obtained a net clinical benefit in terms of acute RHF-related signs and symptoms, progressive renal and liver function improvement and concomitant reduction of high-sensitivity C-Reactive Protein and Interleukin-6 (IL-6) levels. CONCLUSIONS: Acute RHF during SARSCoV-2 infection could be related to a convergent widespread systemic inflammatory response. Thanks to its anti-inflammatory and anti-remodeling properties, levosimendan might represent a viable therapy in this clinical setting, contributing to the dampening of the inflammatory response. [ABSTRACT FROM AUTHOR]

Published
2022

31. Brain-derived neurotrophic factor in patients with acute coronary syndrome

Author

Montone, Rocco Antonio, Camilli, Massimiliano, Del Buono, Marco Giuseppe, Russo, M., Rinaldi, R., Canonico, Francesco, Pedicino, Daniela, Severino, Anna, D'Amario, Domenico, Trani, Carlo, Liuzzo, Giovanna, Crea, Filippo, Niccoli, Giampaolo, Montone R. A., Camilli M., Del Buono M. G., Canonico F. (ORCID:0000-0001-6936-4548), Pedicino D., Severino A., D'Amario D., Trani C. (ORCID:0000-0001-9777-013X), Liuzzo G. (ORCID:0000-0002-5714-0907), Crea F. (ORCID:0000-0001-9404-8846), Niccoli G. (ORCID:0000-0002-3187-6262), Montone, Rocco Antonio, Camilli, Massimiliano, Del Buono, Marco Giuseppe, Russo, M., Rinaldi, R., Canonico, Francesco, Pedicino, Daniela, Severino, Anna, D'Amario, Domenico, Trani, Carlo, Liuzzo, Giovanna, Crea, Filippo, Niccoli, Giampaolo, Montone R. A., Camilli M., Del Buono M. G., Canonico F. (ORCID:0000-0001-6936-4548), Pedicino D., Severino A., D'Amario D., Trani C. (ORCID:0000-0001-9777-013X), Liuzzo G. (ORCID:0000-0002-5714-0907), Crea F. (ORCID:0000-0001-9404-8846), and Niccoli G. (ORCID:0000-0002-3187-6262)

Abstract

Brain-derived neurotrophic factor (BDNF) is a neurotrophic factor highly expressed in coronary plaques, particularly in macrophages, and in activated platelets. Thus, a possible role in the pathogenesis of acute coronary syndrome (ACS) has been suggested. We evaluated systemic BDNF levels according to the different clinical presentations of ACS. Moreover, we assessed the relationship between BDNF levels and the presence of optical coherence tomography (OCT)-defined macrophage infiltrates (MØI) and healed plaques along the culprit vessel. We enrolled consecutive patients presenting with ST-elevation myocardial infarction (STEMI) or non-ST-elevation (NSTE)-ACS. Serum BDNF levels were assessed by enzyme-linked immunosorbent assay. Plaque characteristics of the culprit vessel were assessed by OCT. Among 126 ACS patients (median age 68.00, interquartile range [IQR] 59.75–75.25 years, male 74.6%, 71 (56.3%) were NSTE-ACS and 55 (43.7%) were STEMI. BDNF levels were higher in STEMI patients compared to NSTE-ACS. OCT assessment was performed in 53 (42.1%) patients. Patients with MØI (n = 27) had higher BDNF levels compared to patients without MØI. Furthermore, patients with healed plaques (n = 13) had lower BDNF levels than patients without healed plaques. At multivariate regression analysis BDNF levels independently predicted the presence of MØI (odds ratio [OR] = 2.856; 95% confidence interval [CI] [1.151–7.090], P = 0.024) and the absence of healed plaques (OR = 0.438, 95% CI [0.185–0.992], P= 0.050). Among ACS patients, BDNF levels were higher in patients with STEMI. Moreover, BDNF levels were independently associated with MØI and with the absence of healed plaques along the culprit vessel, suggesting a possible role of BDNF in promoting plaque inflammation, destabilization and occlusive thrombosis.

Published
2020

32. CD8 lymphocytes and plaque erosion: A new piece in the jigsaw

Author

Liuzzo, Giovanna, Pedicino, Daniela, Vinci, Ramona, Crea, Filippo, Liuzzo G. (ORCID:0000-0002-5714-0907), Pedicino D., Vinci R., Crea F. (ORCID:0000-0001-9404-8846), Liuzzo, Giovanna, Pedicino, Daniela, Vinci, Ramona, Crea, Filippo, Liuzzo G. (ORCID:0000-0002-5714-0907), Pedicino D., Vinci R., and Crea F. (ORCID:0000-0001-9404-8846)

Abstract

N/A

Published
2020

33. Clinical, angiographic and echocardiographic correlates of epicardial and microvascular spasm in patients with myocardial ischaemia and non-obstructive coronary arteries

Author

Montone, Rocco Antonio, Niccoli, Giampaolo, Russo, M., Giaccari, Marta, Del Buono, Marco Giuseppe, Meucci, Maria Chiara, Gurguglione, F., Vergallo, Rocco, D'Amario, Domenico, Buffon, Antonino Maria Tommaso, Leone, Antonio Maria, Burzotta, Francesco, Aurigemma, Cristina, Trani, Carlo, Liuzzo, Giovanna, Lanza, Gaetano Antonio, Crea, Filippo, Montone R. A., Niccoli G. (ORCID:0000-0002-3187-6262), Giaccari M., Del Buono M. G., Meucci M. C., Vergallo R., D'Amario D., Buffon A. (ORCID:0000-0002-6910-8357), Leone A. M. (ORCID:0000-0002-1276-9883), Burzotta F. (ORCID:0000-0002-6569-9401), Aurigemma C., Trani C. (ORCID:0000-0001-9777-013X), Liuzzo G. (ORCID:0000-0002-5714-0907), Lanza G. A. (ORCID:0000-0003-2187-6653), Crea F. (ORCID:0000-0001-9404-8846), Montone, Rocco Antonio, Niccoli, Giampaolo, Russo, M., Giaccari, Marta, Del Buono, Marco Giuseppe, Meucci, Maria Chiara, Gurguglione, F., Vergallo, Rocco, D'Amario, Domenico, Buffon, Antonino Maria Tommaso, Leone, Antonio Maria, Burzotta, Francesco, Aurigemma, Cristina, Trani, Carlo, Liuzzo, Giovanna, Lanza, Gaetano Antonio, Crea, Filippo, Montone R. A., Niccoli G. (ORCID:0000-0002-3187-6262), Giaccari M., Del Buono M. G., Meucci M. C., Vergallo R., D'Amario D., Buffon A. (ORCID:0000-0002-6910-8357), Leone A. M. (ORCID:0000-0002-1276-9883), Burzotta F. (ORCID:0000-0002-6569-9401), Aurigemma C., Trani C. (ORCID:0000-0001-9777-013X), Liuzzo G. (ORCID:0000-0002-5714-0907), Lanza G. A. (ORCID:0000-0003-2187-6653), and Crea F. (ORCID:0000-0001-9404-8846)

Abstract

Background: Coronary vasomotor dysfunction represents an important mechanism responsible for myocardial ischaemia in patients with non-obstructive coronary artery disease (CAD). The use of invasive provocative tests allows identifying patients with epicardial or microvascular spasm. Of note, clinical characteristics associated with the occurrence of epicardial or microvascular spasm have still not completely clarified. Methods and results: We prospectively enrolled consecutive patients undergoing coronary angiography for suspected myocardial ischaemia/necrosis with evidence of non-obstructive CAD and undergoing intracoronary provocative test for suspected vasomotor dysfunction. Patients with a positive provocative test were enrolled. Clinical, echocardiographic and angiographic characteristics of patients were evaluated according to the pattern of vasomotor dysfunction (epicardial vs. microvascular spasm). We included 120 patients [68 patients with stable angina and 52 patients with myocardial infarction and non-obstructive coronary arteries (MINOCA)]. In particular, 77 (64.2%) patients had a provocative test positive for epicardial spasm and 43 (35.8%) patients for microvascular spasm. Patients with epicardial spasm were more frequently males, smokers, had higher rates of diffuse coronary atherosclerosis at angiography and more frequently presented with MINOCA. On the other hand, patients with microvascular spasm presented more frequently diastolic dysfunction. At multivariate logistic regression analysis male sex, smoking, and diffuse coronary atherosclerosis were independent predictors for the occurrence of epicardial spasm. Conclusions: Our study showed that specific clinical features are associated with different responses to intracoronary provocative test. Epicardial spasm is more frequent in males and in MINOCA patients, whereas microvascular spasm is more frequent in patients with stable angina and is associated with diastolic dysfunction.

Published
2020

34. Non invasive ventilation and right ventricle function in cardiogenic pulmonary edema: an echocardiographic perspective to select the "right" ventilatory support

Author

Pedicino, D, primary, Angelini, A, additional, Russo, G, additional, D"aiello, A, additional, Rocco, E, additional, Ciampi, P, additional, Ponzo, M, additional, Graziani, F, additional, Locorotondo, G, additional, Sanna, T, additional, Rebuzzi, AG, additional, Lombardo, A, additional, Massetti, M, additional, Liuzzo, G, additional, and Crea, F, additional

Published
2021
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36. Perilipin-2 is associated with a higher risk of microvascular obstruction in ST-elevation myocardial infarction patients undergoing primary percutaneous coronary intervention

Author

Russo, M, primary, Montone, R.A, additional, D'Amario, D, additional, Camilli, M, additional, Canonico, F, additional, Santamaria, C, additional, Iannaccone, G, additional, Meucci, M.C, additional, Gurgoglione, F, additional, Severino, A, additional, Liuzzo, G, additional, Niccoli, G, additional, and Crea, F, additional

Published
2020
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38. Plaque instability in acute coronary syndromes: a possible pathogenic role of gut microbial communities

Author

Pisano, E, primary, Severino, A, additional, Bugli, F, additional, Pedicino, D, additional, Paroni Sterbini, F, additional, Martini, C, additional, Vinci, R, additional, Canonico, F, additional, Bonanni, A, additional, D'Aiello, A, additional, Ciampi, P, additional, Ponzo, M, additional, Sanguinetti, M, additional, Crea, F, additional, and Liuzzo, G, additional

Published
2020
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39. Meta-inflammation in monocytes of patients with Acute Coronary Syndrome

Author

Canonico, F, primary, Vinci, R, additional, Pedicino, D, additional, Pisano, E, additional, Ciampi, P, additional, Bonanni, A, additional, Ponzo, M, additional, D'Aiello, A, additional, Di Sario, M, additional, Severino, A, additional, D'Amario, D, additional, Niccoli, G, additional, Biasucci, L.M, additional, Crea, F, additional, and Liuzzo, G, additional

Published
2020
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41. Fluid-dynamics and biological features of unstable plaques: different shear stress for different plaques

Author

Russo, G, primary, Pedicino, D, additional, Burzotta, F, additional, Lodi Rizzini, M, additional, Genuardi, L, additional, Vinci, R, additional, Bologna, M, additional, D'Aiello, A, additional, Gallo, D, additional, Chiastra, C, additional, Aurigemma, C, additional, Bonanni, A, additional, Trani, C, additional, Liuzzo, G, additional, and Crea, F, additional

Published
2020
Full Text
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