Antonio Abbate

Richmond VA Medical Center, Ричмонд, Virginia, United States

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Publications (314)2075.51 Total impact

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    ABSTRACT: Heart failure (HF) is a clinical syndrome characterized by dyspnea, fatigue, exercise intolerance and cardiac dysfunction. Unhealthy diet has been associated with increased risk of obesity and heart disease, but whether it directly affects cardiac function, and promotes the development and progression of HF is unknown. We fed 8-week old male or female CD-1 mice with a standard diet (SD) or a diet rich in saturated fat and sugar, resembling a "Western" diet (WD). Cardiac systolic and diastolic function was measured at baseline and 4 and 8weeks by Doppler echocardiography, and left ventricular (LV) end-diastolic pressure (EDP) by cardiac catheterization prior to sacrifice. An additional group of mice received WD for 4weeks followed by SD (wash-out) for 8weeks. WD-fed mice experienced a significant decreased in LV ejection fraction (LVEF), reflecting impaired systolic function, and a significant increase in isovolumetric relaxation time (IRT), myocardial performance index (MPI), and LVEDP, showing impaired diastolic function, without any sex-related differences. Switching to a SD after 4weeks of WD partially reversed the cardiac systolic and diastolic dysfunction. A diet rich in saturated fat and sugars (WD) impairs cardiac systolic and diastolic function in the mouse. Further studies are required to define the mechanism through which diet affects cardiac function, and whether dietary interventions can be used in patients with, or at risk for, HF. Published by Elsevier Ireland Ltd.
    International journal of cardiology 11/2015; 198. DOI:10.1016/j.ijcard.2015.06.136 · 6.18 Impact Factor
  • International journal of cardiology 08/2015; 201:328-330. DOI:10.1016/j.ijcard.2015.08.070 · 6.18 Impact Factor
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    ABSTRACT: Effective primary and secondary prevention and advances in cardiac surgery have significantly improved the care and outcomes of patients with myocardial ischemia. While timely reperfusion has proved to be an invaluable tool, ischemia–reperfusion injury represents a mechanism that may limit its effectiveness. Numerous experimental studies have shown effective protection from ischemia–reperfusion injury in animal models, but translation into clinical practice has been less successful. This article summarizes the role of ischemia–reperfusion injury in the pathophysiology of ischemic heart disease and gives an overview of the various modalities that have been developed in order to provide myocardial protection from reperfusion injury in clinical practice.
    Expert Review of Cardiovascular Therapy 07/2015; DOI:10.1586/14779072.2015.1070669
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    ABSTRACT: Heart failure (HF) with preserved ejection fraction (HFpEF) is a clinical syndrome of HF symptoms associated with impaired diastolic function. Although it represents approximately 50% of patients with HF, the mechanisms of disease are poorly understood and therapies are generally ineffective in reducing HF progression. Animal models of HFpEF not due to pressure or volume overload are lacking therefore limiting in-depth understanding of the pathophysiologic mechanisms and the development of novel therapies. We hypothesize that a continuous infusion of low dose angiotensin II (ATII) is sufficient to induce left ventricular (LV) diastolic dysfunction and HFpEF, without increasing blood pressure or inducing LV hypertrophy or dilatation. Osmotic pumps were implanted subcutaneously in eight-week-old male mice assigned to the ATII (0.2 mg/Kg/day) or volume-matched vehicle (N=8/group) for 4 weeks. We measured systolic and diastolic arterial blood pressures through a tail-cuff transducer, LV dimensions and ejection fraction (LVEF) through echocardiography, and LV relaxation through pulsed-wave Doppler and LV catheterization. Myocardial fibrosis and cardiomyocyte cross-sectional area were measured. ATII infusion had no effects on systemic arterial blood pressure. ATII induced significant impairment in LV diastolic function as measured by an increase (worsening) in LV isovolumetric relaxation time (IRT), myocardial performance index (MPI), tau (τ) and LVEDP without altering LV dimensions, mass, or EF. Chronic infusion of low dose ATII recapitulates the HFpEF phenotype in the mouse, without increasing systemic arterial blood pressure. This mouse model may provide insight into the mechanisms of HFpEF. Copyright © 2015, American Journal of Physiology - Heart and Circulatory Physiology.
    AJP Heart and Circulatory Physiology 07/2015; DOI:10.1152/ajpheart.00282.2015 · 4.01 Impact Factor
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    ABSTRACT: Abstract BACKGROUND: Cardiovascular research is the main shaper of clinical evidence underpinning decision making, with its cyclic progression of junior researchers to mature faculty members. Despite efforts at improving cardiovascular research training, several unmet needs persist. We aimed to appraise current perceptions on cardiovascular research training with an international survey. METHODS AND RESULTS: We administered a 20-closed-question survey to mentors and mentees belonging to different international institutions. A total of 247 (12%) surveys were available (out of 2,000 invitations). Overall, mentees and mentors were reasonably satisfied with the educational and research resources. Significant differences were found analyzing results according to gender, geographic area, training and full-time researcher status. Specifically, women proved significantly less satisfied than men, disclosed access to fewer resources and less support from mentors (all P<0.05). People working in institutions not located in North America or Northern/Central Europe were significantly less satisfied and disclosed much less support (both P<0.05). Those in training reported limited opportunities for collaboration (P = 0.009), and non-full-time researchers disclosed more limited access to tutors and formal grant writing training (both P<0.05). CONCLUSIONS: Several potential biases appear to be present in the way training in cardiovascular research is provided worldwide, including one against women. If confirmed, these data require proactive measures to decrease discriminations and improve the cardiovascular research training quality. PMID: 26186203 [PubMed - as supplied by publisher
    PLoS ONE 07/2015; 10(7). DOI:10.1371/journal.pone.0131900 · 3.23 Impact Factor
  • Antonio Abbate · Allison C Morton · David C Crossman
    The Lancet 06/2015; 385(9987):2573-4. DOI:10.1016/S0140-6736(15)61153-9 · 45.22 Impact Factor
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    ABSTRACT: Abstract Objectives. To provide a comprehensive appraisal of the evidence from secondary research on cardiac regenerative therapy. Study Design and Setting. Overview of systematic reviews of controlled clinical trials concerning stem cell administration or mobilization in patients with cardiovascular disease. Results. After a systematic database search, we short-listed 41 reviews (660 patients). Twenty-two (54%) reviews focused on acute myocardial infarction (AMI), 19 (46%) on chronic ischemic heart disease (IHD) or heart failure (HF), 29 (71%) on bone marrow-derived stem-cells (BMSC), and 36 (88%) to randomized trials only. Substantial variability among reviews was found for validity (AMSTAR score: median 9 [minimum 3]; 1st quartile 9; 3rd quartile 10; maximum 11), effect estimates (change in ejection fraction from baseline to follow-up: 3.47% [0.02%; 2.90%; 4.22%; 6.11%]), and citations (Web of Science yearly citations: 4.1 [0; 2.2; 6.5; 68.9]). No significant association was found between these three features. However, reviews focusing on BMSC therapy had higher validity scores (P = 0.008) and showed more pronounced effect estimates (P = 0.002). Higher citations were associated with journal impact factor (P = 0.007), corresponding author from North America/Europe (P = 0.022), and inclusion of nonrandomized trials (P = 0.046). Conclusions. Substantial heterogeneity is apparent among these reviews in terms of quality and effect estimates. Go to: 1. Introduction
    BioMed Research International 06/2015; · 2.71 Impact Factor
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    ABSTRACT: Patients with advanced liver cirrhosis may develop a clinical syndrome characterized by a blunted contractile responsiveness to stress and/or altered diastolic relaxation, called "cirrhotic cardiomyopathy." This syndrome, which is initially asymptomatic, is often misdiagnosed due to the presence of symptoms that characterize other disorders present in patients with advanced liver cirrhosis, such as exercise intolerance, fatigue, and dyspnea. Stress and other conditions such as liver transplantation and transjugular intrahepatic portosystemic shunt (TIPS) may unmask this syndrome. Liver transplantation in this group of patients results in a clinical improvement and can be a cure for the cardiomyopathy. However, post-transplant prognosis depends on the identification of cirrhotics with cardiomyopathy in the pre-transplant phase; an early diagnosis of cirrhotic cardiomyopathy in the pre-transplant phase may avoid an acute onset or worsening of cardiac failure after liver transplantation. Since a preserved left ventricular ejection fraction may mask the presence of cirrhotic cardiomyopathy, the use of newer noninvasive diagnostic techniques (i.e. tissue Doppler, myocardial strain) is necessary to identify cirrhotics with this syndrome, in the pre-transplant phase. A pre-transplant treatment of heart failure in cirrhotics with cardiomyopathy improves the quality of life in this phase and reduces the complications during and immediately after liver transplantation. Since specific therapies for cirrhotic cardiomyopathy are lacking, due to the absence of a clear understanding of the pathophysiology of the cardiomyopathy, further research in this field is required. Copyright © 2015 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
    Journal of Cardiology 06/2015; DOI:10.1016/j.jjcc.2015.04.016 · 2.57 Impact Factor
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    ABSTRACT: Asymptomatic patients with human immunodeficiency virus (HIV) infection are at increased risk of vascular disease. Whether asymptomatic HIV patients have increased prevalence or structural differences in coronary artery plaques is not clear. Pubmed, Cochrane and Google Scholar were searched for articles evaluating asymptomatic HIV patients evaluated with coronary computed tomography. The prevalence of coronary stenosis (defined as >30% and >50%), of calcified coronary plaques (CCP) viewed as more 'stable' plaques, and of non-calcified coronary plaques (NCP) viewed as more 'vulnerable' plaques were the end points of interest. 9 studies with 1229 HIV patients and 1029 controls were included. No significant differences were detected about baseline cardiovascular risk profile. The prevalence of significant coronary stenosis >30% or >50% did not differ between HIV+ and HIV- patients (42% [37-44] and 46% [35-52] with an Odds Ratio [OR] of 1.38 [0.86-2.20] for >30% stenosis) and (15% [9-21] and 14% [7-22] with an OR of 1.11 [0.81-1.52]), respectively. The prevalence of calcified coronary plaques (CCP) (31% [24-32] and 21% [14-30] with an OR of 1.17 [0.63-2.16]) also did not differ among HIV+ and HIV- patients. On the contrary rates of NCP were >3-fold higher in HIV-positive patients [58% (48-60) and 17% (14-27) with an OR of 3.26 (1-30-8.18)], with an inverse relationship with CD4 cell count at meta-regression (Beta -0.20 [-0.35-0.18], p 0.04). Asymptomatic HIV patients present a similar burden of coronary stenosis and calcified coronary artery plaques but significantly higher rates of non-calcific coronary plaques at computed tomography. The association between HIV infection, reduced CD4 cell counts and higher prevalence on non-calcific coronary artery plaques may shed light into the pathogenesis in HIV-associated coronary artery disease, stressing the importance of primary prevention in this population. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Atherosclerosis 05/2015; 240(1). DOI:10.1016/j.atherosclerosis.2015.03.019 · 3.97 Impact Factor
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    ABSTRACT: Sterile inflammation resulting from myocardial injury activates the NLRP3 inflammasome and amplifies the inflammatory response mediating further damage. We used two experimental models of ischemic injury (acute myocardial infarction [AMI] with and without reperfusion) and a model of non-ischemic injury due to doxorubicin 10 mg/Kg, to determine whether the NLRP3 inflammasome preserved cardiac function after injury. Treatment with the NLRP3 inflammasome inhibitor in the reperfused AMI model caused a significant reduction in infarct size measured at pathology or as serum cardiac troponin I level (-56% and -82% respectively, both p<0.001), and preserved LV fractional shortening (LVFS, 31±2 vs vehicle 26±1%, p=0.003). In the non-reperfused AMI model treatment with the NLRP3 inhibitor significantly limited LV systolic dysfunction at 7 days (LVFS of 20±2 vs 14±1%, p=0.002), without a significant effect on infarct size. In the DOX model, a significant increase in myocardial interstitial fibrosis and a decline in systolic function were seen in vehicle-treated mice, whereas treatment with the NLRP3 inhibitor significantly reduced fibrosis (-80%, p=0.001) and preserved systolic function (LVFS 35±2 vs vehicle 27±2%, p=0.017). Pharmacological inhibition of the NLRP3 inflammasome limits cell death and LV systolic dysfunction following ischemic and non-ischemic injury in the mouse.
    Journal of cardiovascular pharmacology 04/2015; Publish Ahead of Print. DOI:10.1097/FJC.0000000000000247 · 2.11 Impact Factor
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    Journal of Endovascular Therapy 04/2015; 22(2):240-2. DOI:10.1177/1526602815573217 · 3.59 Impact Factor
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    ABSTRACT: Thoracic X-Ray Therapy (XRT), used in cancer treatment, is associated with increased risk of heart failure. XRT-mediated injury to the heart induces an inflammatory response leading to cardiomyopathy. The aim of this study was to determine the role of Interleukin (IL)-1 in response to XRT injury to the heart and on the cardiomyopathy development in the mouse.Female mice with genetic deletion of the Interleukin-1 receptor type I (IL-1R1 Knock Out mice [IL-1R1 KO]), and treatment with recombinant human IL-1 receptor antagonist, anakinra 10 mg/kg twice daily for 7 days, were used as independent approaches to determine the role of IL-1. Wild type (wt) or IL-1R1 KO mice were treated with a single session of XRT (20 or 14 Gray [Gy]). Echocardiography (before and after isoproterenol challenge) and left ventricular (LV) catheterization were performed to evaluate changes in LV dimensions and function. Masson's trichrome was used to assess myocardial fibrosis and pericardial thickening.After 20 Gy, the contractile reserve was impaired in wt mice at day 3, and the LV ejection fraction (EF) was reduced after 4 months when compared with sham-XRT. IL-1R1 KO mice had preserved contractile reserve at 3 days and 4 months and LVEF at 4 months after XRT. Anakinra treatment for 1 day before and 7 days after XRT prevented the impairment in contractile reserve. A significant increase in LV end-diastolic pressure (LVEDP), associated with increased myocardial interstitial fibrosis and pericardial thickening, was observed in wt mice, as well as in IL-1R1 KO or anakinra-treated mice.In conclusion, induction of IL-1 by XRT mediates the development of some, such as the contractile impairment, but not all aspects of the XRT-induced cardiomyopathy, such as myocardial fibrosis or pericardial thickening.
    Molecular Medicine 03/2015; DOI:10.2119/molmed.2014.00243 · 4.82 Impact Factor
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    ABSTRACT: HIV patients are exposed to a higher risk of adverse cardiovascular events, due to complex interactions between traditional risk factors and HIV infection itself in terms of ongoing endothelial dysfunctional immune activation/inflammation and increased risk of thrombosis. On the other hand, long-span antiretroviral therapy administration still raises questions on its long-term safety in an era in which life expectancy is becoming longer and longer while treatment of non-HIV-related serious events is increasingly raising concern. In this article, we will critically analyse the current knowledge of pathological and clinical aspects pertaining to the increased risk of cardiovascular events associated with HIV.
    03/2015; 2(1):e000174-e000174. DOI:10.1136/openhrt-2014-000174
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    ABSTRACT: Inflammation and altered immunity are recognized components of severe pulmonary arterial hypertension in human patients and in animal models of PAH. While eicosanoid metabolites of cyclooxygenase and lipoxygenase pathways have been identified in the lungs from pulmonary hypertensive animals their role in the pathogenesis of severe angioobliterative PAH has not been examined. Here we investigated whether a cyclooxygenase-2 (COX-2) inhibitor or diethylcarbamazine (DEC), that is known for its 5-lipoxygenase inhibiting and antioxidant actions, modify the development of PAH in the Sugen 5416/hypoxia (SuHx) rat model. The COX-2 inhibitor SC-58125 had little effect on the right ventricular pressure and did not prevent the development of pulmonary angioobliteration. In contrast, DEC blunted the muscularization of pulmonary arterioles and reduced the number of fully obliterated lung vessels. DEC treatment of SuHx rats, after the lung vascular disease had been established, reduced the degree of PAH, the number of obliterated arterioles and the degree of perivascular inflammation. We conclude that the non-specific anti-inflammatory drug DEC affects developing PAH and is partially effective once angioobliterative PAH has been established.
    PLoS ONE 03/2015; 10(3):e0120157. DOI:10.1371/journal.pone.0120157 · 3.23 Impact Factor
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    ABSTRACT: Despite momentous breakthroughs in unraveling the pathophysiology of many chronic conditions and developing novel therapeutic agents, everyday clinical practice is still fraught with inadequate or inappropriate use of treatments with proven benefits. Aspirin is a paradigmatic example, as it is used for the primary and secondary prevention of cardiovascular disease and appears to have a beneficial impact on cancer risk. Yet, underuse, non-compliance or cessation of aspirin are not uncommon, may have an important clinical impact, and are not aggressively prevented or managed. Increasing the awareness of the extent and impact of aspirin underuse, non-compliance or cessation, and intensifying efforts at preventing them are worthy goals likely to yield significant benefits on cardiovascular morbidity and mortality worldwide, and possibly also on cancer outcomes.
    International Journal of Cardiology 03/2015; 182. DOI:10.1016/j.ijcard.2014.12.091 · 6.18 Impact Factor
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    ABSTRACT: The mechanisms involved in the development of severe angioobliterative pulmonary arterial hypertension (PAH) are multicellular and complex. Many of the features of human severe PAH, including angioobliteration, lung perivascular inflammation, and right heart failure, are reproduced in the Sugen 5416/chronic hypoxia (SuHx) rat model. Here we address, at first glance, the confusing and paradoxical aspect of the model, namely, that treatment of rats with the antiangiogenic vascular endothelial growth factor (VEGF) receptor 1 and 2 kinase inhibitor, Sugen 5416, when combined with chronic hypoxia, causes angioproliferative pulmonary vascular disease. We postulated that signaling through the unblocked VEGF receptor VEGFR3 (or flt4) could account for some of the pulmonary arteriolar lumen-occluding cell growth. We also considered that Sugen 5416-induced VEGFR1 and VEGFR2 blockade could alter the expression pattern of VEGF isoform proteins. Indeed, in the lungs of SuHx rats we found increased expression of the ligand proteins VEGF-C and VEGF-D as well as enhanced expression of the VEGFR3 protein. In contrast, in the failing right ventricle of SuHx rats there was a profound decrease in the expression of VEGF-B and VEGF-D in addition to the previously described reduction in VEGF-A expression. MAZ51, an inhibitor of VEGFR3 phosphorylation and VEGFR3 signaling, largely prevented the development of angioobliteration in the SuHx model; however, obliterated vessels did not reopen when animals with established PAH were treated with the VEGFR3 inhibitor. Part of the mechanism of vasoobliteration in the SuHx model occurs via VEGFR3. VEGFR1/VEGFR2 inhibition can be initially antiangiogenic by inducing lung vessel endothelial cell apoptosis; however, it can be subsequently angiogenic via VEGF-C and VEGF-D signaling through VEGFR3.
    03/2015; 5(1):101-116. DOI:10.1086/679704
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    ABSTRACT: After acute myocardial infarction, ventricular remodeling is characterized by changes at the molecular, structural, geometrical and functional level that determine progression to heart failure. Inflammation plays a key role in wound healing and scar formation, affecting ventricular remodeling. Several, rather different, components of the inflammatory response were studied as biomarkers in ST-elevation acute myocardial infarction. Widely available and inexpensive tests, such as leukocyte count at admission, as well as more sophisticated immunoassays provide powerful predictors of adverse outcome in patients with ST-elevation acute myocardial infarction. We review the value of inflammatory markers in ST-elevation acute myocardial infarction and their association with ventricular remodeling, heart failure and sudden death. In conclusion, the use of these biomarkers may identify subjects at greater risk of adverse events and perhaps provide an insight into the mechanisms of disease progression. © The European Society of Cardiology 2015.
    European Heart Journal: Acute Cardiovascular Care 02/2015; DOI:10.1177/2048872615568965
  • Giuseppe Biondi-Zoccai · Giacomo Frati · Antonio Abbate
    JACC Cardiovascular Interventions 02/2015; 8(3). DOI:10.1016/j.jcin.2014.12.005 · 7.44 Impact Factor
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    ABSTRACT: Abstract Clinical decision-making requires synthesis of an often complex evidence base. Novel tools have been developed building upon the historical approach of reviewing the literature focusing on a specific topic. Stemming from qualitative reviews, systematic reviews of randomized clinical trials, typically encompassing statistical pooling with pairwise meta-analysis, have been devised and are now considered one of the uppermost ladders in the hierarchy of clinical evidence. In the last decade, the exponential growth in randomized trials and the introduction of original computational methods have created the novel opportunity to compare indirectly competing treatments, as well as combining effect estimates stemming from head-to-head trials with those obtained by indirect comparisons. These methods include adjusted indirect comparison meta-analysis, network meta-analysis, and mixed treatment comparison. While still the focus of intense research and debate, they represent a powerful tool for evidence synthesis and comparative effectiveness in cardiovascular research, and thus are likely to become increasingly popular and impactful in shaping research agenda and clinical practice. This is clearly highlighted by a number of recent landmark network meta-analyses on smoking cessation therapies, coronary stents, and management of patent foramen ovale in patients with history of cryptogenic stroke. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. KEYWORDS: Adjusted indirect comparison meta-analysis; Evidence-based medicine; Mixed treatment comparison; Network meta-analysis; Systematic review PMID: 25585376 [PubMed - as supplied by publisher]
    International Journal of Cardiology 01/2015; · 6.18 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Clinical decision-making requires synthesis of an often complex evidence base. Novel tools have been developed building upon the historical approach of reviewing the literature focusing on a specific topic. Stemming from qualitative reviews, systematic reviews of randomized clinical trials, typically encompassing statistical pooling with pairwise meta-analysis, have been devised and are now considered one of the uppermost ladders in the hierarchy of clinical evidence. In the last decade, the exponential growth in randomized trials and the introduction of original computational methods have created the novel opportunity to compare indirectly competing treatments, as well as combining effect estimates stemming from head-to-head trials with those obtained by indirect comparisons. These methods include adjusted indirect comparison meta-analysis, network meta-analysis, and mixed treatment comparison. While still the focus of intense research and debate, they represent a powerful tool for evidence synthesis and comparative effectiveness in cardiovascular research, and thus are likely to become increasingly popular and impactful in shaping research agenda and clinical practice. This is clearly highlighted by a number of recent landmark network meta-analyses on smoking cessation therapies, coronary stents, and management of patent foramen ovale in patients with history of cryptogenic stroke. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    International Journal of Cardiology 01/2015; 182C:309-314. DOI:10.1016/j.ijcard.2015.01.023 · 6.18 Impact Factor

Publication Stats

5k Citations
2,075.51 Total Impact Points

Institutions

  • 2007–2015
    • Richmond VA Medical Center
      Ричмонд, Virginia, United States
  • 2005–2015
    • Virginia Commonwealth University
      • • Division of Cardiology
      • • VCU Medical center
      • • Department of Internal Medicine
      • • School of Medicine
      Ричмонд, Virginia, United States
    • University of Verona
      Verona, Veneto, Italy
  • 2005–2014
    • Università degli Studi di Torino
      • Department of Medical Science
      Torino, Piedmont, Italy
  • 2002–2011
    • Catholic University of the Sacred Heart
      • Institute of Cardiology
      Roma, Latium, Italy
    • Universitá degli Studi Internazionali di Roma
      Roma, Latium, Italy
  • 2010
    • Julphar School of Pharmacy
      Richmond, California, United States
  • 2009
    • Mount Sinai School of Medicine
      • Department of Radiology
      Manhattan, New York, United States
  • 2003–2009
    • The Catholic University of America
      Washington, Washington, D.C., United States
    • Sacred Heart University
      Феърфилд, Connecticut, United States
  • 2003–2007
    • Università degli Studi di Trieste
      Trst, Friuli Venezia Giulia, Italy
  • 2002–2003
    • Second University of Naples
      Caserta, Campania, Italy
  • 2001–2002
    • LIUCBM Libera Università Campus Bio-Medico di Roma
      • Unit of Medical Oncology
      Roma, Latium, Italy