Antonio Abbate

Richmond VA Medical Center, Ричмонд, Virginia, United States

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Publications (334)2171.84 Total impact

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    ABSTRACT: Successful reperfusion is the most effective strategy to reduce ischemic injury in acute myocardial infarction (AMI). Ischemic injury, however, also triggers a secondary ischemia–independent injury, known as reperfusion injury, contributing to the overall infarct size. We hypothesize that inhibition of the Nod-like Receptor Protein-3 (NLRP3) inflammasome limits infarct size following myocardial ischemia/reperfusion (I/R), by inhibiting the inflammatory component of the reperfusion injury.
    No preview · Article · Feb 2016
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    ABSTRACT: Aim: The post-cardiac arrest syndrome is a complex set of pathophysiological processes including a systemic inflammatory response. The goal of the current investigation was to test the hypothesis that early inflammatory markers are independently associated with in-hospital mortality and poor neurological outcome in patients initially resuscitated from out-of-hospital cardiac arrest. Methods: This was a preplanned analysis of data collected from a prospective observational multicenter study in adult out-of-hospital cardiac arrest patients. Blood was drawn at baseline, 12 and 24hours after return of spontaneous circulation and plasma levels of interleukin (IL)-1β, IL-1 receptor antagonist (IL-1Ra), IL-6, IL-8, IL-10 and tumor necrosis factor (TNF)-α were measured. The primary outcome measure for the current study was survival to hospital discharge. We utilized a mixed linear model to compare the levels of cytokines in survivors and non-survivors over time. We used multivariable logistic regression to assess the association between IL-6 levels and mortality. Results: A total of 102 patients were analyzed. Non-survivors and patients with poor functional outcome had statistical significant higher IL-1Ra, IL-6, IL-8, and IL-10 levels (all p<0.001) at all time points (0, 12 and 24hours) compared to survivors. Baseline IL-6 levels were a good predictor of mortality (AUC=0.83 [95%CI: 0.75-0.92]). Baseline IL-6 levels were strongly associated with mortality in multivariable analysis (OR: 2.58 [95%CI: 1.93-3.45], p<0.001) but were not associated with neurological outcome in multivariable analysis (OR: 1.33 [95%CI: 0.62-2.86], p=0.47). Conclusion: Early inflammatory markers, especially IL-6, are higher in patients with a poor outcome after OHCA. IL-6 remained associated with mortality, but not functional outcome, in multivariable analysis adjusting for patient and event characteristics.
    No preview · Article · Jan 2016 · Resuscitation
  • Stefano Toldo · Carlo Marchetti · Antonio Abbate

    No preview · Article · Jan 2016 · Biochemical and Biophysical Research Communications
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    Full-text · Article · Jan 2016
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    ABSTRACT: The peptide hormone relaxin has traditionally been linked to the maternal adaptation of the cardiovascular system during the first trimester of pregnancy. By promoting nitric oxide formation through different molecular signaling events, relaxin has been proposed as a pleiotropic and cardioprotective hormone in the setting of many cardiovascular diseases. In fact, preclinical studies were able to demonstrate that relaxin promotes vasodilatation and angiogenesis, ameliorates ischemia/reperfusion injury, and regulates extracellular matrix turnover and remodeling. In the RELAX-AHF phase 3 clinical trial, serelaxin (recombinant human relaxin) was shown to be safe, and it exerted survival benefits in patients with acute heart failure. RELAX-AHF-2 is currently ongoing, and it aims to address a larger population and evaluate harder clinical outcomes. Besides heart failure, acute myocardial infarction, peripheral arterial disease, and stable coronary disease could be target diseases for treatment with serelaxin in future clinical trials.
    No preview · Article · Nov 2015 · Journal of Cardiovascular Pharmacology and Therapeutics
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    ABSTRACT: Background&aims: Infectious acute kidney injury (AKI) is a life threatening complication of cirrhosis with limited therapeutic options. The aim of this study was to develop a model of infectious AKI in cirrhotic mice. Methods: Cirrhosis was established by intra-gastric administration of carbon tetrachloride (CCl4 ). Systemic hemodynamics was assessed invasively while cardiac function was assessed by echocardiography. AKI was induced using varying doses of lipopolysaccharide (LPS) titrated to produce 50% lethality. Renal function was assessed from serum creatinine and urine output. Renal injury was evaluated by urinalysis (proteinuria and casts) and renal histology. These mice were compared to: (1) normal mice, (2) normal mice+LPS, and (3) mice treated with CCl4 alone. Results: Cirrhosis with increased cardiac output, decreased systemic vascular resistance, activation of renin-angiotensin-aldosterone axis developed after 12 weeks of CCl4 administration. LPS injection produced a dose-dependent increase in mortality (33% at 2mg/kg vs. 80% at 6mg/kg) without urine (casts or proteinuria) or histological evidence of tubular injury. 2 mg/kg LPS injection produced a rise in creatinine (0.79±0.27 mg/dl in CCl4 +LPS compared to 0.45±0.14 in CCl4 alone, p<0.05) and a decrease in urine output (0.86±0.4 mL/16 hours in CCl4 +LPS compared to 1.70±0.7 mL/16 hours in CCl4 mice, p<0.05). Urine output remained low in mice that died while it recovered over 48-72 hours in those that recovered. Control mice treated with 2 mg/Kg LPS did not experience AKI. Conclusions: Cirrhotic CCl4 treated mice develop functional AKI and mimic most of the features of infectious AKI following LPS injection. This article is protected by copyright. All rights reserved.
    No preview · Article · Nov 2015 · Liver international: official journal of the International Association for the Study of the Liver
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    ABSTRACT: Patients with heart failure (HF) have evidence of chronic systemic inflammation. Whether inflammation contributes to the exercise intolerance in patients with HF is, however, not well established. We hypothesized that the levels of C-reactive protein (CRP), an established inflammatory biomarker, predict impaired cardiopulmonary exercise performance, in patients with chronic systolic HF. We measured CRP using high-sensitivity particle-enhanced immunonephelometry in 16 patients with ischemic heart disease (previous myocardial infarction) and chronic systolic HF, defined as a left ventricular ejection fraction ≤50% and New York Heart Association class II-III symptoms. All subjects with CRP >2 mg/L, reflecting systemic inflammation, underwent cardiopulmonary exercise testing using a symptom-limited ramp protocol. CRP levels predicted shorter exercise times (R = -0.65, p = 0.006), lower oxygen consumption (VO2) at the anaerobic threshold (R = -0.66, p = 0.005), and lower peak VO2 (R = -0.70, p = 0.002), reflecting worse cardiovascular performance. CRP levels also significantly correlated with an elevated ventilation/carbon dioxide production slope (R = +0.64, p = 0.008), a reduced oxygen uptake efficiency slope (R = -0.55, p = 0.026), and reduced end-tidal CO2 level at rest and with exercise (R = -0.759, p = 0.001 and R = -0.739, p = 0.001, respectively), reflecting impaired gas exchange. In conclusion, the intensity of systemic inflammation, measured as CRP plasma levels, is associated with cardiopulmonary exercise performance, in patients with ischemic heart disease and chronic systolic HF. These data provide the rationale for targeted anti-inflammatory treatments in HF.
    No preview · Article · Nov 2015 · The American journal of cardiology
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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.
    No preview · Article · Nov 2015 · International journal of cardiology
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    ABSTRACT: Coronary artery spasm is a rare but potentially fatal disease. Herein, we report a case of recurrent ST-segment myocardial infarctions and ventricular fibrillation complicating severe multivessel coronary artery spasm successfully treated with bilateral thoracic surgical sympathectomy.
    No preview · Article · Oct 2015 · The American journal of cardiology
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    ABSTRACT: The exponential increase in publications focusing on important clinical issues represents a major challenge for patients, physicians, and decision-makers, despite the braggadocio of many experts. Meta-analysis, when conducted within the context of a systematic review, offers an efficient and potent tool to summarize the clinical evidence accrued on a specific clinical question. Despite their many strengths, which include statistical precision, external validity, and the opportunity to analyze subgroups and moderators, meta-analyses also have many limitations. In addition, they are criticized because potentially an exercise in "mega-silliness", mixing "apples and oranges", unable to improve the quality of primary studies (in keeping with the say "garbage in-garbage out"), and focusing on an "average patient" who is only hypothetical. Yet, it is evident that meta-analyses will continue to play a key role in informing decision making whenever the best approach is not self-evident. Thus, it is mandatory to know their main features in order to use them critically and constructively, without being dominated nor scared.
    No preview · Article · Sep 2015 · Giornale italiano di cardiologia (2006)
  • Ignacio M. Seropian · Antonio Abbate

    No preview · Article · Sep 2015 · Circulation
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    ABSTRACT: Overweight and obesity are usually defined as a body mass index (BMI) ≥ 25 kg/m 2 and ≥ 30 kg/m 2 , respectively [1]. The World Health Organization (WHO) more broadlydefines these categories as abnormal or excessive amounts of fat mass (FM) [1]. Regardless of definition, obesity is recognized as a significant risk factor for developingtype 2 diabetes mellitus, hypertension, dyslipidemia and cardio-vascular disease [1-6]. Heart failure (HF), defined as " a complex clinical syndrome that results from any structural or functional impairment of ventricular filling and/or ejection of blood " , affects 38 million people worldwide, including 5.7 million in the United States [7]. HF is the most common cause of hospital admissions for Americans age 65 years and older [7,8]. A strong relationship exists between HF and obesity [5,6]. For every 1 kg/m 2 increase in BMI, the risk of developing HF increases by 5-7% [4], and almost half of all patients diagnosed with HF are obese [6]. While an abnormally high BMI is a risk factor for HF, overweight and obesity exert protective effects after the onset of HF. This phenomenon is commonly termed the " obesity paradox " [4,9-15]. In this editorial we describe the mechanisms through which obesity adversely affects cardiac function and discuss the contribution of body composition to the obesity paradox. In obese individuals, increases in central blood volume (CBV), stroke volume (SV), and, as a result, cardiac output (CO), are accompanied by a reduction in systemic vascular resistance (SVR) without a significant increase in heart rate [4,9-15]. This persistent increase in CO results in an increased cardiac workload that evolves into left ventricular (LV) dilatation, followed by a compensatory hypertrophic response [4,16-18]. These hemodynamic changes seem to be mostly related to an increased amount of lean mass (LM) (a surrogate for skeletal muscle mass) [10-14]. Higher levels of LM, and not FM, have been associated with increased blood flow [19] and possibly CBV, SV and CO. It is necessary to note that BMI does not distinguish between LM and FM and that an increased BMI may indicate an increased amount of LM, FM or a combination of both [20-27]. This distinction is important since low levels of LM are indicative of a poor prognosis in individuals with normal or reduced levels of FM and low levels of LM (i.e., sarcopenia) [28,30] or increased levels of FM and reduced amount of LM (i.e., sarcopenic obesity) [29,30]. Obesity appears to affect diastolic function to a greater extent than systolic function [31-33]. Obesity can potentially impair diastolic function as a result of endocrine-like secretion of pro-inflammatory adipokines or cytokines from adipose tissue [34]. Increased levels of interleukins (IL)-1 and-18 as well as tumor necrosis factor-α have been observed in obese patients [34-37]. In obese patients with HF with preserved ejection fraction and diastolic dysfunction, blockade of the IL-1 receptor with anakinra, a recombinant IL-1 receptor
    Full-text · Article · Sep 2015 · Cardiology

  • No preview · Article · Aug 2015 · International journal of cardiology
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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.
    No preview · Article · Jul 2015 · Expert Review of Cardiovascular Therapy
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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.
    No preview · Article · Jul 2015 · AJP Heart and Circulatory Physiology
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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
    Full-text · Article · Jul 2015 · PLoS ONE
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    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.
    Full-text · Article · Jul 2015
  • Antonio Abbate · Allison C Morton · David C Crossman

    No preview · Article · Jun 2015 · The Lancet
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    Dave L. Dixon · Antonio Abbate

    Preview · Article · Jun 2015
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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
    Full-text · Article · Jun 2015 · BioMed Research International

Publication Stats

7k Citations
2,171.84 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
  • 2013
    • Sapienza University of Rome
      • Department of Medico-Surgical Sciences and Biotechnologies
      Roma, Latium, Italy
  • 2012
    • Kanazawa Medical University
      Kanazawa, Ishikawa, Japan
  • 2010
    • Julphar School of Pharmacy
      Richmond, California, United States
  • 2009
    • Mount Sinai School of Medicine
      • Department of Radiology
      Manhattan, New York, United States
  • 2003-2005
    • The Catholic University of America
      Washington, Washington, D.C., United States
  • 2002-2005
    • Catholic University of the Sacred Heart
      • • Institute of Cardiology
      • • School of Cardiac Surgery
      Milano, Lombardy, Italy
    • Second University of Naples
      Caserta, Campania, Italy
    • Universitá degli Studi Internazionali di Roma
      Roma, Latium, Italy
  • 2002-2003
    • Sacred Heart University
      Феърфилд, Connecticut, United States
  • 2000-2002
    • LIUCBM Libera Università Campus Bio-Medico di Roma
      • Unit of Medical Oncology
      Roma, Latium, Italy