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Professor Andrew Boyle

Professor of Cardiovascular Medicine & Head of Discipline

School of Medicine and Public Health

Career Summary

Biography

Professor Andrew Boyle is a cardiologist and researcher who studies left ventricular remodeling, the process by which the heart weakens and becomes ineffective following heart attacks and with advancing age.  In particular, his research focuses on the molecular and cellular mechanisms of fibrosis and stem cell function in the heart. His clinical focus is on treating patients with acute coronary syndromes including coronary stenting, and transcatheter aortic valve implantation. 

Andrew received his medical degree from Monash University and then completed cardiology advanced training in Melbourne. It was during this time he noticed that early treatments for heart attack were very successful at keeping patients alive, but the late heart failure that ensued was difficult to treat. He became interested in the emerging research field of stem cell therapy for heart disease, with a view to regenerating the damaged heart muscle that occurred during a heart attack. He undertook a PhD at the University of Melbourne studying cardiac regeneration, and then moved to the US and continued this study as a fellow at Johns Hopkins University. He then joined the faculty at the University of California San Francisco, becoming Associate Professor of Medicine, where his laboratory focused on the effects of ageing on left ventricular remodeling, funded by the US National Institutes of Health. After 7 years there, he moved to the University of Newcastle and the Hunter Medical Research Institute (HMRI) where he now continues this research. Andrew has a research laboratory based at HMRI where he studies pre-clinical models of left ventricular remodeling, and he also performs clinical research and interventional procedures at the John Hunter Hospital.

Research Expertise
Professor Andrew Boyle is a cardiologist who performs basic science, translational and clinical research. His basic science laboratory and translational research are based at HMRI, and clinical research at the John Hunter Hospital. The basic science program focuses on left ventricular remodelling, the structural and functional changes that occur after a heart attack and with age. Several preclinical models are used in the laboratory. In particular, the molecular and cellular changes of apoptosis, cardiac stem cell function and cardiac fibrosis are studied, with a view toward cardiac regeneration. The translational research program focuses on comparison between patients and preclinical models, and moving novel findings toward potential therapeutic application. The clinical research program focuses on cardiovascular outcomes following heart attacks, and testing novel therapies in these patients.

Teaching Expertise
Andrew teaches medical and biomedical science undergraduate students, as well as interns, residents, registrars and fellows in cardiology. He has considerable experience in supervising research higher degree students in his research laboratory. There are a number of available projects for research higher degree students.

Administrative Expertise


Collaborations
Andrew has ongoing research collaborations with the University of Melbourne, the Medical University of Graz (Austria), the University of California San Francisco, University of Miami and with researchers at two centres in China.

Qualifications

  • PhD (Medicine Denistry & Health Sciences), University of Melbourne
  • Bachelor of Medicine, Bachelor of Surgery (Hons), Monash University
  • Registered Medical Practitioner, Australian Health Practitioner Regulation Agency

Keywords

  • cardiac fibrosis
  • cardiology
  • interventional cardiology
  • left ventricular remodeling
  • medical students
  • myocardial infarction

Languages

  • English (Fluent)

Fields of Research

Code Description Percentage
110201 Cardiology (incl. Cardiovascular Diseases) 100

Professional Experience

UON Appointment

Title Organisation / Department
Professor of Cardiovascular Medicine & Head of Discipline University of Newcastle
School of Medicine and Public Health
Australia

Academic appointment

Dates Title Organisation / Department
1/01/2010 -  Fellow - Society for Cardiac Angiography and Intervention Society for Cardiac Angiography and Intervention
United States
1/01/2009 -  Fellow - American Heart Association American Heart Association
United States
1/01/2008 -  Fellow - American College of Cardiology American College of Cardiology
United States
1/10/2006 - 1/12/2013 Associate Professor of Medicine University of California San Francisco
United States
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Chapter (6 outputs)

Year Citation Altmetrics Link
2017 Boyle A, 'Acute Myocardial Infarction', Current Diagnosis and Treatment in Cardiology, McGraw Hill, New York (2017)
2014 Shih HHJ, Boyle AJ, 'Aging-related changes in cellular and molecular mechanisms of postinfarction remodeling: Implications for heart failure therapy', Aging and Heart Failure: Mechanisms and Management 427-437 (2014)

© Springer Science+Business Media New York 2014. The normal course of aging is well known to result in decreased cardiac function; decreased capacity to tolerate insults, such as ... [more]

© Springer Science+Business Media New York 2014. The normal course of aging is well known to result in decreased cardiac function; decreased capacity to tolerate insults, such as myocardial infarction (MI); and a higher prevalence of pathological remodeling post-MI. Recent progress in aging biology has allowed investigators to understand the effect of aging from the molecular, organelle, and cellular levels that ultimately result in organ dysfunction. In this chapter, we will review the natural course of cellular and molecular changes in the heart that predispose an aging heart toward adverse remodeling, the age-related differences in the postinfarction remodeling process, the clinical implications of aging and postinfarction remodeling, and future targets for heart failure therapy in the aged population.

DOI 10.1007/978-1-4939-0268-2
2014 Boyle AJ, Jaffe A, 'Acute Myocardial INfarction', Current Diagnosis and Treatment in Cardiology, McGraw Hill, New York (2014)
2012 Parasher PS, Boyle AJ, 'Vascular access: Arterial, venous, and ultrasound guidance', Handbook of Endovascular Peripheral Interventions 1-30 (2012)
DOI 10.1007/978-1-4614-0839-0_1
2011 Lao D, Boyle A, 'Antithrombotic Therapy for Non-ST-Elevation Acute Coronary Syndrome', Inpatient Anticoagulation 223-240 (2011)
DOI 10.1002/9781118067178.ch11
2010 Boyle AJ, McNiece IK, Hare JM, 'Mesenchymal stem cell therapy for cardiac repair.', 65-84 (2010) [C1]

Stem cell therapy for repair of damaged cardiac tissue is an attractive option to improve the health of the growing number of heart failure patients. Mesenchymal stem cells (MSCs)... [more]

Stem cell therapy for repair of damaged cardiac tissue is an attractive option to improve the health of the growing number of heart failure patients. Mesenchymal stem cells (MSCs) possess unique properties that may make them a better option for cardiac repair than other cell types. Unlike other adult stem cells, they appear to escape allorecognition by the immune system and they have immune-modulating properties, thus making it possible to consider them for use as an allogeneic cell therapy product. There is a large and growing body of preclinical and early clinical experience with MSC therapy that shows great promise in realizing the potential of stem cell therapy to effect repair of damaged cardiac tissue. This review discusses the mechanism of action of MSC therapy and summarizes the current literature in the field.

Citations Scopus - 49
Show 3 more chapters

Journal article (107 outputs)

Year Citation Altmetrics Link
2019 Jackson N, McGee M, Ahmed W, Davies A, Leitch J, Mills M, et al., 'Groin Haemostasis With a Purse String Suture for Patients Following Catheter Ablation Procedures (GITAR Study)', Heart Lung and Circulation, 28 777-783 (2019)

© 2018 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ) Background: The most frequent com... [more]

© 2018 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ) Background: The most frequent complications from percutaneous electrophysiology procedures relate to vascular access. We sought to perform the first randomised controlled trial for femoral venous haemostasis utilising a simple and novel purse string suture (PSS) technique. Methods: We randomised 200 consecutive patients who were referred for electrophysiology procedures at two different hospitals to either 10 minutes of manual pressure or a PSS over the femoral vein and determined the incidence of vascular access site complications. Results: The mean age was 61.8 ± 12.1 years and 138 (69%) were male. Bleeding requiring addition pressure or a FemStop (Abbott Laboratories, Abbott Park, IL, USA) for complete haemostasis occurred in 17/99 (17%) patients in the PSS arm and 19/101 (19%) patients in the manual pressure arm (p = 0.72). There were no cases of haematoma prolonging hospital stay, arterio-venous fistula, pseudoaneurysm or retroperitoneal bleeding. The mean duration to achieve haemostasis was 45 seconds in the PSS arm and 10 minutes 44 seconds in the manual pressure arm (p < 0.001). Pain/discomfort associated with haemostasis occurred in 15/99 (15%) patients in the PSS arm and in 29/101 (29%) patients receiving manual pressure (p = 0.03). Conclusions: In this randomised trial we demonstrate that an easy to perform PSS is as effective at achieving haemostasis as 10 minutes of manual pressure for catheter ablation procedures. The PSS is considerably faster to perform and is more comfortable for patients than manual pressure.

DOI 10.1016/j.hlc.2018.03.011
Citations Web of Science - 1
Co-authors John Attia
2019 Wong R, Al-Omary M, Baker D, Spratt N, Boyle A, Baker N, et al., 'Cognitive dysfunction is associated with abnormal responses in cerebral blood flow in patients with single ventricular physiology: Novel insights from transcranial Doppler ultrasound.', Congenit Heart Dis, 14 638-644 (2019)
DOI 10.1111/chd.12763
Co-authors Peter Howe, Neil Spratt, Rachel Wong
2019 Davies AJ, Butel-Simoes L, Naudin C, Al-Omary M, Khan A, Bastian B, et al., 'Trends in the Incidence of First Acute Myocardial Infarction in Metropolitan and Regional Areas of the Hunter Region', Heart Lung and Circulation, 28 e37-e39 (2019) [C1]

© 2018 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ) Introduction: There is conflictin... [more]

© 2018 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ) Introduction: There is conflicting information regarding the contemporary incidence of first acute myocardial infarction (AMI) in Australia. We sought to document the regional variations in first AMI incidence in a large health district. Methods: We identified all patients presenting with first AMI in the Hunter region of New South Wales from 2004 to 2013. We calculated age and gender adjusted incidence of AMI and evaluated differences between patients from regional and metropolitan areas. We assessed 30-day and 12-month outcomes, including mortality, through linkage with the NSW Registry of Births Deaths and Marriages. Results: The incidence of first AMI in regional areas was persistently higher throughout the study compared to metropolitan areas (IRR 1.244; 95% CI 1.14¿1.35; p = 0.001). There were no significant differences between regional and metropolitan areas in 30-day and 12-month outcomes following presentation with first AMI. Conclusions: The study demonstrates persistently higher rates in regional compared to metropolitan areas, supporting the need for implementation of targeted intervention and prevention strategies.

DOI 10.1016/j.hlc.2018.02.022
2019 Whitehead N, Williams T, Brienesse S, Ferreira D, Murray N, Inder K, et al., 'Contemporary Trends in Stroke complicating Cardiac Catheterization.', Intern Med J, (2019)
DOI 10.1111/imj.14405
Co-authors Kerry Inder, Neil Spratt
2019 Williams T, Savage L, Whitehead N, Orvad H, Cummins C, Faddy S, et al., 'Missed Acute Myocardial Infarction (MAMI) in a rural and regional setting', IJC Heart and Vasculature, 22 177-180 (2019)

© 2019 Background: Delay in treatment and/or failure to provide reperfusion in ST-segment elevation myocardial infarction (STEMI) impacts on morbidity and mortality. This occurs m... [more]

© 2019 Background: Delay in treatment and/or failure to provide reperfusion in ST-segment elevation myocardial infarction (STEMI) impacts on morbidity and mortality. This occurs more often outside metropolitan areas yet the reasons for this are unclear. This study aimed to describe factors associated with missed diagnosis of acute myocardial infarction (MAMI) in a rural and regional setting. Methods: Using a retrospective cohort design, patients who presented with STEMI and failed to receive reperfusion therapy within four hours were identified as MAMI. Univariate analyses were undertaken to identify differences in clinical characteristics between the treated STEMI group and the MAMI group. Mortality, 30-day readmission rates and length of hospital stay are reported. Results: Of 100 patients identified as MAMI (70 male, 30 female), 24 died in hospital. Demographics and time from symptom onset were similar in the treated STEMI and MAMI groups. Of the MAMI patients who died, rural hospitals recorded the highest inpatient mortality (69.6% p = 0.008). MAMI patients compared to treated STEMI patients had higher 30 day readmission (31.6% vs 3.3%, p = 0.001) and longer length of stay (5.5 vs 4.3 days p = 0.029). Inaccurate identification of STEMI on electrocardiogram (72%) and diagnostic uncertainty (65%) were associated with MAMI. The Glasgow algorithm to identify STEMI was utilised on 57% of occasions, with 93% accuracy. Conclusion: Mortality following MAMI is high particularly in smaller rural hospitals. MAMI results in increased length of stay and readmission rate. Electrocardiogram interpretation and diagnostic accuracy require improvement to determine if this improves patient outcomes.

DOI 10.1016/j.ijcha.2019.02.013
Citations Scopus - 1Web of Science - 1
Co-authors Kerry Inder
2019 Ezad S, McGee M, Boyle AJ, 'Takotsubo Syndrome Associated with ST Elevation Myocardial Infarction', CASE REPORTS IN CARDIOLOGY, (2019)
DOI 10.1155/2019/1010243
2019 Hardy SA, Mabotuwana NS, Murtha LA, Coulter B, Sanchez-Bezanilla S, Al-Omary MS, et al., 'Novel role of extracellular matrix protein 1 (ECM1) in cardiac aging and myocardial infarction', PLoS ONE, 14 (2019)

© 2019 Hardy et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and repro... [more]

© 2019 Hardy et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Introduction The prevalence of heart failure increases in the aging population and following myocardial infarction (MI), yet the extracellular matrix (ECM) remodeling underpinning the development of aging- and MI-associated cardiac fibrosis remains poorly understood. A link between inflammation and fibrosis in the heart has long been appreciated, but has mechanistically remained undefined. We investigated the expression of a novel protein, extracellular matrix protein 1 (ECM1) in the aging and infarcted heart. Methods Young adult (3-month old) and aging (18-month old) C57BL/6 mice were assessed. Young mice were subjected to left anterior descending artery-ligation to induce MI, or transverse aortic constriction (TAC) surgery to induce pressure-overload cardiomyopathy. Left ventricle (LV) tissue was collected early and late post-MI/TAC. Bone marrow cells (BMCs) were isolated from young healthy mice, and subject to flow cytometry. Human cardiac fibroblast (CFb), myocyte, and coronary artery endothelial & smooth muscle cell lines were cultured; human CFbs were treated with recombinant ECM1. Primary mouse CFbs were cultured and treated with recombinant angiotensin-II or TGF-ß1. Immunoblotting, qPCR and mRNA fluorescent in-situ hybridization (mRNA-FISH) were conducted on LV tissue and cells. Results ECM1 expression was upregulated in the aging LV, and in the infarct zone of the LV early post-MI. No significant differences in ECM1 expression were found late post-MI or at any time-point post-TAC. ECM1 was not expressed in any resident cardiac cells, but ECM1 was highly expressed in BMCs, with high ECM1 expression in granulocytes. Flow cytometry of bone marrow revealed ECM1 expression in large granular leucocytes. mRNA-FISH revealed that ECM1 was indeed expressed by inflammatory cells in the infarct zone at day-3 post-MI. ECM1 stimulation of CFbs induced ERK1/2 and AKT activation and collagen-I expression, suggesting a pro-fibrotic role. Conclusions ECM1 expression is increased in ageing and infarcted hearts but is not expressed by resident cardiac cells. Instead it is expressed by bone marrow-derived granulocytes. ECM1 is sufficient to induce cardiac fibroblast stimulation in vitro. Our findings suggest ECM1 is released from infiltrating inflammatory cells, which leads to cardiac fibroblast stimulation and fibrosis in aging and MI. ECM1 may be a novel intermediary between inflammation and fibrosis.

DOI 10.1371/journal.pone.0212230
Co-authors Lucy Murtha, Philip Hansbro, Malcolm Starkey
2019 McGee M, Ferreira D, Tvedten O, Mahmoodi E, Whitehead N, Baker D, et al., 'Specificity of Myocardial Perfusion Imaging: Issues With Proposed MBS Item Review', HEART LUNG AND CIRCULATION, 28 E23-E25 (2019)
DOI 10.1016/j.hlc.2018.04.304
2019 Ezad S, Al-Omary MS, Davies AJ, Leitch J, Sverdlov AL, Boyle AJ, 'Heart failure admissions following ST segment elevation myocardial infarction', Australian Journal of Rural Health, 27 99-100 (2019)
DOI 10.1111/ajr.12456
Co-authors Aaron Sverdlov
2019 de Waal K, Crendal E, Boyle A, 'Left ventricular vortex formation in preterm infants assessed by blood speckle imaging.', Echocardiography, 36 1364-1371 (2019) [C1]
DOI 10.1111/echo.14391
2019 Khan A, Brienesse S, Boyle A, Collins N, 'Percutaneous treatment of saphenous vein graft aneurysm: Contemporary procedural considerations.', Catheter Cardiovasc Interv, 93 927-932 (2019)
DOI 10.1002/ccd.28128
2019 Papolos A, Fan E, Wagle RR, Foster E, Boyle AJ, Yeghiazarians Y, et al., 'Echocardiographic determination of pulmonary arterial capacitance.', Int J Cardiovasc Imaging, 35 1581-1586 (2019)
DOI 10.1007/s10554-019-01595-9
2018 Murtha L, Morten M, Schuliga M, Mabotuwana N, Hardy S, Waters D, et al., 'The Role of Pathological Aging in Cardiac and Pulmonary Fibrosis', Aging and Disease, 10 (2018)
Citations Scopus - 1
Co-authors Doan Ngo, Darryl Knight, Aaron Sverdlov, Lucy Murtha, Michael Schuliga
2018 Khan AA, Boyle AJ, 'Letter by Khan and Boyle Regarding Article, "Early Use of N-Acetylcysteine (NAC) With Nitrate Therapy in Patients Undergoing Primary Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction Reduces Myocardial Infarct Size (The NACIAM Trial [N-Acetylcysteine in Acute Myocardial Infarction])"', CIRCULATION, 137 1418-1419 (2018)
DOI 10.1161/CIRCULATIONAHA.117.032281
2018 Al-Omary MS, Davies AJ, Evans TJ, Bastian B, Fletcher PJ, Attia J, Boyle AJ, 'Mortality and Readmission Following Hospitalisation for Heart Failure in Australia: A Systematic Review and Meta-Analysis', Heart Lung and Circulation, 27 917-927 (2018) [C1]

© 2018 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ) Background: Heart failure (HF) is... [more]

© 2018 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ) Background: Heart failure (HF) is a common, costly condition with an increasing burden on Australian health care system resources. Knowledge of the burden of HF on patients and on the health system is important for resource allocation. This study is the first systematic review to estimate the mortality and readmission rates after hospitalisation for HF in the Australian population. Methods: We searched for studies of HF hospitalisation in Australia published between January 1990 and May 2016, using a systematic search of PubMed, Medline, Scopus, Web of Science, EMBASE and Cochrane Library databases. Studies reporting 30-day and/or 1-year outcomes for mortality or readmission following hospitalisation were eligible and included in this study. Results: Out of 2889 articles matching the initial search criteria, a total of 13 studies representing 67,255 patients were included in the final analysis. The pooled mean age of heart failure patients was 76.3 years and 51% were male (n = 34,271). The pooled estimated 30-day and 1-year all-cause mortality were 8% and 25% respectively. The pooled estimated 30-day and 1-year all-cause readmission rates were 20% and 56% respectively. There is a high prevalence of comorbidities in heart failure patients. There were limited data on readmission and mortality in rural patients and Indigenous people. Conclusions: Heart failure hospitalisations in Australia are followed by substantial readmission and mortality rates.

DOI 10.1016/j.hlc.2018.01.009
Citations Scopus - 2Web of Science - 2
Co-authors John Attia
2018 Potter MDE, Brienesse SC, Walker MM, Boyle A, Talley NJ, 'Effect of the gluten-free diet on cardiovascular risk factors in patients with coeliac disease: A systematic review', Journal of Gastroenterology and Hepatology (Australia), 33 781-791 (2018) [C1]
DOI 10.1111/jgh.14039
Citations Scopus - 12Web of Science - 9
Co-authors Nicholas Talley, Marjorie Walker
2018 Al-Omary MS, Khan AA, Davies AJ, Fletcher PJ, Mcivor D, Bastian B, et al., 'Outcomes following heart failure hospitalization in a regional Australian setting between 2005 and 2014.', ESC heart failure, 5 271-278 (2018) [C1]
DOI 10.1002/ehf2.12239
Citations Scopus - 4Web of Science - 3
Co-authors Aaron Sverdlov, Christopher Oldmeadow, John Attia
2018 Ezad S, Williams TD, Condon J, Boyle AJ, Collins NJ, 'Common themes in patients requiring urgent cardiothoracic surgery after percutaneous coronary interventions: Case series and review of the literature', CARDIOVASCULAR REVASCULARIZATION MEDICINE, 19 976-979 (2018)
DOI 10.1016/j.carrev.2018.03.017
2018 Brienesse SC, Davies AJ, Khan A, Boyle AJ, 'Prognostic Value of LVEDP in Acute Myocardial Infarction: a Systematic Review and Meta-Analysis', Journal of Cardiovascular Translational Research, 11 33-35 (2018) [C1]

© 2017, Springer Science+Business Media, LLC, part of Springer Nature. Left ventricular end-diastolic pressure (LVEDP) is an easily obtained, physiologically integrative measure o... [more]

© 2017, Springer Science+Business Media, LLC, part of Springer Nature. Left ventricular end-diastolic pressure (LVEDP) is an easily obtained, physiologically integrative measure of total LV function. LVEDP may be a useful prognostic measure in patients with acute myocardial infarction and utilised to guide medical therapy and assess risk for post myocardial infarction heart failure. To assess the utility of LVEDP as a prognostic measure in patients presenting with acute myocardial infarction. We performed an unrestricted search of electronic databases (1946 to March 2017) using a predefined search strategy. Publications were included if patients had an acute coronary syndrome and LVEDP was measured by cardiac catheterisation and included outcome data specifying major adverse cardiac events. Two reviewers performed independent study selection, data abstraction and quality assessment by using the Cochrane tool for randomised trials and the ROBINS-I tool for non-randomised studies. Our search identified 8637 patients in seven studies. In patients with elevated LVEDP and STEMI, there was a significantly increased risk of 30-day death (three studies, 5372 participants; RR 1.9; 95% CI 1.4¿2.7; p < 0.001; I2 = 35.3%) and heart failure (two studies, 2574 participants; RR 2.9; 95% CI 1.9¿4.5; p = < 0.001; I2 = 0.0%). There was no significant increase in risk of 30¿day reinfarction (RR 1.25; 95% CI 0.77¿2.1; p = 0.37; I2 = 41.3%). Elevated LVEDP measured during cardiac catheterisation for acute myocardial infarction appears to be a predictor of heart failure and mortality.

DOI 10.1007/s12265-017-9776-7
Citations Scopus - 2Web of Science - 2
2018 de Waal K, Phad N, Boyle A, 'Left atrium function and deformation in very preterm infants with and without volume load', Echocardiography, 35 1818-1826 (2018) [C1]

© 2018 Wiley Periodicals, Inc. Background: Left atrium (LA) function can be assessed by volumetric measurements, conventional and tissue Doppler, and more recently, deformation im... [more]

© 2018 Wiley Periodicals, Inc. Background: Left atrium (LA) function can be assessed by volumetric measurements, conventional and tissue Doppler, and more recently, deformation imaging using two-dimensional speckle tracking echocardiography (2DSTE). 2DSTE allows for measurement of volume and deformation and can quantify the contribution of the reservoir, conduit, and contraction phase. A common cause for LA dysfunction in very preterm infants is volume overload with a patent ductus arteriosus (PDA). The aim of this study was to explore the feasibility and reliability of LA 2DSTE in preterm infants, and describe LA function with and without PDA volume load. Methods: We prospectively recruited preterm infants <30¿weeks of gestation referred for assessment of a possible PDA. A cardiac ultrasound was performed at day 3 and in week 4 of life and analyzed using conventional techniques and 2DSTE. Results: Forty-eight infants (32 with PDA) were included. LA 2DSTE analysis was feasible in 96% of measurements with good reliability of strain and volume parameters. Strain rate was less reliable. Poorer LA contraction and reservoir function was associated with larger LA volume index, higher inflow over the mitral valve at early diastole, higher EA ratio, and higher Ee¿ ratio. Poorer conduit function was associated with higher Ee¿ ratio. A larger PDA diameter was found to be an independent contributor to deteriorating LA contraction and reservoir function. Conclusion: LA 2DSTE analysis is feasible in preterm infants and provides detailed information on atrium mechanics. Further studies are needed to explore the clinical value of these new parameters in this population.

DOI 10.1111/echo.14140
2018 Khan AA, Davies AJ, Whitehead NJ, McGee M, Al-Omary MS, Baker D, et al., 'Targeting elevated left ventricular end-diastolic pressure following primary percutaneous coronary intervention for ST-segment elevation myocardial infarction - a phase one safety and feasibility study.', European heart journal. Acute cardiovascular care, 2048872618819657 (2018)
DOI 10.1177/2048872618819657
Co-authors Ian Renner, Tazeen Majeed, John Attia
2017 Shrestha U, Sciammarella M, Alhassen F, Yeghiazarians Y, Ellin J, Verdin E, et al., 'Measurement of absolute myocardial blood flow in humans using dynamic cardiac SPECT and

© 2015, American Society of Nuclear Cardiology. Background: The objective of this study was to measure myocardial blood flow (MBF) in humans using 99mTc-tetrofosmin and dynamic si... [more]

© 2015, American Society of Nuclear Cardiology. Background: The objective of this study was to measure myocardial blood flow (MBF) in humans using 99mTc-tetrofosmin and dynamic single-photon emission computed tomography (SPECT). Methods: Dynamic SPECT using 99mTc-tetrofosmin and dynamic positron emission tomography (PET) was performed on a group of 16 patients. The SPECT data were reconstructed using a 4D-spatiotemporal iterative reconstruction method. The data corresponding to 9 patients were used to determine the flow-extraction curve for 99mTc-tefrofosmin while data from the remaining 7 patients were used for method validation. The nonlinear tracer correction parameters A and B for 99mTc-tefrofosmin were estimated for the 9 patients by fitting the flow-extraction curve K1=F(1-Aexp(-BF)) for K1 values estimated with 99mTc-tefrofosmin using SPECT and MBF values estimated with 13N-NH3 using PET. These parameters were then used to calculate MBF and coronary flow reserve (CFR) in three coronary territories (LAD, RCA, and LCX) using SPECT for an independent cohort of 7 patients. The results were then compared with that estimated with 13N-NH3 PET. The flow-dependent permeability surface-area product (PS) for 99mTc-tefrofosmin was also estimated. Results: The estimated flow-extraction parameters for 99mTc-tefrofosmin were found to be A¿=¿0.91¿±¿0.11, B¿=¿0.34¿±¿0.20 (R2¿=¿0.49). The range of MBF in LAD, RCA, and LCX was 0.44-3.81¿mL/min/g. The MBF between PET and SPECT in the group of independent cohort of 7 patients showed statistically significant correlation, r¿=¿0.71 (P¿<¿.001). However, the corresponding CFR correlation was moderate r¿=¿0.39 yet statistically significant (P¿=¿.037). The PS for 99mTc-tefrofosmin was (0.019¿±¿0.10)*MBF¿+¿(0.32¿±¿0.16). Conclusions: Dynamic cardiac SPECT using 99mTc-tetrofosmin and a clinical two-headed SPECT/CT scanner can be a useful tool for estimation of MBF.

DOI 10.1007/s12350-015-0320-3
Citations Scopus - 20Web of Science - 19
2017 Khan AA, Fletcher PJ, Boyle AJ, 'Pre-hospital thrombolysis in ST-segment elevation myocardial infarction: A regional Australian experience', Medical Journal of Australia, 206 369-369.e1 (2017)
DOI 10.5694/MJA16.01260
Citations Scopus - 1
2017 Murtha LA, Schuliga MJ, Mabotuwana NS, Hardy SA, Waters DW, Burgess JK, et al., 'The processes and mechanisms of cardiac and pulmonary fibrosis', Frontiers in Physiology, 8 1-15 (2017) [C1]
DOI 10.3389/fphys.2017.00777
Citations Scopus - 27Web of Science - 23
Co-authors Michael Schuliga, Lucy Murtha, Darryl Knight
2017 Wong R, Ahmad W, Davies A, Spratt N, Boyle A, Levi C, et al., 'Assessment of cerebral blood flow in adult patients with aortic coarctation', Cardiology in the Young, 27 1606-1613 (2017) [C1]

© Cambridge University Press 2017. Background Survival into adult life in patients with aortic coarctation is typical following surgical and catheter-based techniques to relieve o... [more]

© Cambridge University Press 2017. Background Survival into adult life in patients with aortic coarctation is typical following surgical and catheter-based techniques to relieve obstruction. Late sequelae are recognised, including stroke, hypertension, and intracerebral aneurysm formation, with the underlying mechanisms being unclear. We hypothesised that patients with a history of aortic coarctation may have abnormalities of cerebral blood flow compared with controls. Methods Patients with a history of aortic coarctation underwent assessment of cerebral vascular function. Vascular responsiveness of intracranial vessels to hypercapnia and degree of cerebral artery stiffness using Doppler-derived pulsatility indices were used. Response to photic stimuli was used to assess neurovascular coupling, which reflects endothelial function in response to neuronal activation. Patient results were compared with age- and sex-matched controls. Results A total of 13 adult patients (males=10; 77%) along with 13 controls underwent evaluation. The mean age was 36.1±3.7 years in the patient group. Patients with a background of aortic coarctation were noted to have increased pulse pressure on blood pressure assessment at baseline with increased intracranial artery stiffness compared with controls. Patients with a history of aortic coarctation had less reactive cerebral vasculature to hypercapnic stimuli and impaired neurovascular coupling compared with controls. Results Adult patients with aortic coarctation had increased intracranial artery stiffness compared with controls, in addition to cerebral vasculature showing less responsiveness to hypercapnic and photic stimuli. Further studies are required to assess the aetiology and consequences of these documented abnormalities in cerebral blood flow in terms of stroke risk, cerebral aneurysm formation, and cognitive dysfunction.

DOI 10.1017/S1047951117000920
Citations Scopus - 2Web of Science - 3
Co-authors Rachel Wong, Christopher Levi, Peter Howe, Neil Spratt
2017 Zhang X, Khan AA, Haq EU, Rahim A, Hu D, Attia J, et al., 'Increasing mortality from ischaemic heart disease in China from 2004 to 2010: disproportionate rise in rural areas and elderly subjects. 438 million person-years follow-up.', European heart journal. Quality of care & clinical outcomes, 3 47-52 (2017) [C1]
DOI 10.1093/ehjqcco/qcw041
Citations Scopus - 1
Co-authors John Attia, Christopher Oldmeadow
2017 de Waal K, Phad N, Collins N, Boyle A, 'Cardiac remodeling in preterm infants with prolonged exposure to a patent ductus arteriosus', Congenital Heart Disease, 12 364-372 (2017) [C1]

© 2017 Wiley Periodicals, Inc. Background: Sustained volume load due to a patent ductus arteriosus (PDA) leads to cardiac remodeling. Remodeling changes can become pathological an... [more]

© 2017 Wiley Periodicals, Inc. Background: Sustained volume load due to a patent ductus arteriosus (PDA) leads to cardiac remodeling. Remodeling changes can become pathological and are associated with cardiovascular disease progression. Data on remodeling changes in preterm infants is not available. Methods: Clinical and echocardiography data were collected in preterm infants <30 weeks gestation on postnatal day 3 and then every 7¿14 days until closure of the ductus arteriosus. Images were analyzed using conventional techniques and speckle tracking. Remodeling changes of infants with prolonged (>14 days) exposure to a PDA were compared to control infants without a PDA. Results: Thirty out of 189 infants had prolonged exposure to a PDA. The left heart remodeled to a larger and more spherical shape and thus significantly increased in volume. Most changes occurred in the first 4 weeks, plateaued, and then returned to control values. Systolic function and estimates of filling pressure increased and effective arterial elastance reduced with a PDA, however contractility was unchanged. Wall thickness increased after 4 weeks of increased volume exposure. Conclusion: The preterm PDA induces early and significant remodeling of the left heart. A compensated cardiac physiology was seen with preserved systolic function, suggesting adaptive rather than pathological remodeling changes with prolonged exposure to a PDA.

DOI 10.1111/chd.12454
Citations Scopus - 7Web of Science - 6
2017 Al-Omary MS, Davies AJ, Khan AA, McGee M, Bastian B, Leitch J, et al., 'Heart Failure Hospitalisations in the Hunter New England Area Over 10 years. A Changing Trend', HEART LUNG AND CIRCULATION, 26 627-630 (2017)
DOI 10.1016/j.hlc.2016.10.005
Citations Scopus - 3Web of Science - 3
Co-authors John Attia
2017 Geng X, Ye J, Yeghiazarians Y, Shih H, Hwang J, Sievers R, et al., 'Myocardial Production and Release of Stem Cell Factor Following Myocardial Infarction', Journal of Biomaterials and Tissue Engineering, 7 77-82 (2017)
DOI 10.1166/jbt.2017.1543
Citations Scopus - 1Web of Science - 1
2017 Davies AJ, Naudin C, Al-Omary M, Khan A, Oldmeadow C, Jones M, et al., 'Disparities in the incidence of acute myocardial infarction: long-term trends from the Hunter region', Internal Medicine Journal, 47 557-562 (2017) [C1]

© 2017 Royal Australasian College of Physicians Background: Trends in the incidence of acute myocardial infarction (AMI) provide important information for healthcare providers and... [more]

© 2017 Royal Australasian College of Physicians Background: Trends in the incidence of acute myocardial infarction (AMI) provide important information for healthcare providers and can allow for accurate planning of future health needs and targeted interventions in areas with an excess burden of cardiovascular disease. Aim: To investigate the regional variations in AMI incidence in the Hunter region. Methods: Incident cases of AMI identified between 1996 and 2013 from the Hunter New England Health Cardiac and Stroke Outcomes Unit were prospectively collected for this study. We calculated crude and age-adjusted incidence of AMI over an 18-year period and explored differences in remoteness, age, sex and indigenous status. Results: During 1996¿2013, a total of 15 480 cases of AMI were identified. There was a significantly higher incidence of AMI in patients from regional areas compared to patients from metropolitan areas. More importantly, while rates of AMI declined by 28% in metropolitan patients, they increased by 8% in regional patients. Males had higher rates of AMI throughout the study period than females, however there was trend over time towards a reduction in AMI incidence in males that was not seen in females. The age-adjusted incidence of AMI for indigenous patients increased by 48% from 2007 to 2013, compared to a 23% decrease in non-indigenous patients. Conclusion: Between 1996 and 2013 in the Hunter region, the adjusted incidence of AMI increased for regional patients compared to metropolitan patients with a trend towards a higher adjusted incidence of AMI in the indigenous population.

DOI 10.1111/imj.13399
Citations Scopus - 2Web of Science - 2
Co-authors Christopher Oldmeadow
2017 Geng X, Hwang J, Ye J, Shih H, Coulter B, Naudin C, et al., 'Aging is protective against pressure overload cardiomyopathy via adaptive extracellular matrix remodeling', AMERICAN JOURNAL OF CARDIOVASCULAR DISEASE, 7 72-82 (2017) [C1]
Citations Web of Science - 4
2016 Miles S, Ahmad W, Bailey A, Hatton R, Boyle A, Collins N, 'Sleep-Disordered Breathing in Patients with Pulmonary Valve Incompetence Complicating Congenital Heart Disease', Congenital Heart Disease, 11 678-682 (2016) [C1]

© 2016 Wiley Periodicals, Inc. Objective: Long standing pulmonary regurgitation results in deleterious effects on right heart size and function with late consequences of right hea... [more]

© 2016 Wiley Periodicals, Inc. Objective: Long standing pulmonary regurgitation results in deleterious effects on right heart size and function with late consequences of right heart volume overload including ventricular dilatation, propensity to arrhythmia and right heart failure. As sleep disordered breathing may predispose to elevations in pulmonary vascular resistance and associated negative effects on right ventricular function, we sought to assess this in patients with underlying congenital heart disease. Design: We performed a pilot study to evaluate the incidence of sleep-disordered breathing in a patient population with a history of long standing pulmonary valve incompetence in patients with congenital heart disease using overnight oximetry. Patients. Patients with a background of tetralogy of Fallot repair or residual pulmonary incompetence following previous pulmonary valve intervention for congenital pulmonary stenosis were included. Results: Twenty-two patients underwent overnight oximetry. The mean age of the cohort was 34.3 ± 15.2 years with no patients observed to have severe underlying pulmonary hypertension. Abnormal overnight oximetry was seen in 13/22 patients (59.1%) with 2/22 (9.1%) patients considered to have severe abnormalities. Conclusions: An important proportion of patients with a background of pulmonary incompetence complicating congenital heart disease are prone to the development of sleep-disordered breathing as assessed by overnight oximetry. Further study into the prevalence and mechanisms of sleep-disordered breathing in a larger cohort are warranted.

DOI 10.1111/chd.12369
Citations Scopus - 1Web of Science - 1
2016 de Waal K, Phad N, Collins N, Boyle A, 'Myocardial function during bradycardia events in preterm infants', Early Human Development, 98 17-21 (2016) [C1]

© 2016 Elsevier Ireland Ltd. Background Transient bradycardia episodes are common in preterm infants and often secondary to apnea. Decreased ventilation with resultant hypoxemia i... [more]

© 2016 Elsevier Ireland Ltd. Background Transient bradycardia episodes are common in preterm infants and often secondary to apnea. Decreased ventilation with resultant hypoxemia is believed to be the predominant mechanism. Sudden bradycardias without apnea are also reported, possibly due to vagal stimulation. Point of care ultrasound is used to diagnose and follow cardiovascular complications in preterm infants. Inadvertently, the operator would sometimes capture bradycardia events. This study reports on left ventricular function during such events. Methods We retrospectively reviewed our cardiac ultrasound database for bradycardia events. Apical four or three chamber images before, during and after a bradycardia event were analysed with speckle tracking software which provides systolic and diastolic parameters of myocardial motion, deformation and volume. Results Over a 2¿year period, 15 bradycardia events were noted in 14 patients with a median gestational age of 26¿weeks (range 23 to 29). Heart rate decreased by an average of 43% (171/min to 98/min). Myocardial velocity and longitudinal strain rate during the atrial component of diastole were reduced during bradycardia. Longitudinal strain during systole was increased and radial deformation was unchanged. Ventricular volumes and ejection fraction did not change. Most parameters returned to baseline values after the event. Longitudinal systolic strain rate remained lower and stroke volume was 12% higher compared to baseline. Conclusion Parameters of systolic contractility and stroke volume were maintained and parameters of atrial contractility were reduced during mild to moderate bradycardia in preterm infants. Bradycardia reduces total cardiac output with a compensatory increase detected following the event.

DOI 10.1016/j.earlhumdev.2016.05.002
2016 Khan AA, Williams T, Savage L, Stewart P, Ashraf A, Davies AJ, et al., 'Pre-hospital thrombolysis in ST-segment elevation myocardial infarction: A regional Australian experience', Medical Journal of Australia, 205 121-125 (2016) [C1]

© 2016 AMPCo Pty Ltd. Objective: The system of care in the Hunter New England Local Health District for patients with ST-segment elevation myocardial infarction (STEMI) foresees p... [more]

© 2016 AMPCo Pty Ltd. Objective: The system of care in the Hunter New England Local Health District for patients with ST-segment elevation myocardial infarction (STEMI) foresees pre-hospital thrombolysis (PHT) administered by paramedics to patients more than 60 minutes from the cardiac catheterisation laboratory (CCL), and primary percutaneous coronary intervention (PCI) at the CCL for others. We assessed the safety and effectiveness of the pre-hospital diagnosis strategy, which allocates patients to PHT or primary PCI according to travel time to the CCL. Design, setting and participants: Prospective, non-randomised, consecutive, single-centre case series of STEMI patients diagnosed on the basis of a pre-hospital electrocardiogram (ECG), from August 2008 to August 2013. All patients were treated at the tertiary referral hospital (John Hunter Hospital, Newcastle). Main outcome measures: The primary efficacy endpoint was all-cause mortality at 12 months; the primary safety endpoint was bleeding. Results: STEMI was diagnosed in 484 patients on the basis of pre-hospital ECG; 150 were administered PHT and 334 underwent primary PCI. The median time from first medical contact (FMC) to PHT was 35 minutes (IQR, 28¿43 min) and to balloon inflation 130 minutes (IQR, 100¿150 min). In the PHT group, 37 patients (27%) needed rescue PCI (median time, 4 h; IQR, 3¿5 h). The 12-month all-cause mortality rate was 7.0% (PHT, 6.7%; PCI, 7.2%). The incidence of major bleeding (TIMI criteria) in the PHT group was 1.3%; no patients in the primary PCI group experienced major bleeding. Conclusion: PHT can be delivered safely by paramedical staff in regional and rural Australia with good clinical outcomes.

DOI 10.5694/mja15.01336
Citations Scopus - 6Web of Science - 6
Co-authors Christopher Oldmeadow, John Attia
2015 Genet M, Lee LC, Ge L, Acevedo-Bolton G, Jeung N, Martin A, et al., 'A Novel Method for Quantifying Smooth Regional Variations in Myocardial Contractility Within an Infarcted Human Left Ventricle Based on Delay-Enhanced Magnetic Resonance Imaging', JOURNAL OF BIOMECHANICAL ENGINEERING-TRANSACTIONS OF THE ASME, 137 (2015) [C1]
DOI 10.1115/1.4030667
Citations Scopus - 11Web of Science - 10
2015 Zhang Y, Sivakumaran P, Newcomb AE, Hernandez D, Harris N, Khanabdali R, et al., 'Cardiac Repair with a Novel Population of Mesenchymal Stem Cells Resident in the Human Heart', Stem Cells, 33 3100-3113 (2015) [C1]

© 2015 AlphaMed Press. Cardiac resident stem cells (CRSCs) hold much promise to treat heart disease but this remains a controversial field. Here, we describe a novel population of... [more]

© 2015 AlphaMed Press. Cardiac resident stem cells (CRSCs) hold much promise to treat heart disease but this remains a controversial field. Here, we describe a novel population of CRSCs, which are positive for W8B2 antigen and were obtained from adult human atrial appendages. W8B2+ CRSCs exhibit a spindle-shaped morphology, are clonogenic and capable of self-renewal. W8B2+ CRSCs show high expression of mesenchymal but not hematopoietic nor endothelial markers. W8B2+ CRSCs expressed GATA4, HAND2, and TBX5, but not C-KIT, SCA-1, NKX2.5, PDGFRa, ISL1, or WT1. W8B2+ CRSCs can differentiate into cardiovascular lineages and secrete a range of cytokines implicated in angiogenesis, chemotaxis, inflammation, extracellular matrix remodeling, cell growth, and survival. In vitro, conditioned medium collected from W8B2+ CRSCs displayed prosurvival, proangiogenic, and promigratory effects on endothelial cells, superior to that of other adult stem cells tested, and additionally promoted survival and proliferation of neonatal rat cardiomyocytes. Intramyocardial transplantation of human W8B2+ CRSCs into immunocompromised rats 1 week after myocardial infarction markedly improved cardiac function (~40% improvement in ejection fraction) and reduced fibrotic scar tissue 4 weeks after infarction. Hearts treated with W8B2+ CRSCs showed less adverse remodeling of the left ventricle, a greater number of proliferating cardiomyocytes (Ki67+cTnT+ cells) in the remote region, higher myocardial vascular density, and greater infiltration of CD163+ cells (a marker for M2 macrophages) into the border zone and scar regions. In summary, W8B2+ CRSCs are distinct from currently known CRSCs found in human hearts, and as such may be an ideal cell source to repair myocardial damage after infarction.

DOI 10.1002/stem.2101
Citations Scopus - 25Web of Science - 25
2014 Gupta V, Feng K, Cheruvu P, Boyer N, Yeghiazarians Y, Ports TA, et al., 'High femoral artery bifurcation predicts contralateral high bifurcation: implications for complex percutaneous cardiovascular procedures requiring large caliber and/or dual access.', J Invasive Cardiol, 26 409-412 (2014) [C1]
Citations Scopus - 3Web of Science - 5
2014 Feng K, Gupta V, Terrazas E, Yeghiazarians Y, Ports T, Gregoratos G, et al., 'Trans-radial versus trans-femoral access in patients with end-stage liver disease undergoing cardiac catheterization', American Journal of Cardiovascular Disease, 4 133-139 (2014) [C1]
Citations Scopus - 3Web of Science - 2
2014 Yeghiazarians Y, Honbo N, Imhof I, Woods B, Aguilera V, Ye J, et al., 'IL-15: A novel prosurvival signaling pathway in cardiomyocytes', Journal of Cardiovascular Pharmacology, 63 406-411 (2014) [C1]

Cardiovascular disease is the leading cause of death in Western countries. A major limitation of current treatments is the inability to efficiently repair or replace dead myocardi... [more]

Cardiovascular disease is the leading cause of death in Western countries. A major limitation of current treatments is the inability to efficiently repair or replace dead myocardium. Recently, stem cell-based therapies have been explored as an avenue to circumvent current therapeutic limitations. Overall, these therapies seem to result in small improvements in the contractile function of the heart. The exact mechanism(s) of action that underlie these improvements remain unknown, and it is believed that paracrine effects play a significant role. Previously, we had reported that an extract derived from bone marrow cells, in the absence of any live cell, contained cardioprotective soluble factors. In this study, we identify IL-15 as a putative cardioprotectant within the bone marrow cells paracrine profile. Using an in vitro culture system, we assessed the ability of IL-15 to protect cardiomyocytes under hypoxic conditions. For the first time, we have identified IL-15 receptors on the surface of cardiomyocytes and delineated the signaling system by which hypoxic cardiomyocytes may be protected from cellular death and rescued from oxidative stress with IL-15 treatment. Copyright © 2013 by Lippincott Williams & Wilkins.

DOI 10.1097/FJC.0000000000000061
Citations Scopus - 5Web of Science - 5
2014 Pandit J, Gupta V, Boyer N, Yeghiazarians Y, Ports TA, Boyle AJ, 'Patient and physician perspectives on outcomes weighting in revascularization. The POWR study', International Journal of Cardiology, (2014) [C3]
DOI 10.1016/j.ijcard.2014.08.096
Citations Scopus - 2Web of Science - 2
2014 Velez E, Boyer N, Acevedo-Bolton G, Hope MD, Boyle A, 'CT-reconstructed three-dimensional printed models of the right subclavian artery and aorta define age-related changes and facilitate benchtop catheter testing', Journal of Invasive Cardiology, 26 E141-E144 (2014) [C1]

BACKGROUND: Severe tortuosity of the right subclavian artery (RSCA) encountered during transradial cardiac catheterization can lead to longer procedures, increased fluoroscopy tim... [more]

BACKGROUND: Severe tortuosity of the right subclavian artery (RSCA) encountered during transradial cardiac catheterization can lead to longer procedures, increased fluoroscopy time, inability to engage the coronary artery ostia, and potentially procedural failure. Increasing age is strongly correlated with subclavian tortuosity; however, the magnitude and direction of age-related changes in aortic and subclavian artery anatomy have not been defined. METHODS: Chest computed tomography (CT) angiograms of 14 patients (6 age <45 years and 8 age =75 years) were evaluated for RSCA tortuosity. Measurements were taken along the midline of the vessel and compared to the straight distance traveled (index of tortuosity = straight distance/midline length). One normal and one tortuous subclavian were selected for three-dimensional printing and various catheters were benchtop tested on both models. RESULTS: The older group had longer (11.95 cm vs 9.6 cm; P<.01) and more tortuous subclavian arteries (lower index of tortuosity, 0.65 vs 0.76; P<.01) with more posterior unfolding (distance to most posterior aspect, 3.74 ± 0.77 cm vs 1.76 ± 0.58 cm; P<.001). Engagement of the coronary arteries of the normal model was significantly easier, with successful engagement of one or both coronaries with every catheter (n=7). Only 2 of 7 catheters (Radial Brachial and Extra Backup 3.0) were able to engage the coronary arteries in the tortuous model. CONCLUSION: Age is associated with elongation, tortuosity, and posterior unfolding of the RSCA. Three-dimensional printing of normal and tortuous arteries is feasible and shows potential to test differences between catheters.

Citations Scopus - 5Web of Science - 4
2014 Whitman IR, Boyle AJ, 'Extreme brachial loop', JACC: Cardiovascular Interventions, 7 334-335 (2014) [C3]
DOI 10.1016/j.jcin.2013.06.021
2013 Ye J, Hom D, Hwang J, Yeghiazarians Y, Lee R, Boyle A, 'Aging Impairs the Proliferative Capacity of Cardiospheres, Cardiac Progenitor Cells and Cardiac Fibroblasts: Implications for Cell Therapy', Journal of Clinical Medicine, 2 103-114 (2013) [C1]
DOI 10.3390/jcm2030103
Citations Scopus - 1
2013 Beyer AT, Ng R, Singh A, Zimmet J, Shunk K, Yeghiazarians Y, et al., 'Topical nitroglycerin and lidocaine to dilate the radial artery prior to transradial cardiac catheterization: A randomized, placebo-controlled, double-blind clinical trial The PRE-DILATE Study', INTERNATIONAL JOURNAL OF CARDIOLOGY, 168 2575-2578 (2013) [C1]
DOI 10.1016/j.ijcard.2013.03.048
Citations Scopus - 19Web of Science - 17
2013 Ye J, Boyle AJ, Shih H, Sievers RE, Wang Z-E, Gormley M, Yeghiazarians Y, 'CD45-positive cells are not an essential component in cardiosphere formation', CELL AND TISSUE RESEARCH, 351 201-205 (2013) [C1]
DOI 10.1007/s00441-012-1511-8
Citations Scopus - 6Web of Science - 6
2013 See F, Watanabe M, Kompa AR, Wang BH, Boyle AJ, Kelly DJ, et al., 'Early and Delayed Tranilast Treatment Reduces Pathological Fibrosis Following Myocardial Infarction', HEART LUNG AND CIRCULATION, 22 122-132 (2013) [C1]
DOI 10.1016/j.hlc.2012.08.054
Citations Scopus - 16Web of Science - 14
2013 Nazer B, Boyle A, 'Treatment of recurrent radial artery pseudoaneurysms by prolonged mechanical compression', Journal of Invasive Cardiology, 25 358-359 (2013) [C3]

As radial artery pseudoaneurysm (PA) is a rare complication of transradial catheterization, data on their management are sparse. Here, we report the case of a 77-year-old woman wh... [more]

As radial artery pseudoaneurysm (PA) is a rare complication of transradial catheterization, data on their management are sparse. Here, we report the case of a 77-year-old woman who underwent right transradial diagnostic cardiac catheterization, and subsequently developed a symptomatic PA. She underwent initial treatment with 20 minutes of mechanical compression with a Hemoband (Hemoband Corporation) with initial success. Three weeks later, she developed recurrence of her PA, and was treated with 24 hours of mechanical compression, wearing the Hemoband as an outpatient, with sustained resolution of the PA confirmed by ultrasound 1 month later, and no neurologic or further vascular complications. In addition to demonstrating that an initial PA as well as its recurrence can be treated with prolonged mechanical compression, we review the literature regarding radial artery PAs and their treatment.

Citations Scopus - 7
2013 Natal-Hernandez L, Meadows J, Shunk KA, Boyle AJ, 'Percutaneous Retrograde Recanalization of a Chronic Total Coronary Artery Occlusion in a 7 Year Old', Cardiovascular Revascularization Medicine, 14 113-117 (2013) [C3]

The arterial switch operation for correction of transposition of the great arteries can be complicated by late stenosis or occlusion of the coronary arteries that are re-implanted... [more]

The arterial switch operation for correction of transposition of the great arteries can be complicated by late stenosis or occlusion of the coronary arteries that are re-implanted to the new aorta. We report the case of a young boy who underwent this operation as a neonate and was found to have an occluded anomalous left anterior descending artery (LAD) before age 3. Subsequent bypass surgery was complicated by anastomotic stricture and kinking of the left internal mammary artery graft to the LAD. At age 7, the LAD territory showed reversible ischemia on nuclear perfusion testing and he was referred for percutaneous coronary intervention. A combined approach with pediatric and adult interventional cardiologists resulted in successful retrograde PCI to recanalize the chronic total occlusion of the LAD. Important features of this technique in pediatric patients are discussed. © 2013 Elsevier Inc.

DOI 10.1016/j.carrev.2012.12.007
Citations Scopus - 2
2013 Boyer N, Beyer A, Gupta V, Dehghani H, Hindnavis V, Shunk K, et al., 'The effects of intra-arterial vasodilators on radial artery size and spasm: Implications for contemporary use of trans-radial access for coronary angiography and percutaneous coronary intervention', Cardiovascular Revascularization Medicine, 14 321-324 (2013) [C1]

Background: Transradial access (TRA) offers advantages including decreased vascular complications, reduced length of hospital stay, and reduced cost. The size of the radial artery... [more]

Background: Transradial access (TRA) offers advantages including decreased vascular complications, reduced length of hospital stay, and reduced cost. The size of the radial artery (RA) limits the equipment that can be used via TRA. Intra-arterial (IA) vasodilators prevent and treat RA spasm, yet are not uniformly used in TRA and their effect on the absolute size of the RA remains unknown. Methods and materials: 121 patients undergoing TRA for cardiac catheterization were included. 78 patients underwent RA angiography prior to administration of IA vasodilators ('no vasodilator' group), 43 patients underwent radial angiography after administration of an IA verapamil and nitroglycerin cocktail ('vasodilator' group). Quantitative angiography was used to compare the RA diameters. Results: Clinical characteristics were similar between the groups, except that patients in the 'no vasodilator' cohort were taller (1.67 ± 0.1. m vs. 1.73 ± 0.1. m, p = 0.002), and heavier (84.9 ± 18.2. kg vs. 75 ± 17.1. kg, p = 0.003). In the 'vasodilator' group the proximal RA diameter was larger (2.29 ± 0.47. mm vs. 2.09 ± 0.41. mm, p = 0.02) as was the narrowest segment (1.83 ± 0.56. mm vs 1.39 ± 0.43, p < 0.0001) compared to the 'no vasodilator' group. At the RA origin, 79.4% of those in the 'vasodilator' group were larger than a 6. Fr guide catheter, compared to 51.4% in the 'no vasodilator' group (p = 0.004). At the narrowest segment a higher percentage of RAs in the 'vasodilator' group were larger than a 5. Fr guide catheter (65.1% vs 26.9%, p < 0.001) and a 6. Fr catheter (34.9% vs 10.3%, p = 0.001). Conclusion: IA vasodilators increase pre-procedural RA diameter in patients undergoing cardiac catheterization via TRA. This increase in diameter has important implications for procedural planning. Summary for Table of Contents: Boyer et al. performed a blinded controlled clinical trial investigating the effects of intra-arterial vasodilators on radial artery size and spasm during cardiac catheterization. The study demonstrates that intra-arterial vasodilators significantly increased the radial artery size throughout the entire course of the vessel and significantly decreased the amount of radial artery spasm. The authors conclude that these findings support the use of intra-arterial vasodilators during cardiac catheterization and have important implications for emerging technologies such as larger bore sheathless radial procedures. © 2013 Elsevier Inc.

DOI 10.1016/j.carrev.2013.08.009
Citations Scopus - 11
2013 Boyle AJ, Hwang J, Ye J, Shih H, Jun K, Zhang Y, et al., 'The effects of aging on apoptosis following myocardial infarction', Cardiovascular Therapeutics, 31 (2013) [C1]
DOI 10.1111/1755-5922.12043
Citations Scopus - 5Web of Science - 6
2012 Dehghani H, Boyle AJ, 'Percutaneous device closure of secundum atrial septal defect in older adults', American Journal of Cardiovascular Disease, 2 133-142 (2012) [D1]
2012 Angeli FS, Zhang Y, Sievers R, Jun K, Yim S, Boyle A, Yeghiazarians Y, 'Injection of human bone marrow and mononuclear cell extract into infarcted mouse hearts results in functional improvement', Open Cardiovascular Medicine Journal, 6 38-43 (2012) [C1]

Background: We have previously shown that mouse whole bone marrow cell (BMC) extract results in improvement of cardiac function and decreases scar size in a mouse model of myocard... [more]

Background: We have previously shown that mouse whole bone marrow cell (BMC) extract results in improvement of cardiac function and decreases scar size in a mouse model of myocardial infarction (MI), in the absence of intact cells. It is not clear if these results are translatable to extracts from human BMC (hBMC) or mononuclear cells (hMNC), which would have significant clinical implications. Methods: Male C57BL/6J (10-12 weeks old) mice were included in this study. MI was created by permanent ligation of the left anterior descending artery. Animals were randomized into three groups to receive ultrasound-guided myocardial injections with either hBMCs extract (n=6), hMNCs extract (n=8) or control with 0.5% bovine serum albumin (BSA) (n=7). Cardiac function was assessed by echocardiography at baseline, 2 and 28 days post-MI. Infarct size and vascularity was assessed at 28 days post-MI. Results: hBMC and hMNC extract preserve cardiac function and result in smaller scar size post-MI when compared with the control group. Conclusions: The current study for the first time reports that hBMC and hMNC extracts improve cardiac function post-MI in a mouse MI model. Further studies are necessary to fully address the potential clinical benefits of these therapies. © Angeli et al.; Licensee Bentham Open.

DOI 10.2174/1874192401206010038
Citations Scopus - 6
2012 Ye J, Boyle A, Shih H, Sievers RE, Zhang Y, Prasad M, et al., 'Sca-1 + cardiosphere-derived cells are enriched for isl1-expressing cardiac precursors and improve cardiac function after myocardial injury', PLoS ONE, 7 (2012) [C1]
DOI 10.1371/journal.pone.0030329
Citations Scopus - 58Web of Science - 47
2012 Nazer B, Hayward RM, Boyle AJ, 'Simultaneous thrombotic culprit lesions in two separate coronary arteries in a patient with ST-elevation myocardial infarction', European Heart Journal, 33 2622 (2012) [C3]
DOI 10.1093/eurheartj/ehs251
Citations Scopus - 2
2012 Koskenvuo JW, Sievers RE, Zhang Y, Angeli FS, Lee B, Shih H, et al., 'Fractionation of mouse bone-marrow cells limits functional efficacy in non-reperfused mouse model of acute myocardial infarction', ANNALS OF MEDICINE, 44 829-835 (2012) [C1]
DOI 10.3109/07853890.2012.672026
Citations Scopus - 4Web of Science - 3
2012 Majure DT, Hallaux M, Yeghiazarians Y, Boyle AJ, 'Topical nitroglycerin and lidocaine locally vasodilate the radial artery without affecting systemic blood pressure: A dose-finding phase I study', Journal of Critical Care, 27 9-13 (2012) [C1]
DOI 10.1016/j.jcrc.2012.04.019
Citations Scopus - 5Web of Science - 6
2012 Wang TY, Masoudi FA, Messenger JC, Shunk KA, Boyle A, Brennan JM, et al., 'Percutaneous Coronary Intervention and Drug-Eluting Stent Use Among Patients \= 85 Years of Age in the United States', JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 59 105-112 (2012) [C1]
DOI 10.1016/j.jacc.2011.10.853
Citations Scopus - 31Web of Science - 26
2012 Yeghiazarians Y, Gaur M, Zhang Y, Sievers RE, Ritner C, Prasad M, et al., 'Myocardial improvement with human embryonic stem cell-derived cardiomyocytes enriched by p38MAPK inhibition', CYTOTHERAPY, 14 223-231 (2012) [C1]
DOI 10.3109/14653249.2011.623690
Citations Scopus - 30Web of Science - 29
2011 Zellner C, Yeghiazarians Y, Ports TA, Ursell P, Boyle AJ, 'Sterile radial artery granuloma after transradial cardiac catheterization', Cardiovascular Revascularization Medicine, 12 187-189 (2011) [C1]

Transradial cardiac catheterization has lower rates of arterial access site complications than transfemoral procedures. However, there are complications that are unique to the tra... [more]

Transradial cardiac catheterization has lower rates of arterial access site complications than transfemoral procedures. However, there are complications that are unique to the transradial route. We present the case of a sterile granuloma occurring at the site of radial arterial access as a reaction to the hydrophilic coating on the sheath. The clinical presentation was suggestive of an infected pseudoaneurysm. Awareness of this entity may help clinicians avoid unnecessary surgical procedures, as these granulomata are transient self-limiting reactions. © 2011 Elsevier Inc.

DOI 10.1016/j.carrev.2010.06.003
Citations Scopus - 8
2011 Shih H, Lee B, Lee RJ, Boyle AJ, 'The Aging Heart and Post-Infarction Left Ventricular Remodeling', JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 57 9-17 (2011) [C1]
DOI 10.1016/j.jacc.2010.08.623
Citations Scopus - 118Web of Science - 105
2011 Mirsky R, Jahn S, Koskenvuo JW, Sievers RE, Yim SM, Ritner C, et al., 'Treatment of pulmonary arterial hypertension with circulating angiogenic cells', AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 301 L12-L19 (2011) [C1]
DOI 10.1152/ajplung.00215.2010
Citations Scopus - 17Web of Science - 16
2011 Boyle AJ, Yeghiazarians Y, Shih H, Hwang J, Ye J, Sievers R, et al., 'Myocardial production and release of MCP-1 and SDF-1 following myocardial infarction: Differences between mice and man', Journal of Translational Medicine, 9 (2011) [C1]
DOI 10.1186/1479-5876-9-150
Citations Scopus - 18Web of Science - 18
2011 Koskenvuo JW, Mirsky R, Zhang Y, Helenius H, Angeli FS, De Marco T, et al., 'Evidence of diminished coronary flow in pulmonary hypertension - explaining angina pectoris in this patient group?', CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, 31 477-484 (2011) [C1]
DOI 10.1111/j.1475-097X.2011.01049.x
Citations Scopus - 1Web of Science - 1
2011 Boyle AJ, Shih H, Hwang J, Ye J, Lee B, Zhang Y, et al., 'Cardiomyopathy of aging in the mammalian heart is characterized by myocardial hypertrophy, fibrosis and a predisposition towards cardiomyocyte apoptosis and autophagy', EXPERIMENTAL GERONTOLOGY, 46 549-559 (2011) [C1]
DOI 10.1016/j.exger.2011.02.010
Citations Scopus - 72Web of Science - 71
2011 Zhang Y, Sievers RE, Prasad M, Mirsky R, Shih H, Wong ML, et al., 'Timing of bone marrow cell therapy is more important than repeated injections after myocardial infarction', CARDIOVASCULAR PATHOLOGY, 20 204-212 (2011) [C1]
DOI 10.1016/j.carpath.2010.06.007
Citations Scopus - 19Web of Science - 27
2010 boyle A, mcniece I, 'Mesenchymal Stem Cell Therapy for Cardiac Repair', Methods in Molecular Biology, 660 65 (2010)
Citations Scopus - 68
2010 Heiss C, Jahn S, Taylor M, Real WM, Angeli FS, Wong ML, et al., 'Improvement of Endothelial Function With Dietary Flavanols Is Associated With Mobilization of Circulating Angiogenic Cells in Patients With Coronary Artery Disease', JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 56 218-224 (2010) [C1]
DOI 10.1016/j.jacc.2010.03.039
Citations Scopus - 128Web of Science - 122
2010 Angeli FS, Amabile N, Shapiro M, Mirsky R, Bartlett L, Zhang Y, et al., 'Cytokine Combination Therapy with Erythropoietin and Granulocyte Colony Stimulating Factor in a Porcine Model of Acute Myocardial Infarction', CARDIOVASCULAR DRUGS AND THERAPY, 24 409-420 (2010) [C1]
DOI 10.1007/s10557-010-6263-7
Citations Scopus - 9Web of Science - 7
2010 Angeli FS, Smith C, Amabile N, Shapiro M, Bartlett L, Virmani R, et al., 'Granulocyte colony stimulating factor in myocardial infarction with low ejection fraction', CYTOKINE, 51 278-285 (2010) [C1]
DOI 10.1016/j.cyto.2010.06.003
Citations Scopus - 9Web of Science - 7
2010 Angeli FS, Amabile N, Burjonroppa S, Shapiro M, Bartlett L, Zhang Y, et al., 'Prolonged Therapy With Erythropoietin is Safe and Prevents Deterioration of Left Ventricular Systolic Function in a Porcine Model of Myocardial Infarction', JOURNAL OF CARDIAC FAILURE, 16 579-589 (2010) [C1]
DOI 10.1016/j.cardfail.2010.02.008
Citations Scopus - 8Web of Science - 8
2010 Yeghiazarians Y, Khan M, Angeli FS, Zhang Y, Jahn S, Prasad M, et al., 'Cytokine Combination Therapy With Long-Acting Erythropoietin and Granulocyte Colony Stimulating Factor Improves Cardiac Function But is Not Superior Than Monotherapy in a Mouse Model of Acute Myocardial Infarction', JOURNAL OF CARDIAC FAILURE, 16 669-678 (2010) [C1]
DOI 10.1016/j.cardfail.2010.03.008
Citations Scopus - 13Web of Science - 11
2010 Zellner C, Ports TA, Yeghiazarians Y, Boyle AJ, 'Sterile Radial Artery Granuloma After Transradial Procedures: A Unique and Avoidable Complication', CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, 76 673-676 (2010) [C1]
DOI 10.1002/ccd.22730
Citations Scopus - 11Web of Science - 9
2010 Yong CM, Sharma M, Ochoa V, Abnousi F, Roberts J, Bass NM, et al., 'Multivessel Coronary Artery Disease Predicts Mortality, Length of Stay, and Pressor Requirements After Liver Transplantation', LIVER TRANSPLANTATION, 16 1242-1248 (2010) [C1]
DOI 10.1002/lt.22152
Citations Scopus - 34Web of Science - 33
2010 Koskenvuo JW, Mirsky R, Zhang Y, Angeli FS, Jahn S, Alastalo T-P, et al., 'A comparison of echocardiography to invasive measurement in the evaluation of pulmonary arterial hypertension in a rat model', INTERNATIONAL JOURNAL OF CARDIOVASCULAR IMAGING, 26 509-518 (2010) [C1]
DOI 10.1007/s10554-010-9596-1
Citations Scopus - 42Web of Science - 36
2010 Yong CM, Boyle AJ, 'Factor Xa Inhibitors in Acute Coronary Syndromes and Venous Thromboembolism', CURRENT VASCULAR PHARMACOLOGY, 8 5-11 (2010) [C1]
DOI 10.2174/157016110790226688
Citations Scopus - 10Web of Science - 6
2010 Hatzistergos KE, Quevedo H, Oskouei BN, Hu Q, Feigenbaum GS, Margitich IS, et al., 'Bone Marrow Mesenchymal Stem Cells Stimulate Cardiac Stem Cell Proliferation and Differentiation', CIRCULATION RESEARCH, 107 913-+ (2010) [C1]
DOI 10.1161/CIRCRESAHA.110.222703
Citations Scopus - 487Web of Science - 451
2010 Martin JH, Connelly KA, Boyle A, Kompa A, Zhang Y, Kelly D, et al., 'Effect of Atorvastatin on Cardiac Remodelling and Mortality in Rats Following Hyperglycemia and Myocardial Infarction', INTERNATIONAL JOURNAL OF CARDIOLOGY, 143 353-360 (2010) [C1]
DOI 10.1016/j.ijcard.2009.03.098
Citations Scopus - 7Web of Science - 7
Co-authors Jen Martin
2009 Angeli FS, Shapiro M, Amabile N, Orcino G, Smith CS, Tacy T, et al., 'Left ventricular remodeling after myocardial infarction: Characterization of a swine model on ß-blocker therapy', Comparative Medicine, 59 272-279 (2009) [C1]

Current guidelines recommend ß blockers for patients after myocardial infarction (MI). Novel therapies for heart failure should be tested in combination with this medication befor... [more]

Current guidelines recommend ß blockers for patients after myocardial infarction (MI). Novel therapies for heart failure should be tested in combination with this medication before entering clinical trials. In this methodologic study, we sought to describe the time course of systolic and diastolic parameters of cardiac performance over a 6-wk period in closed-chest model of swine MI treated with a ß blocker. Myocardial infarction in pigs (n = 10) was induced by 90-min balloon occlusion of the left anterior descending coronary artery. Echocardiography and pressure-volume data were collected before and at 1 and 6 wk after MI; histopathology was assessed at 6 wk. Left-ventricular (LV) volume increased significantly over 6 wk, with significant decreases in ejection fraction, wall motion index, stroke work, rate of pressure development (dP/dtmax), preload recruitable stroke work, and mechanical efficiency. Impairment of diastolic function was manifested by a significant increase in the exponential ß coefficient of the LV end-diastolic pressure-volume relation and reduction of LV pressure decay. At 6 wk, histopathologic analysis showed that the size of the infarct area was 16.3% ± 4.4%, and the LV mass and myocyte cross-sectional area in both the infarct border and remote zones were increased compared with those of noninfarcted pigs (n = 5). These findings suggest a dynamic pattern of remodeling over time in a closed-chest ischemia-reperfusion swine model of acute MI on ß-blocker therapy and may guide future studies. Copyright 2009 by the American Association for Laboratory Animal Science.

Citations Scopus - 14
2009 Sharma M, Yong C, Majure D, Zellner C, Roberts JP, Bass NM, et al., 'Safety of Cardiac Catheterization in Patients With End-Stage Liver Disease Awaiting Liver Transplantation', AMERICAN JOURNAL OF CARDIOLOGY, 103 742-746 (2009) [C1]
DOI 10.1016/j.amjcard.2008.10.037
Citations Scopus - 50Web of Science - 42
2009 Yeghiazarians Y, Zhang Y, Prasad M, Shih H, Saini SA, Takagawa J, et al., 'Injection of Bone Marrow Cell Extract Into Infarcted Hearts Results in Functional Improvement Comparable to Intact Cell Therapy', MOLECULAR THERAPY, 17 1250-1256 (2009) [C1]
DOI 10.1038/mt.2009.85
Citations Scopus - 64Web of Science - 66
2008 Zellner C, Boyle A, Yeghiazarians Y, 'Magnesium sulfate for transradial cardiac catheterization: Teaching an old dog new tricks', Journal of Invasive Cardiology, 20 543-544 (2008) [C3]
Citations Scopus - 2
2008 Sharma M, Sakhuja R, Teitel D, Boyle A, 'Percutaneous arterial closure for inadvertent cannulation of the subclavian artery - A call for caution', Journal of Invasive Cardiology, 20 (2008) [C1]
Citations Scopus - 5
2008 Schuleri KH, Boyle AJ, Centola M, Amado LC, Evers R, Zimmet JM, et al., 'The Adult Gottingen Minipig as a Model for Chronic Heart Failure After Myocardial Infarction: Focus on Cardiovascular Imaging and Regenerative Therapies', COMPARATIVE MEDICINE, 58 568-579 (2008) [C1]
Citations Scopus - 41Web of Science - 44
2008 Schuleri KH, Amado LC, Boyle AJ, Centola M, Saliaris AP, Gutman MR, et al., 'Early improvement in cardiac tissue perfusion due to mesenchymal stem cells', American Journal of Physiology - Heart and Circulatory Physiology, 294 (2008) [C1]

The underlying mechanism(s) of improved left ventricular function (LV) due to mesenchymal stem cell (MSC) administration after myocardial infarction (MI) remains highly controvers... [more]

The underlying mechanism(s) of improved left ventricular function (LV) due to mesenchymal stem cell (MSC) administration after myocardial infarction (MI) remains highly controversial. Myocardial regeneration and neovascularization, which leads to increased tissue perfusion, are proposed mechanisms. Here we demonstrate that delivery of MSCs 3 days after MI increased tissue perfusion in a manner that preceded improved LV function in a porcine model. MI was induced in pigs by 60-min occlusion of the left anterior descending coronary artery, followed by reperfusion. Pigs were assigned to receive intramyocardial injection of allogeneic MSCs (200 million, ~15 injections) (n = 10), placebo (n = 6), or no intervention (n = 8). Resting myocardial blood flow (MBF) was serially assessed by first-pass perfusion magnetic resonance imaging (MRI) over an 8-wk period. Over the first week, resting MBF in the infarct area of MSC-treated pigs increased compared with placebo-injected and untreated animals [0.17 ± 0.03, 0.09 ± 0.01, and 0.08 ± 0.01, respectively, signal intensity ratio of MI to left ventricular blood pool (LVBP); P < 0.01 vs. placebo, P < 0.01 vs. nontreated]. In contrast, the signal intensity ratios of the three groups were indistinguishable at weeks 4 and 8. However, MSC-treated animals showed larger, more mature vessels and less apoptosis in the infarct zones and improved regional and global LV function at week 8. Together these findings suggest that an early increase in tissue perfusion precedes improvements in LV function and a reduction in apoptosis in MSC-treated hearts. Cardiac MRI-based measures of blood flow may be a useful tool to predict a successful myocardial regenerative process after MSC treatment. Copyright © 2008 the American Physiological Society.

DOI 10.1152/ajpheart.00762.2007
Citations Scopus - 120
2008 Bart BA, Goldsmith SR, Boyle A, Costanzo MR, 'Renal Function and Ultrafiltration', Journal of Cardiac Failure, 14 533-534 (2008)
DOI 10.1016/j.cardfail.2008.03.005
2008 Boyle AJ, Schuleri KH, Lienard J, Vaillant R, Chan MY, Zimmet JM, et al., 'Quantitative Automated Assessment of Myocardial Perfusion at Cardiac Catheterization', AMERICAN JOURNAL OF CARDIOLOGY, 102 980-987 (2008) [C1]
DOI 10.1016/j.amjcard.2008.05.064
Citations Scopus - 8Web of Science - 8
2007 Boyle AJ, Chan MY, Dib J, Kapur NK, Kraft S, Vaillant R, et al., 'Assessment of a novel angiographic image stabilization system for percutaneous coronary intervention', Journal of Interventional Cardiology, 20 153-157 (2007)

Background: Optimization of coronary images for percutaneous coronary intervention (PCI) remains difficult due to cardiac motion throughout the respiratory and cardiac cycles. We ... [more]

Background: Optimization of coronary images for percutaneous coronary intervention (PCI) remains difficult due to cardiac motion throughout the respiratory and cardiac cycles. We tested a novel system to stabilize angiographic images at the region of interest in order to assist during PCI. Methods: Patients undergoing PCI to the right coronary artery (RCA) (group 1, n = 22) or complex PCI (group 2, n = 16) were prospectively enrolled and the angiographic image sequences of patients who died suddenly of confirmed or presumed stent thrombosis following PCI (group 3, n = 16) were retrospectively reviewed. All image sequences were analyzed off-line by three cardiologists before and after image stabilization for accuracy of stent placement, presence of residual edge dissection, and adequacy of procedural outcome. Results: Image stabilization was successful in 100% of cases in a mean time of 95 ± 71 seconds and was considered to be helpful in 13.6% of group 1, in 18.3% of group 2, and in 10% of group 3 cases. There was good correlation between observers with a kappa statistic of 0.85 to 1.0 for all observations. However, there was no difference in the reviewers' opinions of stent placement, presence of edge dissection, or adequacy of procedural result when comparing the standard angiographic views and the stabilized images. In particular, no previously unrecognized edge dissections were apparent in group 3 with stabilized display. Conclusion: Image stabilization centered on the region of interest was considered helpful in a small subset of patients, particularly the complex PCI patients. However, no differences in objective parameters could be demonstrated. © 2007, the Author.

DOI 10.1111/j.1540-8183.2007.00242.x
2007 Burjonroppa SC, Boyle AJ, Yeghiazarians Y, 'Is it time to burst the "balloon" for high-risk patients?', Journal of Invasive Cardiology, 19 347-348 (2007)
2007 Connelly KA, Boyle AJ, Kelly DJ, 'Angiotensin II and the cardiac complications of diabetes mellitus', Current Pharmaceutical Design, 13 2721-2729 (2007)

The prevalence of diabetes has reached epidemic proportions in the developed world and is expect to increase to 5.4% by 2025. This has resulted in an unprecedented number of patie... [more]

The prevalence of diabetes has reached epidemic proportions in the developed world and is expect to increase to 5.4% by 2025. This has resulted in an unprecedented number of patients experiencing the macro- and micro-vascular complications of diabetes, such as renal, retinal, neurological and cardiac dysfunction. Premature coronary artery disease and cardiac failure are vastly over-represented in the diabetic population, with significant morbidity and mortality. In fact, the rate of cardiac events in patients with diabetes is equivalent to non-diabetic patients with a previous myocardial infarction. Epidemiological evidence, combined with the results of large scale trials blocking the renin-angiotensin system (RAS) have provided data to support the hypothesis that angiotensin II and its interaction with the metabolic changes associated with diabetes mellitus is responsible for the pathogenesis of many of these complications. This review focuses on the role of the RAS and the development of diabetic cardiac disease. © 2007 Bentham Science Publishers Ltd.

DOI 10.2174/138161207781662984
Citations Scopus - 19
2007 Schuleri KH, Boyle AJ, Hare JM, 'Mesenchymal stem cells for cardiac regenerative therapy', Handbook of Experimental Pharmacology, 180 195-218 (2007)

Until recently, the concept of treating the injured or failing heart by generating new functional myocardium was considered physiologically impossible. Major scientific strides in... [more]

Until recently, the concept of treating the injured or failing heart by generating new functional myocardium was considered physiologically impossible. Major scientific strides in the past few years have challenged the concept that the heart is a post-mitotic organ, leading to the hypothesis that cardiac regeneration could be therapeutically achieved. Bone marrow-derived adult stem cells were among the first cell populations that were used to test this hypothesis. Animal studies and early clinical experience support the concept that therapeutically delivered mesenchymal stem cells (MSCs) safely improve heart function after an acute myocardial infarction (MI). MSCs produce a variety of cardio-protective signalling molecules, and have the ability to differentiate into both myocyte and vascular lineages. Additionally, MSCs are attractive as a cellular vehicle for gene delivery, cell transplantation or for tissue engineering because they offer several practical advantages. They can be obtained in relatively large numbers through standard clinical procedures, and they are easily expanded in culture. The multi-lineage potential of MSC, in combination with their immunoprivileged status, make MSCs a promising source for cell therapy in cardiac diseases. Here we provide an overview of biological characteristics of MSCs, experimental animal studies and early clinical trials with MSCs. In addition, we discuss the routes of cell delivery, cell tracking experiments and current knowledge of the mechanistic underpinnings of their action. © 2007 Springer-Verlag Berlin Heidelberg.

DOI 10.1007/978-3-540-68976-8-9
Citations Scopus - 78
2006 Kocher AA, Schuster MD, Bonaros N, Lietz K, Xiang G, Martens TP, et al., 'Myocardial homing and neovascularization by human bone marrow angioblasts is regulated by IL-8/Gro CXC chemokines', Journal of Molecular and Cellular Cardiology, 40 455-464 (2006)

In the adult, new blood vessel formation can occur either through angiogenesis from pre-existing mature endothelium or vasculogenesis mediated by bone marrow-derived endothelial p... [more]

In the adult, new blood vessel formation can occur either through angiogenesis from pre-existing mature endothelium or vasculogenesis mediated by bone marrow-derived endothelial precursors. We recently isolated endothelial progenitor cells, or angioblasts, in human adult bone marrow which have selective migratory properties for ischemic tissues, including myocardium, to where they home and induce vasculogenesis. Here we show that myocardial production of the IL-8/Gro-alpha CXC chemokine family is significantly increased after acute ischemia, and that this provides a chemoattractant gradient for bone marrow-derived endothelial progenitors, or angioblasts. This chemokine-mediated homing of bone marrow angioblasts to the ischemic heart regulates their ability to induce myocardial neovascularization, protection against cardiomyocyte apoptosis, and functional cardiac recovery. Together, our results indicate that CXC chemokines play a central role in regulating vasculogenesis in the adult, and suggest that manipulation of interactions between chemokines and their receptors on autologous human bone marrow-derived angioblasts could augment neovascularization of ischemic myocardial tissue. © 2006 Elsevier Ltd. All rights reserved.

DOI 10.1016/j.yjmcc.2005.11.013
Citations Scopus - 122
2006 Amado LC, Schuleri KH, Saliaris AP, Boyle AJ, Helm R, Oskouei B, et al., 'Multimodality noninvasive imaging demonstrates in vivo cardiac regeneration after mesenchymal stem cell therapy', JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 48 2116-2124 (2006)
DOI 10.1016/j.jacc.2006.06.073
Citations Scopus - 125Web of Science - 115
2006 Dib J, Boyle AJ, Chan M, Resar JR, 'Coronary air embolism: A case report and review of the literature', CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, 68 897-900 (2006)
DOI 10.1002/ccd.20880
Citations Scopus - 18Web of Science - 16
2006 Wilson AM, Ryan MC, Boyle AJ, 'The novel role of C-reactive protein in cardiovascular disease: Risk marker or pathogen', INTERNATIONAL JOURNAL OF CARDIOLOGY, 106 291-297 (2006)
DOI 10.1016/j.ijcard.2005.01.068
Citations Scopus - 143Web of Science - 120
2006 Boyle AJ, Whitbourn R, Schlicht S, Krum H, Kocher A, Nandurkar H, et al., 'Intra-coronary high-dose CD34+stem cells in patients with chronic ischemic heart disease: A 12-month follow-up', INTERNATIONAL JOURNAL OF CARDIOLOGY, 109 21-27 (2006)
DOI 10.1016/j.ijcard.2005.05.024
Citations Scopus - 91Web of Science - 76
2006 Boyle AJ, Chan M, Dib J, Resar J, 'Catheter-induced coronary artery dissection: Risk factors, prevention and management', Journal of Invasive Cardiology, 18 500-503 (2006)

Guide catheter-induced dissection of the coronary arteries is an uncommon but potentially catastrophic complication of diagnostic and interventional cardiac catheterization. Sever... [more]

Guide catheter-induced dissection of the coronary arteries is an uncommon but potentially catastrophic complication of diagnostic and interventional cardiac catheterization. Several factors placing the individual at higher risk of this complication have been identified. We discuss these risk factors and utilize them to propose methods to prevent dissections. Management options of coronary artery dissection are also discussed.

Citations Scopus - 40
2006 Boyle AJ, Schulman SP, Hare JM, 'Is stem cell therapy ready for patients? Stem cell therapy for cardiac repair - Ready for the next step', CIRCULATION, 114 339-352 (2006)
DOI 10.1161/CIRCULATIONAHA.105.590653
Citations Scopus - 149Web of Science - 126
2005 Xiang G, Seki T, Schuster MD, Witkowski P, Boyle AJ, See F, et al., 'Catalytic degradation of vitamin D up-regulated protein 1 mRNA enhances cardiomyocyte survival and prevents left ventricular remodeling after myocardial ischemia', Journal of Biological Chemistry, 280 39394-39402 (2005)

Vitamin D3 up-regulated protein 1 (VDUP1) is a key mediator of oxidative stress on various cellular processes via downstream effects on apoptosis signaling kinase 1 (ASK1) and p38... [more]

Vitamin D3 up-regulated protein 1 (VDUP1) is a key mediator of oxidative stress on various cellular processes via downstream effects on apoptosis signaling kinase 1 (ASK1) and p38 mitogen-activated protein kinase (MAPK). Here, we report that VDUP1 expression is significantly increased in rat hearts following acute myocardial ischemia, suggesting it may have important regulatory effects on cardiac physiological processes during periods of oxidative stress. Transfection of H9C2 cardiomyoblasts with a sequence-specific VDUP1 DNA enzyme to down-regulate VDUP1 mRNA expression significantly reduced apoptosis and enhanced cell survival under conditions of H2O2 stress, and these effects involved inhibition of ASK1 activity. Direct intracardiac injection of the DNA enzyme at the time of acute myocardial infarction reduced myocardial VDUP1 mRNA expression and resulted in prolonged reduction in cardiomyocyte apoptosis and ASK1 activity. Moreover, down-regulation of VDUP1 was accompanied by significant reduction in cardiac expression of pro-collagen type I a2 mRNA level, as well as marked reduction in myocardial scar formation. These features were accompanied by significant improvement in cardiac function. Together, these results suggest a direct role for VDUP1 in the adverse effects of ischemia and oxidative stress on cardiomyocyte survival, left ventricular collagen deposition, and cardiac function. Strategies to inhibit VDUP1 expression and/or function during acute ischemic events may be beneficial to cardiac functional recovery and prevention of left ventricular remodeling. © 2005 by The American Society for Biochemistry and Molecular Biology, Inc.

DOI 10.1074/jbc.M502966200
Citations Scopus - 56
2005 Boyle AJ, Kelly DJ, Zhang Y, Cox AJ, Gow RM, Way K, et al., 'Inhibition of protein kinase C reduces left ventricular fibrosis and dysfunction following myocardial infarction', Journal of Molecular and Cellular Cardiology, 39 213-221 (2005)

Despite current therapies, chronic heart failure (CHF) remains a major complication of myocardial infarction (MI). The pathological changes that follow MI extend to regions remote... [more]

Despite current therapies, chronic heart failure (CHF) remains a major complication of myocardial infarction (MI). The pathological changes that follow MI extend to regions remote from the site of infarction (non-infarct zone, NIZ) where fibrosis is a prominent finding. Although the mechanisms underling this adverse remodeling are incompletely understood, activation of protein kinase C has recently been implicated in its pathogenesis. MI was induced in Sprague-Dawley rats by ligation of the left anterior descending coronary artery. One week post-MI, animals were randomized to receive the PKC-inhibitor, ruboxistaurin (LY333531) for 4 weeks, or no treatment. When compared with sham-operated animals, post-MI rats showed a 33 ± 7% reduction in fractional shortening over a 4 weeks period, that was attenuated by treatment with ruboxistaurin (6 ± 11%, P < 0.05). Increased matrix deposition was noted in the NIZ, particularly in the subendocardial region of post-MI rats, in association with elevated expression of the profibrotic growth factor, transforming growth factor-beta. These findings were also significantly reduced by ruboxistaurin. PKC-inhibition with ruboxistaurin led to attenuation in both the pathological fibrosis and impaired cardiac function that follow experimental MI, suggesting a possible role for this agent in preventing post-infarction heart failure. © 2005 Elsevier Ltd. All rights reserved.

DOI 10.1016/j.yjmcc.2005.03.008
Citations Scopus - 61
2005 Boyle AJ, Schuster M, Witkowski P, Xiang G, Seki T, Way K, Itescu S, 'Additive effects of endothelial progenitor cells combined with ACE inhibition and ß-blockade on left ventricular function following acute myocardial infarction', JRAAS - Journal of the Renin-Angiotensin-Aldosterone System, 6 33-37 (2005)

Animal studies have demonstrated the efficacy of endothelial progenitor cells (EPCs) in preventing left ventricular (LV) remodelling following myocardial infarction (MI). Prelimin... [more]

Animal studies have demonstrated the efficacy of endothelial progenitor cells (EPCs) in preventing left ventricular (LV) remodelling following myocardial infarction (MI). Preliminary human studies are underway, yet no studies have demonstrated efficacy in combination with standard medical therapy, i.e. angiotensin-converting enzyme (ACE) inhibitors and ß-blockers. Nude rats underwent left anterior descending coronary artery ligation to induce MI. Animals were randomised to receive no treatment MI, n=5), quinapril 200 mg/L + metoprolol 2 g/L (ACE/BB, n=5), two million EPCs intravenously (EPC, n=5)or both (ACE/BB + EPC [n=51), then sacrificed after two weeks treatment. ACE/BB resulted in a 75% reduction in fibrosis in the region remote from the MI (p<0.05), but EPC therapy had little effect here. Conversely, EPC therapy induced neovascularisation at the peri-infarct rim, thereby preventing peri-infarct apoptosis by 81% (p<0.05). Acting via different but complementary mechanisms, the combination of ACE/BB + EPCs resulted in a greater overall improvement in LV function on echocardiography than either therapy alone. Clinical triaJs using stem cell therapy in conjunction with standard medical treatment are warranted.

DOI 10.3317/jraas.2005.004
Citations Scopus - 19
2004 Xiang G, Seki T, Schuster M, Witkowski P, Boyle AJ, See F, et al., 'Down-regulation of Plasminogen Activator Inhibitor 1 Expression Promotes Myocardial Neovascularization by Bone Marrow Progenitors', J Biol Chem, 1657-1666 (2004)
DOI 10.1084/jem.20040221
Citations Scopus - 34
2004 La Gerche A, Boyle A, Wilson AM, Prior DL, 'No Evidence of Sustained Myocardial Injury Following an Ironman Distance Triathlon', International Journal of Sports Medicine, 25 45-49 (2004)

We aimed to determine whether an Ironman distance triathlon resulted in sustained myocardial injury detected by electrocardiography, biochemical markers or echocardiographic asses... [more]

We aimed to determine whether an Ironman distance triathlon resulted in sustained myocardial injury detected by electrocardiography, biochemical markers or echocardiographic assessment of left ventricular systolic and diastolic function. Electrocardiograms, blood for analysis of creatine kinase (CK) and its MB fraction, cardiac troponin I (cTn1) and echocardiograms were obtained in 15 male athletes prior to and at a mean of 4.7 days after competing in the Australian Ironman Triathlon. Regional wall motion scores, left ventricular ejection fraction (LVEF) and mitral inflow parameters were determined from the echocardiograms by a blinded investigator. Levels of cTn1 were undetectable in all athletes and total CK was mildly elevated in 7/15 athletes prior to the event. Baseline wall motion, ejection fraction and diastolic filling were normal in all athletes. CK levels were increased post-race (p < 0.05) with a mean post-race level of 451U/l. Levels of cTn1 were undetectable post-race in 14 athletes with a level of 0.9 µg/l recorded in one athlete, although all were within the laboratory's normal range for the assay. Mitral inflow parameters and LVEF did not change post-race and regional wall motion was normal in 14 of 15 athletes. Regional wall motion abnormalities detected in 1 athlete had resolved by 25 days post-race. These findings indicate that ultraendurance exercise does not result in sustained myocardial injury in this group of elite athletes.

DOI 10.1055/s-2003-45236
Citations Scopus - 28
2004 Wilson AM, Boyle AJ, Fox P, 'Management of ischaemic heart disease in women of child-bearing age', Internal Medicine Journal, 34 694-697 (2004)

Ischaemic heart disease is rare in young women but is expected to increase with increasing average age of child bearing. Diagnosis of myocardial ischaemia in this group is complic... [more]

Ischaemic heart disease is rare in young women but is expected to increase with increasing average age of child bearing. Diagnosis of myocardial ischaemia in this group is complicated by limited data about maternal and fetal safety of the standard diagnostic tests routinely used in other patients. Management of these patients remains difficult, as many standard treatments, such as beta- blockers and angiotensin converting enzyme inhibitors are pregnancy category C or D, and there is little experience with many of the newer treatments such as coronary artery stenting, clopidogrel and glycoprotein IIb/IIIa inhibitors in pregnancy. An interesting case of a woman, who had an acute myocardial infarction treated with thrombolysis and coronary artery stenting, and who subsequently became pregnant, is reported here, and other published reports regarding the management of coronary artery disease, both acute and chronic, in pregnant women are explored.

DOI 10.1111/j.1445-5994.2004.00698.x
Citations Scopus - 19
2003 Connelly KA, Boyle A, Wilson A, MacIsaac A, Fox P, Whitbourn R, 'Coronary artery stent thrombosis associated with exercise testing', Heart Lung and Circulation, 12 66-69 (2003)

Chest pain following coronary artery stenting is common, yet finding the cause can be difficult. Exercise testing has long been used in the assessment of chest pain, but its usefu... [more]

Chest pain following coronary artery stenting is common, yet finding the cause can be difficult. Exercise testing has long been used in the assessment of chest pain, but its usefulness in patients who have recently undergone coronary artery stenting is in doubt. A case of exercise testing appearing to precipitate acute stent thrombosis in a patient several weeks post-coronary artery stenting is reported and compared to a similar case in the literature. The role of exercise testing in the assessment of chest pain early after coronary artery stenting is then reviewed.

DOI 10.1046/j.1444-2892.2003.00165.x
Citations Scopus - 3
2002 Boyle AJ, Wilson AM, Connelly K, McGuigan L, Wilson J, Whitbourn R, 'Improvement in timing and effectiveness of external cardiac compressions with a new non-invasive device: the CPR-Ezy', RESUSCITATION, 54 63-67 (2002)
DOI 10.1016/S0300-9572(02)00049-7
Citations Scopus - 57Web of Science - 52
2001 Boyle AJ, Jelinek MV, 'Rethinking the approach to abdominal aortic aneurysms', LANCET, 357 2140-2140 (2001)
DOI 10.1016/S0140-6736(00)05216-8
Citations Scopus - 1Web of Science - 1
2001 Boyle AJ, Wilson AM, Maclsaac AI, Daffy J, Stanley P, 'Mural endocarditis caused by Salmonella virchow: Survival with conservative treatment', Heart Lung and Circulation, 10 161-163 (2001)

We describe a case of endocarditis caused by Salmonella enterica serotype virchow, which was treated conservatively with antibiotics alone. It is the only reported case of surviva... [more]

We describe a case of endocarditis caused by Salmonella enterica serotype virchow, which was treated conservatively with antibiotics alone. It is the only reported case of survival from salmonella endocarditis with conservative treatment, and the first reported case of endocarditis caused by Salmonella virchow. The changing prevalence, virulence patterns and importance of salmonella species in endocarditis are discussed.

DOI 10.1046/j.1444-2892.2001.00099.x
Citations Scopus - 1
Show 104 more journal articles

Conference (14 outputs)

Year Citation Altmetrics Link
2017 Murtha LA, Mabotuwana NR, Hardy SA, Boyle AJ, 'Fibulin-3 as a Potential Therapeutic Target for Cardiac Fibrosis', JOURNAL OF CARDIAC FAILURE, Dallas, TX (2017)
DOI 10.1016/j.cardfail.2017.07.071
Co-authors Lucy Murtha
2017 Murtha LA, Mabotuwana NS, Hardy SA, Boyle AJ, 'Fibulin-3 Plays a Key Role in Cardiac Fibrosis Following Myocardial Infarction in Mice', CIRCULATION, Anaheim, CA (2017)
Co-authors Lucy Murtha
2016 Davies AJ, Boyle A, 'Trends in characteristics and outcomes of elderly patients presenting with acute myocardial infarction', EUROPEAN HEART JOURNAL, Rome, ITALY (2016)
2016 Davies AJ, Boyle A, 'Differences in age and outcomes of aboriginal and non-aboriginal Australians presenting with acute myocardial infarction', EUROPEAN HEART JOURNAL, Rome, ITALY (2016)
2016 Khan AA, Williams T, Savage L, Stewart P, Fletcher P, Boyle A, 'PRE-HOSPITAL THROMBOLYSIS VERSUS PRIMARY PERCUTANEOUS CORONARY INTERVENTION FOR ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION IN REGIONAL AUSTRALIA: REAL WORLD LONG TERM FOLLOW UP', JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Chicago, IL (2016)
DOI 10.1016/S0735-1097(16)30614-3
2014 Esposito M, Shah NN, Korabathina R, Pan C, Paruchuri V, Finley J, et al., 'Quantitative Assessment of Myocardial Perfusion Using Time-Density Curve Analysis After Elective Percutaneous Coronary Intervention', JOURNAL OF INVASIVE CARDIOLOGY (2014) [E3]
Citations Web of Science - 1
2011 Watanabe M, See F, Kompa AR, Boyle AJ, Gilbert RE, Connelly K, et al., 'Delayed Tranilast Treatment Reduces Pathological Fibrosis Following Myocardial Infarction And In Uremic Cardiomyopathy', CIRCULATION (2011) [C3]
2008 Schuleri KH, Amado LC, Boyle AJ, Centola M, Saliaris AP, Gutman MR, et al., 'Early improvement in cardiac tissue perfusion due to mesenchymal stem cells', AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, Amelia Isl, FL (2008) [E1]
DOI 10.1152/ajpheart.00762.2007
Citations Web of Science - 108
2007 Schuleri KH, Centola M, Zimmet JM, Boyle AJ, Feigenbaum GS, Heldman AW, et al., 'Intramyocardial allogeneic mesenchymal stem cells reduce infarct size in a porcine model of chronic ischemic cardiomyopathy', JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, New Orleans, LA (2007)
2007 Schuleri KH, Amado LC, Boyle AJ, Centola M, Zimmet JM, Saliaris AP, et al., 'Early improvement in cardiac tissue perfusion due to mesenchymal stem cells', EUROPEAN HEART JOURNAL (2007) [E3]
2006 Amado LC, Schuleri KH, Saliaris AP, Helm R, Boyle A, Oskouei B, et al., 'Impact of mesenchymal stem cell therapy on scar composition and cardiac regional function', JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Atlanta, GA (2006)
2006 Schuleri KH, Boyle A, Amado LC, Saliaris AP, Oskouei BN, Young RG, et al., 'Allogeneic mesenchymal stem cells improve vessel maturation and reduce apoptosis in regions of ischemically damaged myocardium', JOURNAL OF CARDIAC FAILURE, Seattle, WA (2006)
DOI 10.1016/j.cardfail.2006.06.037
2006 Mazhari R, Schuleri KH, Zimmet JM, Saliaris AP, Amado LC, Boyle AJ, et al., 'Cell tracking following the intramyocardial injection of mesenchymal cells after myocardial infarction', JOURNAL OF CARDIAC FAILURE, Seattle, WA (2006)
DOI 10.1016/j.cardfail.2006.06.067
2006 Mazhari R, Schuleri KH, Zimmet JM, Boyle AJ, Heldman AW, Hare JM, 'Cell tracking following the intramyocardial injection of MSCs after myocardial infarction', CIRCULATION, Chicago, IL (2006)
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Grants and Funding

Summary

Number of grants 31
Total funding $5,474,198

Click on a grant title below to expand the full details for that specific grant.


20193 grants / $606,253

HMRI MRSP Infrastructure Funding Cardiovascular 2019$299,461

Funding body: NSW Ministry of Health

Funding body NSW Ministry of Health
Project Team Professor Ronald Plotnikoff, Professor Andrew Boyle, Professor Dirk Van Helden, Professor Ronald Plotnikoff
Scheme Medical Research Support Program (MRSP)
Role Investigator
Funding Start 2019
Funding Finish 2019
GNo G1801376
Type Of Funding C2220 - Aust StateTerritoryLocal - Other
Category 2220
UON Y

Understanding scar tissue in the heart$263,032

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Andrew Boyle
Scheme Project Grant
Role Lead
Funding Start 2019
Funding Finish 2021
GNo G1900541
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

CaMKII study$43,760

Funding body: Armaron Bio Pty Ltd

Funding body Armaron Bio Pty Ltd
Project Team Professor Andrew Boyle
Scheme Research Grant
Role Lead
Funding Start 2019
Funding Finish 2019
GNo G1901017
Type Of Funding C3111 - Aust For profit
Category 3111
UON Y

201811 grants / $1,462,188

MORACS - Management of Rural Acute Coronary Syndromes$651,155

Funding body: NSW Health

Funding body NSW Health
Scheme Translational Research Grants Scheme
Role Lead
Funding Start 2018
Funding Finish 2020
GNo
Type Of Funding C2210 - Aust StateTerritoryLocal - Own Purpose
Category 2210
UON N

Improving Outcomes Following Hospitalisation for Heart Failure in Regional and Remote NSW – the BEEM-HF Study$479,376

Funding body: NSW Health

Funding body NSW Health
Project Team

Aaron Sverdlov

Scheme Translational Research Grants Scheme
Role Investigator
Funding Start 2018
Funding Finish 2020
GNo
Type Of Funding C2210 - Aust StateTerritoryLocal - Own Purpose
Category 2210
UON N

To develop and test a new paradigm for management of changing Heart Failure disease treatment$99,371

Funding body: Biotronik Australia Pty Ltd

Funding body Biotronik Australia Pty Ltd
Project Team Associate Professor Aaron Sverdlov, Associate Professor Doan Ngo, Professor Andrew Boyle
Scheme Entrepreneurs' Programme: Innovation Connections
Role Investigator
Funding Start 2018
Funding Finish 2018
GNo G1801209
Type Of Funding C3111 - Aust For profit
Category 3111
UON Y

Reduction of End Diastolic Pressure in Acute Myocardial Infarction. The RED PAMI trial.$75,000

Funding body: National Heart Foundation of Australia

Funding body National Heart Foundation of Australia
Project Team Professor Andrew Boyle, Professor James Cameron, Doctor Stuart Moir
Scheme Vanguard Grant
Role Lead
Funding Start 2018
Funding Finish 2018
GNo G1700824
Type Of Funding Aust Competitive - Non Commonwealth
Category 1NS
UON Y

Fellowship in Interventional Cardiology Research at University of Newcastle/John Hunter Hospital$59,479

Funding body: Abbott Australasia Pty Ltd

Funding body Abbott Australasia Pty Ltd
Project Team Professor Andrew Boyle, Dr Nick Collins
Scheme Research Grant
Role Lead
Funding Start 2018
Funding Finish 2018
GNo G1800537
Type Of Funding C3111 - Aust For profit
Category 3111
UON Y

Determining the mechanisms of myocardial infarction induced cardiac fibrosis: what role does fibulin-3 play?$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Lucy Murtha, Professor Andrew Boyle, Associate Professor Doan Ngo, Associate Professor Aaron Sverdlov
Scheme Project Grant
Role Investigator
Funding Start 2018
Funding Finish 2018
GNo G1801370
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Does Heparin influence systemic midkine levels in cardiac patients undergoing angiograms?$20,500

Funding body: Cellmid Ltd

Funding body Cellmid Ltd
Project Team Professor Andrew Boyle, Doctor Theo De Malmanche
Scheme Research Grant
Role Lead
Funding Start 2018
Funding Finish 2018
GNo G1800022
Type Of Funding C3111 - Aust For profit
Category 3111
UON Y

The role of extracellular matrix protein 1 (ECM1) in cardiac fibrosis$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Mr Sean Hardy, Professor Andrew Boyle, Professor Phil Hansbro, Professor Peter Rainer
Scheme Emlyn and Jennie Thomas Postgraduate Medical Research Scholarship
Role Lead
Funding Start 2018
Funding Finish 2019
GNo G1800696
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Reducing elevated diastolic pressure in acute myocardinal infraction - medication arm (RED-PAMI-meds)$17,307

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Professor Andrew Boyle, Doctor Arshad Khan
Scheme Research Grant
Role Lead
Funding Start 2018
Funding Finish 2018
GNo G1800371
Type Of Funding C3112 - Aust Not for profit
Category 3112
UON Y

Assessment of neurovascular function and cognition in adult patients with complex congenital heart disease$10,000

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Dr Nick Collins, Doctor Rachel Wong, Emeritus Professor Peter Howe, Professor Neil Spratt, Professor Andrew Boyle, Conjoint Professor Chris Levi
Scheme Research Grant
Role Investigator
Funding Start 2018
Funding Finish 2018
GNo G1800454
Type Of Funding C3112 - Aust Not for profit
Category 3112
UON Y

A prospective systematic examination of radial artery occlusion, injury and complication post cardiac catheterisation: A nursing led review of procedural complications$5,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Mr Trent Williams, Associate Professor Kerry Inder, Professor Andrew Boyle
Scheme Project Grant
Role Investigator
Funding Start 2018
Funding Finish 2018
GNo G1800458
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

20175 grants / $1,224,878

A randomised clinical trial of STAtin therapy for Reducing Events in the Elderly (STAREE)$977,798

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Andrew Boyle, Prof Sophia Zoungas, Professor Andrew Boyle
Scheme Project Grant
Role Lead
Funding Start 2017
Funding Finish 2020
GNo G1601140
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

HNE Translational research Fellowship for Dr Arshad Khan$137,538

Funding body: Hunter New England Health LHD, NSW Health

Funding body Hunter New England Health LHD, NSW Health
Project Team

Arshad Khan, Andrew Boyle

Scheme Translational Research Fellowship
Role Investigator
Funding Start 2017
Funding Finish 2018
GNo
Type Of Funding Other Public Sector - State
Category 2OPS
UON N

Characterising the role of Fibulin-3 in health and disease$81,750

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Lucy Murtha, Professor Andrew Boyle
Scheme Project Grant
Role Investigator
Funding Start 2017
Funding Finish 2019
GNo G1700327
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Injectable Polymer for Cardiac Regeneration – a Pilot Study$20,000

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Professor Andrew Boyle, Professor Randall Lee
Scheme Research Grant
Role Lead
Funding Start 2017
Funding Finish 2017
GNo G1700571
Type Of Funding C3112 - Aust Not for profit
Category 3112
UON Y

Feasibility and engagement strategies for a cardiovascular disease prevention program targeting a high need, low health literacy rural community.$7,792

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Tracy Schumacher, Associate Professor Leanne Brown, Professor Jennifer May, Professor Clare Collins, Professor Andrew Boyle
Scheme Linkage Pilot Research Grant
Role Investigator
Funding Start 2017
Funding Finish 2018
GNo G1701268
Type Of Funding Internal
Category INTE
UON Y

20163 grants / $303,400

Fibulin-3 and Cardiac Fibrosis$266,655

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Andrew Boyle
Scheme Project Grant
Role Lead
Funding Start 2016
Funding Finish 2018
GNo G1600019
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Profiling Human Cardiac Stem Cells$21,745

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Professor Andrew Boyle, Professor Jennifer Martin
Scheme Research Grant
Role Lead
Funding Start 2016
Funding Finish 2016
GNo G1600704
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

Knockout model for heart fibrosis$15,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Andrew Boyle
Scheme Project Grant
Role Lead
Funding Start 2016
Funding Finish 2016
GNo G1600595
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20152 grants / $45,222

MERINO2 - A randomised controlled trial comparing two different antibiotics for blood stream infections caused by the 'ESCaPM' group of antibiotic resistant Gram negative bacteria$25,222

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Conjoint Professor Josh Davis, Professor Andrew Boyle, Patrick Harris, David Paterson
Scheme Project Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo G1500781
Type Of Funding C3112 - Aust Not for profit
Category 3112
UON Y

Development of a novel model of cardiac scar tissue$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Andrew Boyle
Scheme Project Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500378
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20143 grants / $508,257

Fibulin-3 and Cardiac Fibrosis$302,237

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Andrew Boyle
Scheme Project Grant
Role Lead
Funding Start 2014
Funding Finish 2017
GNo G1400574
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Activation and Rejuvenation of Endogenous Cardiac Stem Cells$200,000

Funding body: National Heart Foundation of Australia

Funding body National Heart Foundation of Australia
Scheme NSW Cardiovascular Research Network Research Development Project Grant
Role Investigator
Funding Start 2014
Funding Finish 2016
GNo
Type Of Funding Other Public Sector - State
Category 2OPS
UON N

2014 International Visitor from University of California (San Francisco), USA$6,020

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Professor Andrew Boyle, Professor Randall Lee
Scheme International Research Visiting Fellowship
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1400864
Type Of Funding Internal
Category INTE
UON Y

20121 grants / $33,000

A New Model of Diastolic Heart Failure$33,000

Funding Body: UCSF CTSI Funding Scheme: SOS Grant - Individual Investigator Description: – (Boyle PI) 7/2012 – 6/2013 $30,000

Funding body: Society for Cardiovascular Angiography and Interventions

Funding body Society for Cardiovascular Angiography and Interventions
Project Team

Andrew Boyle

Scheme Fellows Award
Role Lead
Funding Start 2012
Funding Finish 2013
GNo
Type Of Funding Not Known
Category UNKN
UON N

20082 grants / $1,200,000

The Effects of Aging on Left Ventricular Remodeling Following Myocardial Infarction$700,000

Funding Body: NIH National Institutes of Health Funding Scheme: K08 Description: Aging has detrimental effects of outcomes following heart attacks. We study the cellular and molecular mechanisms that lead to these worse outcomes.

Funding body: NIH National Institutes of Health

Funding body NIH National Institutes of Health
Project Team

Andrew Boyle

Scheme K08
Role Lead
Funding Start 2008
Funding Finish 2013
GNo
Type Of Funding Not Known
Category UNKN
UON N

The Influence of Aging on Pressure Overload Cardiomyopathy$500,000

Research Grant Description: The cellular and molecular aspects of left ventricular remodeling in response to pressure overload were studied, with emphasis on age-related changes.

Funding body: Ellison Medical Foundation

Funding body Ellison Medical Foundation
Project Team

Andrew Boyle

Scheme Research Grant
Role Lead
Funding Start 2008
Funding Finish 2012
GNo
Type Of Funding Not Known
Category UNKN
UON N

20031 grants / $91,000

Novel Therapies for the Prevention and Treatment of Left ventricular Remodelling Following Myocardial Infarction.$91,000

Study of new treatments including bone marrow derived stem cells for treatment of post-infarction heart failure

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team

Andrew Boyle

Scheme Scholarships - Medical and Dental Postgraduate Research
Role Lead
Funding Start 2003
Funding Finish 2005
GNo
Type Of Funding Not Known
Category UNKN
UON N
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Research Supervision

Number of supervisions

Completed0
Current13

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2019 PhD Pathophysiology of Obesity-Induced Cardiometabolic Dysfunction: The Link With Colorectal Cancer PhD (Pharmacy), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2019 Masters Atrial Fibrillation Ablation in Hunter New England Health: The Outcomes of AF Ablation Study and Sedation Versus General Anaesthesia Study M Philosophy (Medicine), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2019 PhD Management of Rural Acute Coronary Syndromes (MORACS) PhD (Nursing), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2019 PhD The Diagnosis and Epidemiology of Blunt Cardiac Injury PhD (Trauma Sciences), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2019 PhD Improving Outcomes following Hospitalisation for Heart Failure in Regional and Remote NSW-the BEEM-HF Study PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2019 Masters The Origin of Extracellular Matrix Protein 1 (ECM) Production in Cardiac Ageing and Myocardial Infarction M Philosophy (Medicine), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2018 PhD Heart Failure Outcomes in Hunter New England Area PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2018 PhD The Impact of Reduction in Left Ventricular End Diastolic Pressure in Patients with ST-segment Elevation Myocardial Infarction. PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2017 PhD The Identification of Novel Proteins Expressed by Human Cardiac Stem and Progenitor Cells to Develop Regenerative Non-Cellular Therapies for Heart Failure PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2017 PhD Nurse-led Detection of Adverse Events following Cardiac Admissions and Procedures in a Regional Australian Health District PhD (Nursing), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2017 PhD Establishment and Application of an In Vitro 3D Model of the Human Heart to Facilitate Discovery of New Therapies for Myocardial Infarction PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2017 PhD Extracellular Matrix Protein 1 (ECM1) in the Ageing and Diseased Mammalian Heart PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2016 Masters Investigation of Vitamin D¿s Significance to Severe Cardiovascular Disease M Philosophy (Nursing), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
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Research Opportunities

Investigating cardiac fibrosis

Honours

Honours

Hunter Medical Research Institute - Public Health

1/01/2019 - 31/12/2019

Contact

Ms Stacey Wilks
University of Newcastle
School of Medicine and Public Health
stacey.wilks@newcastle.edu.au

Regeneration of cardiac tissue

PhD scholarship

PHD

Health

1/01/2019 - 31/12/2021

Contact

Ms Stacey Wilks
University of Newcastle
School of Medicine and Public Health
stacey.wilks@newcastle.edu.au

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News

Newcastle researchers awarded $750,000 to help heart health

December 11, 2017

Six Hunter researchers have secured $750,000 in Heart Foundation funding to investigate heart disease, Australia’s leading cause of death.

Drug trial to reduce scarring after heart scare

December 1, 2015

Hunter heart attack survivors will be among the first in the world to trial a new drug designed to reduce the tissue scarring commonly associated with heart wea

Professor Andrew Boyle

Position

Professor of Cardiovascular Medicine & Head of Discipline
School of Medicine and Public Health
Faculty of Health and Medicine

Contact Details

Email andrew.boyle@newcastle.edu.au
Phone (02) 4921 4205
Fax (02) 4921 4210

Office

Location HMRI

,
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