Search

Your search keyword '"Iles, Leah"' showing total 141 results
Start Over Author "Iles, Leah"
141 results on '"Iles, Leah"'

2. Regression of Diffuse Ventricular Fibrosis Following Restoration of Sinus Rhythm With Catheter Ablation in Patients With Atrial Fibrillation and Systolic Dysfunction: A Substudy of the CAMERA MRI Trial

Author

Prabhu, Sandeep, Costello, Ben T., Taylor, Andrew J., Gutman, Sarah J., Voskoboinik, Aleksandr, McLellan, Alex J.A., Peck, Kah Y., Sugumar, Hariharan, Iles, Leah, Pathik, Bhupesh, Nalliah, Chrishan J., Wong, Geoff R., Azzopardi, Sonia M., Lee, Geoffrey, Mariani, Justin, Kaye, David M., Ling, Liang-Han, Kalman, Jonathan M., and Kistler, Peter M.

Published
2018
Full Text
View/download PDF

14. Myocardial fibrosis in heart failure

Author

Iles, Leah Maree

Subjects
Uncategorized
Abstract

Heart failure is a major contributor to mortality and morbidity, both in Australia and worldwide. Despite significant recent therapeutic advances, many patients ultimately progress to advanced cardiomyopathy. The subsequent burden of end-stage heart failure, with few eligible for cardiac transplantation, necessitates urgent research into the underlying pathophysiology of this important disease. Myocardial fibrosis has previously been identified as fundamental in the development of heart failure, as first described in ischaemic cardiomyopathy. Its importance in non-ischaemic cardiomyopathy has been more recently recognised, with considerable interest in possible therapeutic options to retard progression. In order to further elucidate the consequences of myocardial fibrosis and potential benefits of anti-fibrotic therapies, a non-invasive quantitative method for the analysis of myocardial fibrosis is highly desired. In Chapter 1 of this thesis, I provide an introduction and literature review encompassing the current knowledge of the pathogenesis of heart failure, and the pivotal role of myocardial fibrosis. Chapter 2 outlines the methodology of a novel non-invasive cardiac magnetic resonance (CMR) imaging technique, investigated in this thesis as a potential quantitative assessment of diffuse myocardial fibrosis. In Chapter 3 I report for the first time validation of this CMR imaging technique for the quantification of diffuse myocardial fibrosis. This study compares this prototype CMR sequence in patients with heart failure with control subjects. Additionally, histological confirmation and correlation with diastolic function is reported. Recognising the limitations of comparative histology using endomyocardial biopsy specimens, I then compared histological analysis in explanted hearts with in vivo CMR examination prior to cardiac transplantation. This whole heart analysis allowed not only validation of our novel CMR technique for diffuse myocardial fibrosis, but also for confirmation of an established CMR technique, late gadolinium enhancement (LGE), as representative of regional replacement myocardial fibrosis. Whilst this has been shown to correlate with fibrosis in areas of myocardial infarction, histological validation in non-ischaemic cardiomyopathy is lacking. To extend on my investigation into the consequences of myocardial fibrosis, I studied patients planned for implantation of an internal cardioverter-defibrillator (ICD) for the primary prevention of sudden cardiac death. All patients underwent CMR prior to device implantation, and were followed to monitor for a primary endpoint of appropriate device therapy, with a pre-specified composite secondary endpoint of all-cause mortality, appropriate ICD therapy or cardiac transplantation. Presence of LGE was significantly associated with likelihood of reaching both the primary and secondary endpoints. Finally, in Chapter 6, I report cross-sectional and longitudinal data in a group of patients with non-ischaemic cardiomyopathy. In this study, I present data independently correlating diffuse myocardial fibrosis quantified by CMR with symptoms of heart failure, and both regional and diffuse myocardial fibrosis independently predicting adverse outcomes. Publication of two of these papers has contributed to rapid proliferation of research into this important aspect of heart failure, with both papers highly cited. It is hoped that this doctoral work and ongoing post-doctoral studies will continue to advance our understanding of myocardial fibrosis in heart failure, ultimately with reduction in patient mortality and morbidity.

Published
2017
Full Text
View/download PDF

15. Reduction in mortality from implantable cardioverter-defibrillators in non-ischaemic cardiomyopathy patients is dependent on the presence of left ventricular scar

Author

Gutman, Sarah J, primary, Costello, Benedict T, additional, Papapostolou, Stavroula, additional, Voskoboinik, Aleksandr, additional, Iles, Leah, additional, Ja, Johnson, additional, Hare, James L, additional, Ellims, Andris, additional, Kistler, Peter M, additional, Marwick, Thomas H, additional, and Taylor, Andrew J, additional

Published
2018
Full Text
View/download PDF

17. Reduction in mortality from implantable cardioverter-defibrillators in non-ischaemic cardiomyopathy patients is dependent on the presence of left ventricular scar.

Author

Gutman, Sarah J, Costello, Benedict T, Papapostolou, Stavroula, Voskoboinik, Aleksandr, Iles, Leah, Ja, Johnson, Hare, James L, Ellims, Andris, Kistler, Peter M, Marwick, Thomas H, and Taylor, Andrew J

Abstract

Aims In patients with non-ischaemic cardiomyopathy (NICM), the mortality benefit of a primary prevention implantable cardioverter-defibrillator (ICD) has been challenged. Left ventricular (LV) scar identified by cardiac magnetic resonance (CMR) imaging is associated with a high risk of malignant arrhythmia in NICM. We aimed to determine the impact of LV scar on the mortality benefit from a primary prevention ICD in NICM. Methods and results We recruited 452 consecutive heart failure patients [New York Heart Association (NYHA) Class II/III] with NICM and LV ejection fraction ≤35% from a state-wide CMR service. All patients fulfilled European Society of Cardiology guidelines for primary prevention ICD implantation; however, the decision to implant was at the treating physician's discretion. Baseline clinical and CMR data were recorded prospectively and heart failure mortality risk (MAGGIC score) was calculated. The primary study outcome measurement was all-cause mortality based on presence or absence of ICD, stratified by LV scar. Median follow-up was 37.9 months and there was no difference in MAGGIC score between those who did and did not receive a primary prevention ICD (19.30 ± 5.46 vs. 18.90 ± 5.67, P  = 0.50). In patients without LV scar, ICD implantation was not associated with improved mortality [hazard ratio (HR) = 1.22, 95% confidence interval (CI): 0.53–2.78, P  = 0.64]. In patients with LV scar, ICD implantation was independently associated with reduced mortality (HR = 0.45, 95% CI: 0.26–0.77, P  = 0.003). Conclusions In patients with NICM, primary prevention ICD implantation is only associated with reduced mortality in patients with LV scar. This may enable more effective selection of NICM patients for ICD implantation compared with current guidelines. View large Download slide View large Download slide [ABSTRACT FROM AUTHOR]

Published
2019
Full Text
View/download PDF

18. 176-72: Diffuse Ventricular Fibrosis on Cardiac Magnetic Resonance Imaging Associates with Ventricular Tachycardia in Patients with Hypertrophic Cardiomyopathy

Author

Mclellan, Alex, primary, Ellims, Andris, additional, Prabhu, Sandeep, additional, Voskoboinik, Alex, additional, Iles, Leah, additional, Hare, James, additional, Kaye, David, additional, Macciocca, Ivan, additional, Mariani, Justin, additional, Kalman, Jonathan M., additional, Taylor, Andrew, additional, and Kistler, Peter, additional

Published
2016
Full Text
View/download PDF

21. Magnetic resonance post-contrast T1 mapping in the human atrium: Validation and impact on clinical outcome after catheter ablation for atrial fibrillation

Author

Ling, Liang-han, primary, McLellan, Alex J.A., additional, Taylor, Andrew J., additional, Iles, Leah M., additional, Ellims, Andris H., additional, Kumar, Saurabh, additional, Teh, Andrew, additional, Lee, Geoffrey, additional, Wong, Michael C.G., additional, Azzopardi, Sonia, additional, Sellenger, Michael A., additional, Morton, Joseph B., additional, Kalman, Jonathan M., additional, and Kistler, Peter M., additional

Published
2014
Full Text
View/download PDF

28. Bright Muscle, Weak Heart, Bad Start?

Author

Jaworski, Catherine, primary, Looi, Jen-Li, additional, Iles, Leah M., additional, McLean, Catriona A., additional, Taylor, Andrew J., additional, and Hare, James L., additional

Published
2014
Full Text
View/download PDF

30. Reply

Author

Iles, Leah, Pfluger, Heinz, Lefkovits, Lisa, Butler, Michelle J., Kistler, Peter M., Kaye, David M., and Taylor, Andrew J.

Subjects
Cardiology and Cardiovascular Medicine
Published
2011

32. Sinus rhythm restores ventricular function in patients with cardiomyopathy and no late gadolinium enhancement on cardiac magnetic resonance imaging who undergo catheter ablation for atrial fibrillation

Author

Ling, Liang-Han, primary, Taylor, Andrew J., additional, Ellims, Andris H., additional, Iles, Leah M., additional, McLellan, Alex J.A., additional, Lee, Geoffrey, additional, Kumar, Saurabh, additional, Lee, Geraldine, additional, Teh, Andrew, additional, Medi, Caroline, additional, Kaye, David M., additional, Kalman, Jonathan M., additional, and Kistler, Peter M., additional

Published
2013
Full Text
View/download PDF

37. Diffuse Ventricular Fibrosis in Atrial Fibrillation

Author

Ling, Liang-han, primary, Kistler, Peter M., additional, Ellims, Andris H., additional, Iles, Leah M., additional, Lee, Geraldine, additional, Hughes, Gerard L., additional, Kalman, Jonathan M., additional, Kaye, David M., additional, and Taylor, Andrew J., additional

Published
2012
Full Text
View/download PDF

45. A comprehensive evaluation of myocardial fibrosis in hypertrophic cardiomyopathy with cardiacmagnetic resonance imaging: linking genotype with fibrotic phenotype.

Author

Ellims, Andris H., Iles, Leah M., Ling, Liang-han, Chong, Belinda, Macciocca, Ivan, Slavin, Glenn S., Hare, James L., Kaye, David M., Marasco, Silvana F., McLean, Catriona A., James, Paul A., du Sart, Desirée, and Taylor, Andrew J.

Abstract

Aims In hypertrophic cardiomyopathy (HCM), attempts to associate genotype with phenotype have largely been unsuccessful. More recently, cardiac magnetic resonance (CMR) imaging has enhanced myocardial fibrosis characterization, while next-generation sequencing (NGS) can identify pathogenic HCM mutations. We used CMR and NGS to explore the link between genotype and fibrotic phenotype in HCM. Methods and results One hundred and thirty-nine patients with HCM and 25 healthy controls underwent CMR to quantify regional myocardial fibrosis with late gadolinium enhancement (LGE) and diffuse myocardial fibrosis with post-contrast T1 mapping. Collagen content of myectomy specimens from nine HCM patients was determined. Fifty-six HCM patients underwent NGS for 65 cardiomyopathy genes, including 36 HCM-associated genes. Post-contrast myocardial T1 time correlated histologically with myocardial collagen content (r = −0.70, P = 0.03). Compared with controls, HCM patients had more LGE (4.6 ± 6.1 vs. 0%, P < 0.001) and lower post-contrast T1 time (483 ± 83 vs. 545 ± 49 ms, P < 0.001). LGE negatively correlated with left-ventricular (LV) ejection fraction and outflow tract obstruction, whereas lower post-contrast T1 time, suggestive of more diffuse myocardial fibrosis, was associated with LV diastolic impairment and dyspnoea. Patients with identifiable HCM mutations had more LGE (7.9 ± 8.6 vs. 3.1 ± 4.3%, P = 0.03), but higher post-contrast T1 time (498 ± 81 vs. 451 ± 70 ms, P = 0.03) than patients without. Conclusion In HCM, contrast-enhanced CMR with T1 mapping can non-invasively evaluate regional and diffuse patterns of myocardial fibrosis. These patterns of fibrosis occur independently of each other and exhibit distinct clinical associations. HCM patients with recognized genetic mutations have significantly more regional, but less diffuse myocardial fibrosis than those without. [ABSTRACT FROM AUTHOR]

Published
2014
Full Text
View/download PDF

46. Evaluation of Diffuse Myocardial Fibrosis in Heart Failure With Cardiac Magnetic Resonance Contrast-Enhanced T1 Mapping

Author

Iles, Leah, Pfluger, Heinz, Phrommintikul, Arintaya, Cherayath, Joshi, Aksit, Pelin, Gupta, Sandeep N., Kaye, David M., and Taylor, Andrew J.

Subjects
*CARDIOMYOPATHIES, *MAGNETIC resonance imaging, *CARDIAC magnetic resonance imaging, *MEDICAL research
Abstract

Objectives: The purpose of this study was to investigate a noninvasive method for quantifying diffuse myocardial fibrosis with cardiac magnetic resonance imaging (CMRI). Background: Diffuse myocardial fibrosis is a fundamental process in pathologic remodeling in cardiomyopathy and is postulated to cause increased cardiac stiffness and poor clinical outcomes. Although regional fibrosis is easily imaged with cardiac magnetic resonance, there is currently no noninvasive method for quantifying diffuse myocardial fibrosis. Methods: We performed CMRI on 45 subjects (25 patients with heart failure, 20 control patients), on a clinical 1.5-T CMRI scanner. A prototype T1 mapping sequence was used to calculate the post-contrast myocardial T1 time as an index of diffuse fibrosis; regional fibrosis was identified by delayed contrast enhancement. Regional and global systolic function was assessed by cine CMRI in standard short- and long-axis planes, with echocardiography used to evaluate diastology. An additional 9 subjects underwent CMRI and endomyocardial biopsy for histologic correlation. Results: Post-contrast myocardial T1 times correlated histologically with fibrosis (R = −0.7, p = 0.03) and were shorter in heart failure subjects than controls (383 ± 17 ms vs. 564 ± 23 ms, p < 0.0001). The T1 time of heart failure myocardium was shorter than that in controls even when excluding areas of regional fibrosis (429 ± 22 ms vs. 564 ± 23 ms, p < 0.0001). The post-contrast myocardial T1 time shortened as diastolic function worsened (562 ± 24 ms in normal diastolic function vs. 423 ± 33 ms in impaired diastolic function vs. 368 ± 20 ms in restrictive function, p < 0.001). Conclusions: Contrast-enhanced CMRI T1 mapping identifies changes in myocardial T1 times in heart failure, which appear to reflect diffuse fibrosis. [Copyright &y& Elsevier]

Published
2008
Full Text
View/download PDF

47. Diffuse Ventricular Fibrosis Measured by T1Mapping on Cardiac MRI Predicts Success of Catheter Ablation for Atrial Fibrillation

Author

McLellan, Alex J.A., Ling, Liang-han, Azzopardi, Sonia, Ellims, Andris H., Iles, Leah M., Sellenger, Michael A., Morton, Joseph B., Kalman, Jonathan M., Taylor, Andrew J., and Kistler, Peter M.

Abstract

There is a complex interplay between the atria and ventricles in atrial fibrillation (AF). Cardiac magnetic resonance (CMR) imaging provides detailed tissue characterization, identifying focal ventricular fibrosis with late gadolinium enhancement (ventricular late gadolinium enhancement) and diffuse fibrosis with postcontrast-enhanced T1mapping. The aim of the present study was to investigate the relationship between postcontrast ventricular T1relaxation time on CMR and freedom from AF after pulmonary vein isolation.

Published
2014
Full Text
View/download PDF

49. Diffuse Ventricular Fibrosis in Atrial Fibrillation Noninvasive Evaluation and Relationships With Aging and Systolic Dysfunction

Author

Ling, Liang-han, Kistler, Peter M., Ellims, Andris H., Iles, Leah M., Lee, Geraldine, Hughes, Gerard L., Kalman, Jonathan M., Kaye, David M., and Taylor, Andrew J.

Subjects
cardiovascular system, atrial fibrillation, T1 mapping, ventricular fibrosis, cardiac magnetic resonance
Abstract

ObjectivesThe purpose of this study was to evaluate diffuse myocardial fibrosis of the left ventricle (LV) in patients with atrial fibrillation (AF).BackgroundDiffuse myocardial fibrosis is a hallmark of cardiomyopathy. Unlike replacement fibrosis, it is not visualized on delayed-enhancement cardiac magnetic resonance (CMR) imaging, but may be quantified with contrast-enhanced T1 mapping methods. In atrial fibrillation (AF), it may be induced by arrhythmia or reflect pre-existing cardiomyopathy.MethodsNinety subjects underwent CMR using a clinical 1.5-T scanner: 23 controls, 40 paroxysmal AF patients, and 27 persistent AF patients. Cardiac morphology and function was evaluated from CMR cine imaging. A histologically validated T1 mapping sequence was used to calculate post-contrast T1 relaxation time (T1 time) of the LV myocardium as an index of diffuse myocardial fibrosis.ResultsAge was similar across controls, paroxysmal AF patients, and persistent AF patients (54 ± 12 years, 58 ± 9 years, and 56 ± 10 years, p = NS). Persistent AF patients had larger indexed left atrium volume (55 ± 18 ml vs. 41 ± 12 ml and 47 ± 14 ml) and lower ejection fraction (54 ± 10% vs. 65 ± 6% and 61 ± 8%) than controls and paroxysmal AF patients (p < 0.05). Post-contrast ventricular T1 time differed across all groups (controls, 535 ± 86 ms; paroxysmal AF, 427 ± 95 ms; persistent AF, 360 ± 84 ms; p < 0.001). Univariate predictors of post-contrast ventricular T1 time included age, sex, AF category, ejection fraction, LV mass, congestive heart failure, and body mass index. After multivariate analysis, age, AF category, and ejection fraction remained independent predictors.ConclusionsPost-contrast ventricular T1 mapping identifies diffuse LV fibrosis in patients with AF and provides new insights into the association between AF and adverse ventricular remodeling.

Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results