Robin A P Weir

Publications (27)169.63 Total impact

• Article: Galectin-3 and Cardiac Function in Survivors of Acute Myocardial Infarction.

  Robin A P Weir, Colin J Petrie, C Aengus Murphy, Suzanne Clements, Tracey Steedman, Ashley M Miller, Iain B McInnes, Iain B Squire, Leong L Ng, Henry J Dargie, John J V McMurray
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  ABSTRACT: BACKGROUND: -Galectin-3 is a biomarker associated with inflammation and fibrosis which predicts adverse outcome and relates to biomarkers of extracellular matrix (ECM) turnover in patients with heart failure, particularly when left ventricular [LV] systolic function is preserved. Whether galectin-3 is related to LV remodeling after acute myocardial infarction (AMI) is unknown. METHODS AND RESULTS: -Circulating galectin-3 and various ECM biomarkers were measured in 100 patients (age 58.9±12.0 years, 77% male) admitted with AMI and LV dysfunction, at baseline (mean 46h) and at 24 weeks, with cardiac magnetic resonance imaging at each time-point. LV remodeling was defined as change in LV end-systolic volume index. Relationships between galectin-3, biomarkers and LV remodeling were analyzed across the entire cohort, then according median baseline LV ejection fraction (LVEF). Galectin-3 levels were elevated in 22 patients (22%) at baseline and increased significantly over time from 14.7±5.5 to 16.3±6.6ng/mL (p=0.007). Baseline galectin-3 did not correlate with any LV parameter at baseline or change in any parameter over time. Galectin-3 was positively associated with remodeling in patients with supramedian baseline LVEF (ie. >49.2%; r = 0.40, p = 0.01) but not when LVEF was ≤49.2%. Galectin-3 correlated significantly with matrix metalloproteinase-3 and monocyte chemoattractant protein-1 at baseline, biomarkers that have been shown to relate to LV remodeling in this cohort. CONCLUSIONS: -Galectin-3 correlated significantly with certain biomarkers involved in ECM turnover although no definite relationship was identified with LV remodeling. Whether galectin-3 plays a pathological role in remodeling remains unclear but merits further study. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT00132093.
  Circulation Heart Failure 03/2013; · 6.29 Impact Factor
• Article: Demonstration of Blood Pressure-Independent Non Infarct Myocardial Fibrosis in Primary Aldosteronism: A Cardiac MRI Study.

  E Marie Freel, Patrick B Mark, Robin A P Weir, Emily P McQuarrie, Karen Allan, Henry J Dargie, John D McClure, Alan G Jardine, Eleanor Davies, John M C Connell
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  ABSTRACT: BACKGROUND: -Primary Aldosteronism (PA) is common and associates with excess cardiovascular morbidity independent of blood pressure. Exposure to aldosterone and sodium leads to cardiac fibrosis and hypertrophy in humans and animals possibly mediated by inflammation and oxidative stress. We aimed to clarify the effects of aldosterone excess on myocardial structure and composition in human subjects with PA and essential hypertension (EH) using contrast-enhanced cardiac MRI (CMR) as well as explore the mechanistic basis for any observed differences. METHODS AND RESULTS: -Twenty seven subjects with recently diagnosed PA and 54 EH controls were recruited. Subjects underwent gadolinium-enhanced CMR; non-infarct related myocardial fibrosis was identified by a diffuse pattern of late gadolinium enhancement (LGE). Patients also underwent assessment of pulse wave velocity (PWV), measurement of circulating superoxide anion and C-reactive protein as well as blood pressure and biochemical assessment. Subjects were well matched with no difference in severity nor duration of hypertension. There was a significant increase in the frequency of non-infarct LGE in PA (70%) when compared to EH subjects (13%; p<0.0001) with no difference in LV mass. PWV, superoxide and CRP were significantly higher in PA subjects. CONCLUSIONS: -These data illustrate that PA patients exhibit more frequent myocardial fibrosis as demonstrated by LGE using CMR imaging; this finding is independent of blood pressure. This may be mediated partly through inflammation and oxidative stress. This study highlights the importance of specific targeting of aldosterone excess as well as blood pressure reduction to minimise cardiac morbidity in Primary Aldosteronism.
  Circulation Cardiovascular Imaging 09/2012; · 5.94 Impact Factor
• Article: Interleukin-21--a biomarker of importance in predicting myocardial function following acute infarction?

  Robin A P Weir, Ashley M Miller, Colin J Petrie, Suzanne Clements, Tracey Steedman, Henry J Dargie, Iain B Squire, Leong L Ng, Iain B McInnes, John J V McMurray
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  ABSTRACT: Following acute myocardial infarction (AMI), the acute inflammatory response contributes to wound healing but also to progressive myocardial injury. Interleukin-21 (IL-21) plays a key role in immunoregulation; whether IL-21 is associated with left ventricular (LV) remodelling after AMI is unknown. Plasma IL-21 concentrations were measured in 100 patients (age 58.9 ± 12.0 years, 77% male) admitted with AMI and LV dysfunction, at baseline (mean 46 h) and again at 24 weeks; cardiac magnetic resonance and measurement of B-type natriuretic peptide, monocyte chemoattractant protein-1, matrix metalloproteinase (MMP)-2, -3, -9, and tissue inhibitor of metalloproteinase (TIMP)-1, -2, -4 occurred at both time-points. Remodelling was defined as change in LV end-systolic volume index (ΔLVESVI). Plasma IL-21 concentration was unchanged over time (48.1 [SD 35.4]pg/mL at baseline vs. 48.8 [61.3]pg/mL at 24 weeks, p=0.92). Baseline IL-21 correlated significantly with ΔLVESVI (r=0.30, p=0.005) and change in LV end-diastolic volume index (r=0.33, p=0.003). On multivariate analysis, plasma IL-21 was an independent predictor of remodelling. IL-21 was also significantly associated with higher TIMP-4 concentrations and lower MMP-9 concentrations at baseline. IL-21 predicts adverse remodelling following AMI in patients with LV dysfunction. Whether it plays a direct pathophysiological role in remodelling merits further study.
  Cytokine 06/2012; 60(1):220-5. · 3.02 Impact Factor
• Article: Aldosterone and cortisol predict medium-term left ventricular remodelling following myocardial infarction.

  Robin A P Weir, Ioannis K Tsorlalis, Tracey Steedman, Henry J Dargie, Robert Fraser, John J V McMurray, John M C Connell
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  ABSTRACT: Mineralocorticoid receptor (MR) antagonists improve cardiovascular outcomes in patients with heart failure complicating acute myocardial infarction (AMI) and in chronic heart failure. It is unclear whether these beneficial effects are due solely to aldosterone blockade, as MR has a similar affinity for cortisol. We examined the relationships between plasma and urinary steroid hormones and left ventricular (LV) remodelling in patients with LV dysfunction following AMI. Plasma concentrations of renin, aldosterone, and N-terminal pro-brain natriuretic peptide (NT-proBNP), and 24 h urinary excretion rates of tetrahydroaldosterone (THAldo) and total cortisol metabolites were measured in 93 patients at a mean of 46 h following AMI prior to contrast-enhanced cardiac magnetic resonance (ceCMR). Patients were then randomized to 24 weeks of placebo or eplerenone therapy in addition to standard treatment, after which ceCMR was repeated. In placebo-treated patients, aldosterone, NT-proBNP, and excretion rates of THAldo and total cortisol metabolites were univariate predictors of remodelling (i.e. change in LV end-systolic volume index); aldosterone (P = 0.040) and total cortisol metabolite excretion (P = 0.038) remained independent predictors on multivariate analysis. None of the measured biomarkers predicted remodelling in the presence of eplerenone. Plasma and urinary aldosterone measures, and urinary cortisol metabolites, were not only related to larger infarct volumes and greater infarct remodelling over time, but were also higher in patients with microvascular obstruction on baseline ceCMR. Aldosterone and cortisol are associated with medium-term LV remodelling when measured early after AMI. The beneficial effects of MR antagonism may relate to blockade of both aldosterone- and cortisol-induced MR activation.
  European Journal of Heart Failure 09/2011; 13(12):1305-13. · 4.90 Impact Factor
• Article: Plasma TIMP-4 predicts left ventricular remodeling after acute myocardial infarction.

  Robin A P Weir, Suzanne Clements, Tracey Steedman, Henry J Dargie, John J V McMurray, Iain B Squire, Leong L Ng
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  ABSTRACT: Alterations in the balance between matrix metalloproteinases and their endogenous tissue inhibitors (TIMPs) are associated with left ventricular (LV) remodeling after acute myocardial infarction (AMI). No relationships have been identified between TIMPs and serial postinfarction change in LV function. Plasma concentrations of TIMP-1, -2, -4 were measured at baseline (mean 46 h) and at 24 weeks in 100 patients (age 58.9 ± 12 years, 77% male) admitted with AMI and LV dysfunction, with cardiac magnetic resonance imaging at each time point. TIMP-1 concentration was reduced, whereas TIMP-2 and -4 concentrations were elevated at baseline compared with a reference control population. TIMP-1 decreased and TIMP-2 increased significantly over time; there was an incremental trend in TIMP-4 concentration. Baseline TIMP-4 correlated with change in LV end-systolic volume index (∆LVESVI; r = 0.24; P = .023) and change in LV end-diastolic volume index (∆LVEDVI; r = 0.25; P = .015). ∆TIMP-4 also correlated with ∆LVESVI and with ∆LVEDVI, as did ∆TIMP-2. On multivariable analysis, baseline TIMP-4 concentration was an independent predictor of ∆LVESVI. Plasma TIMP-4 concentration, measured early after AMI, may assist in the prediction of LV remodeling and therefore in the assessment of prognosis. Further study of the role of the TIMPs in the pathophysiology of postinfarction remodeling is warranted.
  Journal of cardiac failure 06/2011; 17(6):465-71. · 3.25 Impact Factor
• Article: Brugada syndrome unmasked by pneumonia.

  Robin A P Weir, Charles A Murphy, Colin J Petrie, Henry J Dargie
  International journal of cardiology 10/2010; 152(1):e16-8. · 7.08 Impact Factor
• Article: Monocyte chemoattractant protein-1: a dichotomous role in cardiac remodeling following acute myocardial infarction in man?

  Robin A P Weir, Charles Aengus Murphy, Colin J Petrie, Thomas N Martin, Suzanne Clements, Tracey Steedman, Galen S Wagner, John J V McMurray, Henry J Dargie
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  ABSTRACT: Monocyte chemoattractant protein-1 (MCP-1) is elevated after acute myocardial infarction (AMI), and potentiates left ventricular (LV) remodeling in murine models of AMI. We examined the relationships between serum MCP-1, change in LV function and biomarkers related to remodeling in a cohort of AMI patients. Serum MCP-1 concentrations were measured in 100 patients (age 58.9+/-12.0 years, 77% male) admitted with AMI and LV dysfunction, at baseline (mean 46 h), 12 and 24 weeks; cardiac magnetic resonance imaging and measurement of matrix metalloproteinase-2 (MMP-2), MMP-3 and MMP-9 occurred at each time-point. MCP-1 increased significantly from 697 [483, 997]pg/mL at baseline to 878 [678, 1130]pg/mL at 24 weeks (p<0.001). MMP-3 concentration increased while MMP-9 decreased significantly over time; MMP-2 concentration did not change significantly. BASELINE MCP-1 correlated with change in (Delta) LV end-systolic volume index (DeltaLVESVI; r= -0.48, p=0.01) and with DeltaLV ejection fraction (DeltaLVEF; r=0.50, p=0.02). However, DeltaMCP-1 correlated positively with DeltaLVESVI (r=0.40, p=0.006) and negatively with DeltaLVEF (r= -0.36, p=0.004). MCP-1 had no relationship with any MMP. MCP-1 may have a dichotomous role following AMI, aiding early infarct healing but potentiating later remodeling, which merits further study before any therapeutic trials of MCP-1 modulation in humans.
  Cytokine 03/2010; 50(2):158-62. · 3.02 Impact Factor
• Article: Drink, drugs, and the QT interval.

  Robin A P Weir, Colin J Petrie, Charles Angus Murphy, Henry J Dargie
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  ABSTRACT: The effects of several prescription and illicitly-used drugs on electrocardiographic repolarization are well documented, most frequently manifested as prolongation of the corrected QT (QTc) interval. The combination of multiple repolarization-modulating drugs taken in high dosage can occasionally lead to extreme abnormalities of the QTc interval and ST-segment on the surface ECG, which can lead to the erroneous diagnosis of underlying myocardial ischemia and inappropriate treatment. We report on one such case in which the acute management of a syncopal patient was detrimentally influenced by misinterpretation of a very unusual ECG.
  Clinical Cardiology 02/2010; 33(2):E50-1. · 2.15 Impact Factor
• Article: Serum soluble ST2: a potential novel mediator in left ventricular and infarct remodeling after acute myocardial infarction.

  Robin A P Weir, Ashley M Miller, Grace E J Murphy, Suzanne Clements, Tracey Steedman, John M C Connell, Iain B McInnes, Henry J Dargie, John J V McMurray
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  ABSTRACT: This study sought to assess, for the first time, the relationship between serum concentrations of the soluble interleukin-1 receptor family member ST2 (sST2) and serial change in left ventricular (LV) function after acute myocardial infarction (AMI). Serum sST2 levels are elevated early after AMI and are associated with lower pre-discharge LV ejection fraction and adverse cardiovascular outcomes. The sST2 levels were measured in 100 patients (mean age 58.9 +/- 12.0 years; 77% male), admitted with AMI with resultant LV systolic dysfunction, at baseline and at 12 and 24 weeks. Patients underwent cardiac magnetic resonance imaging and measurement of N-terminal pro-brain natriuretic peptide, norepinephrine, and aldosterone at each time point. Median sST2 decreased from 263.3 pg/ml at baseline to 140.0 pg/ml at 24 weeks (p < 0.001). Serum sST2 correlated significantly with LV ejection fraction at baseline (r = -0.30, p = 0.002) and 24 weeks (r = -0.23, p = 0.026); change in sST2 correlated with change in LV end-diastolic volume index (r = -0.24, p = 0.023). Level of sST2 was positively associated with infarct volume index at baseline (r = 0.26, p = 0.005) and 24 weeks (r = 0.22, p = 0.037), and with change in infarct volume index (r = -0.28, p = 0.001). Level of sST2 was significantly higher in patients with greater infarct transmurality and endocardial extent, and in the presence of microvascular obstruction. Level of sST2 correlated significantly with norepinephrine and aldosterone, but not with N-terminal pro-brain natriuretic peptide. Measurement of sST2 early after AMI assists in the prediction of medium-term LV functional recovery. Novel relationships were observed between sST2, infarct magnitude/evolution, and aldosterone. Serum sST2 may be of pathophysiological importance in ventricular and infarct remodeling after AMI. (Effects of Eplerenone on Left Ventricular Remodelling Following Heart Attack; NCT00132093).
  Journal of the American College of Cardiology 01/2010; 55(3):243-50. · 14.16 Impact Factor
• Article: Left ventricular remodeling after acute myocardial infarction: does eplerenone have an effect?

  Robin A P Weir, Patrick B Mark, Colin J Petrie, Suzanne Clements, Tracey Steedman, Ian Ford, Leong L Ng, Iain B Squire, Galen S Wagner, John J V McMurray, Henry J Dargie
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  ABSTRACT: Aldosterone antagonism reduces cardiovascular morbidity and mortality in patients with left ventricular (LV) systolic dysfunction and heart failure or diabetes after acute myocardial infarction (AMI). The mechanism of this effect is unclear. We performed a contrast-enhanced cardiac magnetic resonance study to assess the effects of eplerenone on LV remodeling after AMI. One hundred patients (mean age, 58.9 +/- 12 years; 77% male) with LV systolic dysfunction but without heart failure or diabetes were randomized to 24 weeks' double-blind treatment with eplerenone or placebo started 1 to 14 days after AMI. Contrast-enhanced cardiac magnetic resonance was performed, and plasma concentrations of matrix metalloproteinase-2 (MMP-2) and MMP-9 were measured before randomization and at 12 and 24 weeks. Baseline LV ejection fraction was, by chance, significantly higher in eplerenone than in placebo-treated patients. Eplerenone had no effect on the primary end point (change in LV end-systolic volume index); after covariate adjustment, the primary end point fell by 6.1 +/- 2.7 mL/m2 with eplerenone compared to placebo (P = .027), and LV end-diastolic volume index fell by 7.5 +/- 3.4 mL/m2 (P = .031); eplerenone did not significantly influence LV ejection fraction. Eplerenone, after covariate adjustment, significantly decreased MMP-2 and increased MMP-9 over 24 weeks relative to placebo. In a population of patients with AMI with high uptake of contemporary antiremodeling therapy, eplerenone provides modest incremental protection against LV remodeling, only after covariate adjustment.
  American heart journal 07/2009; 157(6):1088-96. · 4.65 Impact Factor
• Article: Plasma apelin concentration is depressed following acute myocardial infarction in man.

  Robin A P Weir, Kwok Shiong Chong, Jonathan R Dalzell, Colin J Petrie, Charles A Murphy, Tracey Steedman, Patrick B Mark, Theresa A McDonagh, Henry J Dargie, John J V McMurray
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  ABSTRACT: Apelin, a novel peptide with a putative role in cardiovascular homeostasis, has gained interest as an endogenous inotrope, but has yet to be described following acute myocardial infarction (AMI) in man. We aimed to characterize plasma apelin concentrations following AMI and to examine its relationship with clinical and prognostic biomarkers. Plasma concentrations of apelin, N-terminal probrain natriuretic peptide (NT-proBNP), norepinephrine, and arginine vasopressin were measured in 100 patients [mean age 58.9 +/- 12 (SD) years, 77% male] admitted with AMI, with echocardiographic left ventricular (LV) ejection fraction <40%, at mean 46 h after admission and at 24 weeks. Cardiac magnetic resonance imaging was performed pre-discharge and at 24 weeks. Thirty-eight subjects with no cardiac history acted as controls. Apelin concentration was reduced early after AMI (0.54 +/- 0.25 vs. 3.22 +/- 3.01 ng/mL, P <0.001) and remained low at 24 weeks, although it did increase significantly from baseline to 0.62 +/- 0.36 ng/mL, P = 0.030. Apelin had no relationship with any parameter of LV function over time. A relationship was found between baseline apelin and norepinephrine (r = 0.26, P = 0.008). Both NT-proBNP and norepinephrine correlated with adverse ventricular function after AMI. Plasma apelin concentration is reduced early after AMI, increases significantly over time, but remains depressed at 24 weeks.
  European Journal of Heart Failure 04/2009; 11(6):551-8. · 4.90 Impact Factor
• Article: Andersen-Tawil syndrome.

  Robin A P Weir, Colin J Petrie, Victoria Murday, Iain N Findlay
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  ABSTRACT: Advances in the understanding of genetic aspects of cardiovascular diseases, together with an increase in the availability of genetic analysis, have resulted in not only increased diagnosis of known inherited conditions, but also the identification of novel syndromes. The combination of potassium-sensitive periodic paralysis, ventricular arrhythmias and dysmorphism, initially described by Andersen and Tawil, represents such a novel condition. We report a case in which genetic analysis led to the diagnosis of Andersen-Tawil syndrome after 15 years of protracted non-invasive and invasive investigations from initial presentation to ultimate diagnosis in a young female. In conclusion, we describe the clinical and genetic features of Andersen-Tawil syndrome and demonstrate the utility of genetic testing in the diagnosis of cardiovascular disease.
  International journal of cardiology 03/2009; 148(1):e13-5. · 7.08 Impact Factor
• Article: Images in cardiovascular medicine. Bursting forth: late-developing acute mediastinal abscess after sternotomy demonstrated by cardiac computed tomography.

  Robin A P Weir, Ross MacDuff, Udim U Nkere, Giles H Roditi
  Circulation 11/2008; 118(17):e673-4. · 14.74 Impact Factor
• Article: Cardiac and extracardiac abnormalities detected by cardiac magnetic resonance in a post-myocardial infarction cohort.

  Robin A P Weir, Thomas N Martin, Colin J Petrie, Aengus Murphy, Suzanne Clements, Tracey Steedman, Galen S Wagner, John J V McMurray, Henry J Dargie
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  ABSTRACT: All patients should undergo formal assessment of ventricular function following acute myocardial infarction (AMI). Cardiac magnetic resonance (CMR) is not widely used as a test before discharge in AMI patients. This study sought to determine the impact of contrast-enhanced CMR (ceCMR) scanning before discharge in addition to standard transthoracic echocardiography (TTE) on patient care following AMI. 100 patients admitted with AMI, all of whom had a left ventricular ejection fraction (LVEF) <40% on TTE, underwent ceCMR imaging before discharge. Abnormalities of clinical relevance detected on ceCMR, which influenced patient management, are reported. Each patient (77% male, mean age 58.9 years, SD 12) underwent TTE and ceCMR at a mean 1.4 (range 0.8-3.2) and 4.2 days (range 2-11), respectively, following admission. ceCMR significantly influenced the management of 24/100 (24%) of the patient cohort, through detection of LV thrombus, right ventricular infarction, intracardiac neoplasia, and a variety of intrathoracic and intra-abdominal pathology. There were no issues regarding safety in this high-risk group of patients. In a cohort of AMI patients with reduced LVEF, ceCMR scanning before discharge improved the management of 24% of the cohort. ceCMR is a useful and safe adjunct to standard care after AMI.
  Cardiology 10/2008; 113(1):1-8. · 1.71 Impact Factor
• Article: Images in clinical medicine. Austin flint murmur.

  Robin A P Weir, Henry J Dargie
  New England Journal of Medicine 10/2008; 359(10):e11. · 53.30 Impact Factor
• Article: Relief of Fontan obstruction demonstrated non-invasively by cardiac magnetic resonance imaging.

  Robin A P Weir, Tracey Steedman, W Stewart Hillis, Lorna Swan
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  ABSTRACT: Greater numbers of children with congenital heart disease are surviving to adulthood. The non-invasive assessment and surveillance of these patients, still based primarily on transthoracic echocardiography, has been significantly enhanced by the advent, and more widespread use of, cardiac magnetic resonance imaging. We report on the influence of cardiac magnetic resonance imaging in the initial evaluation of, and response to treatment in, a patient who had developed an obstruction within her Fontan circuit.
  International journal of cardiology 08/2008; 127(3):e167-9. · 7.08 Impact Factor
• Article: Late-developing massive left ventricular thrombus following myocardial infarction.

  Robin A P Weir, Patrick B Mark, Colin J Petrie, Aengus Murphy, Suzanne Clements, Tracey Steedman, Henry J Dargie
  Clinical Cardiology 06/2008; 31(5):233-4. · 2.15 Impact Factor
• Article: Broken pump or leaky filter? Renal dysfunction in heart failure a contemporary review.

  Colin J Petrie, Partick B Mark, Robin A P Weir
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  ABSTRACT: Renal dysfunction is a frequent and progressive complication of chronic heart failure and is a powerful predictor of cardiovascular mortality. It is intimately associated with cardiovascular disease even in its earliest stages. Although cardiovascular and renal disease share many risk factors, the prognostic implications do not simply reflect widespread atherosclerotic vascular disease as this appears to be as important in those with heart failure secondary to idiopathic dilated cardiomyopathy as it is in those with coronary artery disease. There may be a role in the progression of heart failure, as the deleterious effects of even "mild" renal impairment seem to be borne out in predicting outcome, in a broad range of heart failure patients including those with heart failure and preserved systolic function. Renal dysfunction is both an indication for, as well as frequently limiting intervention with intensive disease modifying therapy. Although renal impairment is common in heart failure and these patients are at higher risk for adverse events including death, they are under represented in clinical trials.
  International journal of cardiology 02/2008; 128(2):154-65. · 7.08 Impact Factor
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  Available from: Patrick B Mark

  Article: Vascular function assessed with cardiovascular magnetic resonance predicts survival in patients with advanced chronic kidney disease.

  Patrick B Mark, Arthur Doyle, Kevin G Blyth, Rajan K Patel, Robin A P Weir, Tracey Steedman, John E Foster, Henry J Dargie, Alan G Jardine
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  ABSTRACT: Increased arterial stiffness is associated with mortality in patients with chronic kidney disease. Cardiovascular magnetic resonance (CMR) permits assessment of the central arteries to measure aortic function. We studied the relationship between central haemodynamics and outcome using CMR in 144 chronic kidney disease patients with estimated glomerular filtration rate <15 ml/min (110 on dialysis). Aortic distensibilty and volumetric arterial strain were calculated from cross sectional aortic volume and pulse pressure measured during the scan. Median follow up after the scan was 24 months. There were no significant differences in aortic distensibilty or aortic volumetric arterial strain between pre-dialysis and dialysis patients. Aortic distensibilty and volumetric arterial strain negatively correlated with age. Aortic distensibilty and volumetric arterial strain were lower in diabetics, patients with ischaemic heart disease and peripheral vascular disease. During follow up there were 20 deaths. Patients who died had lower aortic distensibilty than survivors. In a survival analysis, diabetes, systolic blood pressure and aortic distensibilty were independent predictors of mortality. There were 12 non-fatal cardiovascular events during follow up. Analysing the combined end point of death or a vascular event, diabetes, aortic distensibilty and volumetric arterial strain were predictors of events. Deranged vascular function measured with CMR correlates with cardiovascular risk factors and predicts outcome. CMR measures of vascular function are potential targets for interventions to reduce cardiovascular risk.
  Journal of Cardiovascular Magnetic Resonance 01/2008; 10:39. · 3.72 Impact Factor
• Article: Arrhythmogenic left ventricular false tendon.

  Robin A P Weir, Henry J Dargie, Iain N Findlay
  The Medical journal of Australia 12/2007; 187(10):591. · 2.81 Impact Factor