The New Zealand Heart Failure Registry: Early observations

The New Zealand Heart Failure Registry: Early observations

Abstracts 54 The New Zealand Heart Failure Registry: Early observations G.P. Devlin ∗ , R. Troughton, M. Lund, R. Doughty, on behalf of the NZHFR Inv...

97KB Sizes 0 Downloads 88 Views


54 The New Zealand Heart Failure Registry: Early observations G.P. Devlin ∗ , R. Troughton, M. Lund, R. Doughty, on behalf of the NZHFR Investigators Department of Cardiology, Waikato Hospital, New Zealand Background: The New Zealand Heart Failure Registry (NZHFR) commenced enrolment mid 2006 with the primary aim to improve the medical care of heart failure patients, through a better understanding of patient demographics, management, and in-hospital and postdischarge outcomes. Methods: The NZHFR is a national prospective observational web –based registry. All hospitals in New Zealand admitting patients with acute heart failure have been invited to participate with a minimum and maximum requirement of 5 and 15 consecutive patients recruited per month respectively. Results: At 14/2/2007 118 patients had been enrolled with 90 day follow up data available in 69% (81/118). The mean patient age was 67 years with 2/3rds male .CXR was performed in all patients. Natriuretic peptides were assayed in less than half (55/118) .Recent echocardiography was available in 83% (98/118).Systolic dysfunction was present in 60% (71/118) .In-hospital death was infrequent (3% (3/118).The mean length of hospital stay was 9 days. Medications on discharge are as shown .At 90 days 17% (14/81) had been readmitted with heart failure and a further 12 % (10/81) had died. Meds on discharge ACE Inhibitors

86/ 118 (73%)


14/118 (12%)


89/ 118 (75%)


34 / 118 (29%)


114/118 (97%)

Conclusion: Early observations from the NZHFR are encouraging with an evidence based approach to care. doi:10.1016/j.hlc.2007.06.059 55 Role of ␤-Adrenergic Stimulated Oxidative Stress and Inflammation in Cardiac Hypertrophy and Failure Q. Xu ∗ , L. Fang, H. Kiriazis, X.M. Gao, R.H. Ritchie, A.M. Dart, X.J. Du Baker Heart Research Institute, Melbourne, Australia Refer to ISHR Section doi:10.1016/j.hlc.2007.06.060


Heart, Lung and Circulation 2007;16:S1–S201

Basic Science – Myocardial 56 Increased Connective Tissue Growth Factor Expression Associated with Functional Impairment and Extracellular Matrix Remodelling in Dystrophin-Deficient Heart C.G. Au 1,2,∗ , T.L. Butler 1,2 , J.R. Egan 1,2 , M.C. Sherwood 1 , K.N. North 1,2 , D.S. Winlaw 1,2 1 Kids Heart Research, Children’s Hospital at Westmead, Australia; 2 University of Sydney, NSW, Australia

Introduction: Cardiomyopathy is a major cause of morbidity and mortality in Duchenne muscular dystrophy (DMD), a progressive X-linked neuromuscular disease caused by dystrophin gene mutations. DMD hearts are characterised by extracellular matrix (ECM) expansion and fibrosis. We examined the role of connective tissue growth factor (CTGF) and transforming growth factor (TGF)-␤ in cardiac fibrosis and dysfunction in the dystrophin-deficient mdx mouse model of DMD. Method: Left ventricles of mdx and wildtype mice at 6 weeks (young), 29 weeks (adult) and 43 weeks (old) were analysed by real-time quantitative RT-PCR, immunoblot, immunohistochemistry and mouse echocardiography. Results: Young mdx hearts were histologically and functionally normal. Adult mdx hearts developed fibrosis and increased CTGF expression compared to age-matched controls, and these changes were more severe in old mdx hearts. Dysregulation of CTGF, TGF-␤, matrix metalloproteinase (MMP)-2 and MMP9 were observed in old mdx mice compared to age-matched controls. Notably, impaired ventricular function (fractional shortening) was only observed in old mdx mice. Conclusion: There is a temporal association between increased CTGF expression and fibrosis in dystrophindeficient hearts. CTGF is increased prior to more conventional regulators of ECM remodelling and before the onset of ventricular dysfunction. CTGF is an attractive target for anti-fibrotic therapy in DMD. doi:10.1016/j.hlc.2007.06.061 57 The Transcription Factor Egr-1 is Upregulated by Myocardial Ischaemia Reperfusion Injury in an In Vivo Rat Model Of Diabetes V.L. Benson 1,∗ , A.C. McMahon 1 , L.M. Khachigian 2 , H.C. Lowe 1,2 1 ANZAC Institute, Concord, NSW, Australia; cular Research, NSW, Australia

2 Centre for Vas-

Background: The transcription factor early growth response factor-1 (Egr-1) plays a key role in the response to myocardial ischaemia reperfusion (IR) injury in nondiabetic animals. Egr-1 mediates the action of insulin in vascular endothelial cells and may also have specific