The New Zealand Heart Failure Registry: Two Years On

The New Zealand Heart Failure Registry: Two Years On

Abstracts 431 THE NEW ZEALAND HEART FAILURE REGISTRY: TWO YEARS ON G.P. Devlin 1,∗ , R. Troughton 2 , M. Lund 3 , R. Doughty 4 1 Waikato Hospital, H...

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431 THE NEW ZEALAND HEART FAILURE REGISTRY: TWO YEARS ON G.P. Devlin 1,∗ , R. Troughton 2 , M. Lund 3 , R. Doughty 4 1 Waikato

Hospital, Hamilton, New Zealand 2 Christchurch Hospital, Christchurch, , New Zealand 3 Middlemore Hospital, Auckland, New Zealand 4 Auckland City Hospital, Auckland, New Zealand On behalf of the NZHFR Investigators. 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. Eleven hospitals are currently active. Results: At 12/3/2009 741 patients had been enrolled with 90 day follow up data available in 84% (625/741). The mean patient age was 70 years with 2/3rds male. CXR was performed in 98% of patients. Natriuretic peptides were assayed in 50% (369/741). Recent echocardiography was available in 80% (592/741). Systolic dysfunction was present in 41% (301/741). In-hospital death was infrequent (3% (19/741). The median length of hospital stay was 7 days. Medications on discharge are as shown. Device therapy was low (1% 5/741). At 90 days 89% (555/625) were alive and 14% (88/625) readmitted with heart failure. Compliance was reported in 86% (535/625). Meds on discharge ACE inhibitors ARBs B-blockers Aldosterone antagonist Diuretic

549/741 (74%) 74/741 (10%) 543/741 (73%) 241/741 (33%) 709/741 (96%)

Conclusion: Early observations from the NZHFR are encouraging with an evidence based approach to care and low readmission rates. doi:10.1016/j.hlc.2009.05.433




Willoughby 1 , Adhiraj

Shirazi 2 ,

Mitra Amy Penhall 3 , Rebecca 2 Glenn D. Young , Matthew I. Worthley 1,2 , Joseph B. Selvanayagam 3 , Prashanthan Sanders 1,2 Perry 3 ,

1 University

of Adelaide, Adelaide, Australia Adelaide Hospital, Adelaide, Australia 3 Flinders Medical Centre, Adelaide, Australia 2 Royal

Purpose: Myocardial fibrosis is common in dilated cardiomyopathy and is associated with poor prognosis. Endothelial dysfunction is highly prevalent in heart failure but its causal role remains uncertain. We hypothesise that endothelial dysfunction plays a pathogenic role by promotion of myocardial fibrosis through small vessel ischaemia. Our aim was to examine the relationship between serum markers of myocardial fibrosis and endothelial dysfunction. Methods: Thirty-one subjects with severe chronic heart failure (left ventricular ejection fraction, LVEF ≤35%) were studied. After stabilisation of heart failure, blood samples were obtained and centrifuged for 10 min at 3000 rpm. Serum was aliquoted and frozen at −70 ◦ C. Serum matrix metalloproteinase-9 (MMP-9), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), and von Villebrand factor (vWF) concentrations were measured by enzyme-linked immunosorbent assay. Results: Subjects’ mean age was 67 ± 11 years and 24 (77%) were male. Mean LVEF was 25 ± 8%. Cardiomyopathy was ischaemic in 17 (55%) cases. Mean serum MMP-9, TIMP-1, and vWF concentrations were 1.57 ± 1.8 ng/mL, 1016.7 ± 281.4 ng/mL, and 658.7 ± 263 U/dL, respectively. There was a strong positive linear relationship between MMP-9 and vWF concentrations (r = 0.77, p < 0.001) that was consistent in both ischaemic and non-ischaemic cases. There was no significant association between any serum biomarker and left ventricular volumes or ejection fraction. Conclusions: There is a close linear association between serum markers of myocardial fibrosis and endothelial dysfunction, although not between LV functional indices and serum markers of fibrosis. We raise the hypothesis that myocardial fibrosis is promoted by endothelial dysfunction. Further research is necessary to determine the nature of this relationship. doi:10.1016/j.hlc.2009.05.434


Heart, Lung and Circulation 2009;18S:S1–S286