G. Nelson
Royal North Shore Hospital
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Publication
Featured researches published by G. Nelson.
American Journal of Cardiology | 2009
Gopal Sivagangabalan; Andrew T.L. Ong; Arun Narayan; Norman Sadick; P. Hansen; G. Nelson; Michael S. Flynn; David L. Ross; Steven C. Boyages; Pramesh Kovoor
Shorter reperfusion times lead to better outcomes in patients with ST-elevation myocardial infarction (STEMI). We assessed the efficacy of prehospital triage with bypass of community hospitals and early activation of the cardiac catheterization team on revascularization times, left ventricular (LV) ejection fraction, and survival. Patients with STEMI (624) were divided into 3 groups determined by site of triage: ambulance field triage (163), interventional center emergency department (202), and 3 community hospital emergency departments (259). Compared with community hospital and interventional center triages, ambulance field triage resulted in a significant median decrease in door-to-balloon times of 68 and 27 minutes, respectively (p <0.001). LV ejection fraction was highest in the field triage group (52 +/- 13%) compared with the interventional center (49 +/- 12%) and community hospital (48 +/- 12%, p = 0.017) groups. Thirty-day mortality was lowest in the ambulance field group (3%) compared with the interventional facility (11%) and community hospital (4%, p = 0.007) groups. There was a significant difference in long-term survival with up to 30-month follow-up among the 3 triage groups (p = 0.041). With time-dependent Cox regression modeling the difference in survival was significant only during the first week after STEMI (p = 0.020). Every extra minute of symptom onset to reperfusion time was associated with a relative risk of long-term mortality of 1.003 (95% confidence interval 1.000 to 1.006, p = 0.027). In conclusion, field triage of patient with STEMI decreased revascularization times, which preserved LV function, and improved early survival.
Internal Medicine Journal | 2005
L. Lozzi; Steen Carstensen; Helge H. Rasmussen; G. Nelson
Abstract
European Heart Journal | 2010
Daniel Robaei; Stuart M. Grieve; G. Nelson; Ravinay Bhindi; Gemma A. Figtree
Cocaine causes myocardial injury through multiple mechanisms including vasoconstriction, adrenergic hyper-stimulation, and de novo thrombus formation. This report presents two cases of cocaine-induced coronary artery thrombosis with no underlying stenosis, resulting in substantial myocardial injury.nnA previously well 32-year-old man presented with chest pain which commenced 24 h after intranasal cocaine use. He denied use …
Heart Lung and Circulation | 2013
U. Allahwala; Jawad Mazhar; S. Conte; G. Nelson; Ravinay Bhindi
no disease. Future studies will investigate the underlying mechanisms of cytokines in CAD. http://dx.doi.org/10.1016/j.hlc.2013.05.102
Heart Lung and Circulation | 2009
R. McMahon; C. Yu; H. Nojoumian; S. Hoo; P. Hansen; Helge H. Rasmussen; Michael R. Ward; G. Nelson; Ravinay Bhindi
Background: “Ischaemic Preconditioning” is a well-documented mechanism, which protects viable myocardium that is repeatedly exposed to ischaemic episodes. Patients with multi-vessel disease (MVD) should have been exposed to a higher level of ischaemic burden than similar patients with single vessel disease (SVD). If these patients subsequently present with acute myocardial infarction (AMI), our hypothesis suggests that there should be a reduction in their amount of myocardial injury compared to patients with SVD. Methods: We examined all patients who presented to our institutionwith suspectedAMI to identify (a) presence of MVD or SVD (b) myocardial injury (CK). Results: Between May 2005 and February 2009, 1297 patients underwent coronary angiography for suspected AMI. Complete data was missing in 108 patients. 264 Patients were found to have normal or minor disease in their coronary arteries andwere excluded from this study. Of the remaining925patients, PrimaryPCIwasperformed <6h from symptom onset in 564 patients, 283(SVD) and 281(MVD). The mean CK values for each group were 2020U/L (SVD) and 1915U/L (MVD). Conclusions: Myocardial injury following primary PCI for AMI is similar in patients irrespective of number of concomitant vessels diseased. Based on this result, there is no evidence to support our hypothesis, however a larger study may be needed to fully address this question.
European Heart Journal | 2007
Steen Carstensen; G. Nelson; P. Hansen; Lewis Macken; Stephen Irons; Michael S. Flynn; Pramesh Kovoor; S. Hoo; Michael R. Ward; Helge H. Rasmussen
International Journal of Cardiology | 2012
Rebecca Kozor; G. Nelson; Gemma A. Figtree
Heart Lung and Circulation | 2018
D. Nour; U. Allahwala; Michael R. Ward; P. Hansen; Gemma A. Figtree; Helge H. Rasmussen; G. Nelson; Ravinay Bhindi
Heart Lung and Circulation | 2018
J. Ravindran; U. Allahwalla; P. Hansen; H. Rassmussen; G. Nelson; S. Hoo; Gemma A. Figtree; Ravinay Bhindi; Michael R. Ward
Heart Lung and Circulation | 2017
B. Nkoane-Kelaeng; R. Lembo; Gemma A. Figtree; G. Nelson; Rebecca Kozor