ORCID Profile
0000-0002-0529-6942
Current Organisation
Charles Darwin University
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Publisher: Elsevier BV
Date: 07-2020
Publisher: Elsevier BV
Date: 05-2014
DOI: 10.1016/J.IJCARD.2014.02.015
Abstract: Inflammation is a key pathogenetic factor in atherogenesis. Periodontitis is a chronic inflammatory source which can have systemic impacts. Indigenous Australians have a higher prevalence of periodontal disease and experience cardiovascular disease earlier than non-Indigenous Australians. The aim was to describe the association between severity of periodontal inflammatory disease and measures of arterial structure and function. Periodontal disease in a convenience s le of Indigenous Australians was assessed clinically for those with periodontal disease, the extent of periodontal pockets ≥ 4 mm was stratified into quartiles. Vascular health was measured non-invasively via carotid-dorsalis pedis pulse-wave velocity (PWV), and via B-mode ultrasound of the common carotid intima-media (IMT). Non-fasting blood s les were collected for lipid and inflammatory marker evaluation. Linear regression models were constructed to determine the associations between extent of periodontal pocketing and vascular health, adjusting for traditional cardiovascular common risk factors. 273 Indigenous Australian adults were recruited and complete data was available for 269 participants (154 males), median age 39 years. Arterial stiffness (PWV) significantly increased with increasing extent of periodontal pocketing (p trend=0.001). By contrast, carotid IMT did not differ across quartiles. Periodontal pocketing was associated with central arterial stiffness, a marker of presymptomatic arterial dysfunction, in Indigenous Australian adults with periodontal disease.
Publisher: Elsevier BV
Date: 12-2013
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 10-2014
DOI: 10.1161/HYPERTENSIONAHA.114.03359
Abstract: Observational studies and nonrandomized trials support an association between periodontal disease and atherosclerotic vascular disease. Both diseases occur frequently in Aboriginal Australians. We hypothesized that nonsurgical periodontal therapy would improve measures of arterial function and structure that are subclinical indicators of atherosclerotic vascular disease. This parallel-group, randomized, open label clinical trial enrolled 273 Aboriginal Australians aged ≥18 years with periodontitis. Intervention participants received full-mouth periodontal scaling during a single visit, whereas controls received no treatment. Prespecified primary end points measured 12-month change in carotid intima-media thickness, an indicator of arterial structure, and 3- and 12-month change in pulse wave velocity, an indicator of arterial function. ANCOVA used complete case data to evaluate treatment group differences. End points could be calculated for 169 participants with follow-up data at 3 months and 168 participants at 12 months. Intima-media thickness decreased significantly after 12 months in the intervention group (mean reduction=−0.023 [95% confidence interval {CI}, −0.038 to −0.008] mm) but not in the control group (mean increase=0.002 [95% CI, −0.017 to 0.022] mm). The difference in intima-media thickness change between treatment groups was statistically significant (−0.026 [95% CI, −0.048 to −0.003] mm P =0.03). In contrast, there were no significant differences between treatment groups in pulse wave velocity at 3 months (mean difference, 0.06 [95% CI, −0.17 to 0.29] m/s P =0.594) or 12 months (mean difference, 0.21 [95% CI, −0.01 to 0.43] m/s P =0.062). Periodontal therapy reduced subclinical arterial thickness but not function in Aboriginal Australians with periodontal disease, suggesting periodontal disease and atherosclerosis are significantly associated.
Publisher: Oxford University Press (OUP)
Date: 11-03-2014
Publisher: Elsevier BV
Date: 02-2009
Publisher: Elsevier BV
Date: 05-2008
Publisher: Wiley
Date: 10-2011
Publisher: Oxford University Press (OUP)
Date: 13-09-2016
Abstract: Pathogenesis of severe Plasmodium vivax malaria is poorly understood. Endothelial dysfunction and reduced nitric oxide (NO) bioavailability characterize severe falciparum malaria, but have not been assessed in severe vivax malaria. In patients with severe vivax malaria (n = 9), patients with nonsevere vivax malaria (n = 58), and healthy controls (n = 79), we measured NO-dependent endothelial function by using reactive hyperemia–peripheral arterial tonometry (RH-PAT) and assessed associations with arginine, asymmetric dimethylarginine (ADMA), and hemolysis. The L-arginine level and the L-arginine to ADMA ratio (a measure of L-arginine bioavailability) were reduced in patients with severe vivax malaria and those with nonsevere vivax malaria, compared with healthy controls (median L-arginine level, 65, 66, and 98 µmol/mL, respectively [P = .0001] median L-arginine to ADMA ratio, 115, 125, and 187, respectively [P = .0001]). Endothelial function was impaired in proportion to disease severity (median RH-PAT index, 1.49, 1.73, and 1.97 in patients with severe vivax malaria, those with nonsevere vivax malaria, and healthy controls, respectively P = .018) and was associated with the L-arginine to ADMA ratio. While the posttreatment fall in hemoglobin level was greater in severe vivax malaria as compared to nonsevere vivax malaria (2.5 vs 1 g/dL P = .0001), markers of intravascular hemolysis were not higher in severe disease. Endothelial function is impaired in nonsevere and severe vivax malaria, is associated with reduced L-arginine bioavailability, and may contribute to microvascular pathogenesis. Severe disease appears to be more associated with extravascular hemolysis than with intravascular hemolysis.
Start Date: 2015
End Date: 2015
Funder: Australian Research Council
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