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1.  Cardiovascular disease risk score prediction models for women and its applicability to Asians 
Purpose
Although elevated cardiovascular disease (CVD) risk factors are associated with a higher risk of developing heart conditions across all ethnic groups, variations exist between groups in the distribution and association of risk factors, and also risk levels. This study assessed the 10-year predicted risk in a multiethnic cohort of women and compared the differences in risk between Asian and Caucasian women.
Methods
Information on demographics, medical conditions and treatment, smoking behavior, dietary behavior, and exercise patterns were collected. Physical measurements were also taken. The 10-year risk was calculated using the Framingham model, SCORE (Systematic COronary Risk Evaluation) risk chart for low risk and high risk regions, the general CVD, and simplified general CVD risk score models in 4,354 females aged 20–69 years with no heart disease, diabetes, or stroke at baseline from the third Australian Risk Factor Prevalence Study. Country of birth was used as a surrogate for ethnicity. Nonparametric statistics were used to compare risk levels between ethnic groups.
Results
Asian women generally had lower risk of CVD when compared to Caucasian women. The 10-year predicted risk was, however, similar between Asian and Australian women, for some models. These findings were consistent with Australian CVD prevalence.
Conclusion
In summary, ethnicity needs to be incorporated into CVD risk assessment. Australian standards used to quantify risk and treat women could be applied to Asians in the interim. The SCORE risk chart for low-risk regions and Framingham risk score model for incidence are recommended. The inclusion of other relevant risk variables such as obesity, poor diet/nutrition, and low levels of physical activity may improve risk estimation.
doi:10.2147/IJWH.S55225
PMCID: PMC3956733  PMID: 24648770
cardiovascular disease prevention; risk assessment; epidemiology; Asia; female
2.  Cross vascular risk for first and recurrent hospitalised atherothrombosis determined retrospectively from linked data 
BMJ Open  2013;3(11):e003813.
Objectives
To determine the sex-specific and age-specific risk ratios for the first-ever and recurrent hospitalisation for cerebrovascular, coronary and peripheral arterial disease in persons with other vascular history versus without other vascular history in Western Australia from 2005to 2007.
Design
Cross-sectional linkage study.
Setting
Hospitalised population in a representative Australian State.
Participants
All persons aged 34–85 years between 1 January 2005 and 31 December 2007 were hospitalised with a principal diagnosis of atherothrombosis.
Data sources
Person-linked file of statutory-collected administrative morbidity and mortality records.
Main outcome measures
Sex-specific and age-specific risk ratios for the first-ever and recurrent hospitalisations for symptomatic atherothrombosis of the brain, coronary and periphery using a 15-year look-back period lead to the determining of prior events.
Results
Over 3 years, 40 877 (66% men; 55% first-ever) were hospitalised for atherothrombosis. For each arterial territory, age-specific recurrent rates were higher than the corresponding first-ever rates, with the biggest difference seen in the youngest age groups. For all types of first-ever atherothrombosis, the rates were higher in those with other vascular history and the risk ratios declined with an advancing age (trend: all p<0.0001) and remained significantly >1 even for 75–84 years old. However, for recurrent events, the rates were marginally higher in those with other vascular history and no risk ratio age trend was apparent with several not significantly >1 (trend: all p>0.13).
Conclusions
This study of hospitalised atherothrombosis suggests first-events predominate and that the risk of further events in the same or other arterial territory is very high for all ages and both sexes, accentuating the necessity for an early and sustained active prevention.
doi:10.1136/bmjopen-2013-003813
PMCID: PMC3840350  PMID: 24259391
VASCULAR MEDICINE; PREVENTIVE MEDICINE
3.  Sex in the CCU: women with non‐ST‐segment elevation acute coronary syndrome may do no worse despite less intervention 
Heart  2007;93(11):1327-1328.
See articles on pages 1357 and 1369
doi:10.1136/hrt.2006.106047
PMCID: PMC2016916  PMID: 17933985
4.  Estimated glomerular filtration rate as an independent predictor of atherosclerotic vascular disease in older women 
BMC Nephrology  2012;13:58.
Background
Estimated glomerular filtration rate (eGFR) levels have been shown to predict atherosclerotic vascular disease hospitalization and mortality. We sought to investigate the role of renal function in the prediction of 10-year atherosclerotic vascular hospitalization and deaths in an unselected population of elderly women in and compared these predictions to Framingham equations.
Methods
Complete 10-year verified mortality and hospitalization discharge records for atherosclerotic vascular disease was collected for a prospective study of 1,239 unselected female subject’s ≥ 70 from the Calcium Intake Fracture Outcome Study (CAIFOS) with 10 years of follow-up. eGFR was compared to the current Framingham risk scores.
Results
The eGFR at baseline using the Modification of Diet in Renal Disease Study (MDRD) equation was 65.2 ± 14.5 mL/min/1.73 m2 and 66.3 ± 13.5 mL/min/1.73 m2 using the Chronic Kidney Disease EPIdemiology (CKD-EPI) equation. Over 10 years 30% of participants sustained an ASVD hospitalization or death. For every standard deviation (SD) reduction in eGFR using MDRD the odds ratio (OR) for ASVD hospitalization and deaths increased by 1.34 (1.18-1.53), P < 0.001and 1.31 (1.14-1.50), P < 0.001 in a model adjusted for Framingham 10-year general cardiovascular risk. Addition of eGFR by the MDRD equation to Framingham risk factors improved the net reclassification index by 5.9%, P = 0.018 and the integrated discrimination improvement by 0.010 ± 0.003, P < 0.001 Similar results were seen using the CKD-EPI equation.
Conclusion
Estimated glomerular filtration rate predicts ASVD outcomes independently of Framingham risk score predictions in elderly women and improves clinical prediction particularly of early ASVD.
doi:10.1186/1471-2369-13-58
PMCID: PMC3411430  PMID: 22799523
5.  Hemodynamic Effects of Fenofibrate and Coenzyme Q10 in Type 2 Diabetic Subjects With Left Ventricular Diastolic Dysfunction  
Diabetes Care  2008;31(8):1502-1509.
OBJECTIVE—To investigate the effects of fenofibrate and coenzyme Q10 (CoQ) on diastolic function, ambulatory blood pressure (ABP), and heart rate (HR) in type 2 diabetic subjects with left ventricular diastolic dysfunction (LVDD).
RESEARCH DESIGN AND METHODS—We randomized, double-blind, 74 subjects to fenofibrate 160 mg daily, CoQ 200 mg daily, fenofibrate 160 mg plus CoQ 200 mg daily, or matching placebo for 6 months. Echocardiography (including tissue Doppler imaging) and 24-h ABP and HR monitoring were performed pre- and postintervention.
RESULTS—Neither fenofibrate nor CoQ, alone or in combination, altered early diastolic mitral annular myocardial relaxation velocity (E′), early-to-late mitral inflow velocity ratio (E/A), deceleration time, isovolumic relaxation time, or the ratio of early mitral flow velocity to early diastolic mitral annular myocardial relaxation velocity (E/E′) compared with placebo (P > 0.05). Fenofibrate and CoQ interactively (P = 0.001) lowered 24-h systolic blood pressure (−3.4 ± 0.09 mmHg, P = 0.010), with a prominent nocturnal effect (−5.7 ± 1.5 mmHg, P = 0.006). Fenofibrate (−1.3 ± 0.5 mmHg, P = 0.013) and CoQ (−2.2 ± 0.5 mmHg, P < 0.001) independently lowered 24-h diastolic blood pressure. Fenofibrate reduced 24-h HR (−3.3 ± 0.5 beats/min, P < 0.001), but CoQ had no effect on HR.
CONCLUSIONS—In type 2 diabetic subjects with LVDD, neither fenofibrate nor CoQ, alone or in combination, improved diastolic function significantly. However, fenofibrate and CoQ independently and interactively lowered 24-h blood pressure, and fenofibrate alone reduced 24-h HR.
doi:10.2337/dc08-0118
PMCID: PMC2494652  PMID: 18487480
6.  Fibrosing alveolitis and polymyositis 
Thorax  1970;25(4):504-507.
A case of fibrosing alveolitis and polymyositis is described. We think that this, in association with previously published reports, favours a real and not fortuitous association. The basis for the association may be an abnormality of immunity, but this could not be established in the present case nor from those previously published.
Images
PMCID: PMC472182  PMID: 5485012
7.  A comprehensive investigation of variants in genes encoding adiponectin (ADIPOQ) and its receptors (ADIPOR1/R2), and their association with serum adiponectin, type 2 diabetes, insulin resistance and the metabolic syndrome 
BMC Medical Genetics  2013;14:15.
Background
Low levels of serum adiponectin have been linked to central obesity, insulin resistance, metabolic syndrome, and type 2 diabetes. Variants in ADIPOQ, the gene encoding adiponectin, have been shown to influence serum adiponectin concentration, and along with variants in the adiponectin receptors (ADIPOR1 and ADIPOR2) have been implicated in metabolic syndrome and type 2 diabetes. This study aimed to comprehensively investigate the association of common variants in ADIPOQ, ADIPOR1 and ADIPOR2 with serum adiponectin and insulin resistance syndromes in a large cohort of European-Australian individuals.
Methods
Sixty-four tagging single nucleotide polymorphisms in ADIPOQ, ADIPOR1 and ADIPOR2 were genotyped in two general population cohorts consisting of 2,355 subjects, and one cohort of 967 subjects with type 2 diabetes. The association of tagSNPs with outcomes were evaluated using linear or logistic modelling. Meta-analysis of the three cohorts was performed by random-effects modelling.
Results
Meta-analysis revealed nine genotyped tagSNPs in ADIPOQ significantly associated with serum adiponectin across all cohorts after adjustment for age, gender and BMI, including rs10937273, rs12637534, rs1648707, rs16861209, rs822395, rs17366568, rs3774261, rs6444175 and rs17373414. The results of haplotype-based analyses were also consistent. Overall, the variants in the ADIPOQ gene explained <5% of the variance in serum adiponectin concentration. None of the ADIPOR1/R2 tagSNPs were associated with serum adiponectin. There was no association between any of the genetic variants and insulin resistance or metabolic syndrome. A multi-SNP genotypic risk score for ADIPOQ alleles revealed an association with 3 independent SNPs, rs12637534, rs16861209, rs17366568 and type 2 diabetes after adjusting for adiponectin levels (OR=0.86, 95% CI=(0.75, 0.99), P=0.0134).
Conclusions
Genetic variation in ADIPOQ, but not its receptors, was associated with altered serum adiponectin. However, genetic variation in ADIPOQ and its receptors does not appear to contribute to the risk of insulin resistance or metabolic syndrome but did for type 2 diabetes in a European-Australian population.
doi:10.1186/1471-2350-14-15
PMCID: PMC3598639  PMID: 23351195
Adiponectin; ADIPOQ; ADIPOR; Type 2 diabetes; Insulin resistance and Metabolic syndrome
8.  Under-ascertainment of Aboriginality in records of cardiovascular disease in hospital morbidity and mortality data in Western Australia: a record linkage study 
Background
Measuring the real burden of cardiovascular disease in Australian Aboriginals is complicated by under-identification of Aboriginality in administrative health data collections. Accurate data is essential to measure Australia's progress in its efforts to intervene to improve health outcomes of Australian Aboriginals. We estimated the under-ascertainment of Aboriginal status in linked morbidity and mortality databases in patients hospitalised with cardiovascular disease.
Methods
Persons with public hospital admissions for cardiovascular disease in Western Australia during 2000-2005 (and their 20-year admission history) or who subsequently died were identified from linkage data. The Aboriginal status flag in all records for a given individual was variously used to determine their ethnicity (index positive, and in all records both majority positive or ever positive) and stratified by region, age and gender. The index admission was the baseline comparator.
Results
Index cases comprised 62,692 individuals who shared a total of 778,714 hospital admissions over 20 years, of which 19,809 subsequently died. There were 3,060 (4.9%) persons identified as Aboriginal on index admission. An additional 83 (2.7%) Aboriginal cases were identified through death records, increasing to 3.7% when cases with a positive Aboriginal identifier in the majority (≥50%) of previous hospital admissions over twenty years were added and by 20.8% when those with a positive flag in any record over 20 years were incorporated. These results equated to underestimating Aboriginal status in unlinked index admission by 2.6%, 3.5% and 17.2%, respectively. Deaths classified as Aboriginal in official records would underestimate total Aboriginal deaths by 26.8% (95% Confidence Interval 24.1 to 29.6%).
Conclusions
Combining Aboriginal determinations in morbidity and official death records increases ascertainment of unlinked cardiovascular morbidity in Western Australian Aboriginals. Under-identification of Aboriginal status is high in death records.
doi:10.1186/1471-2288-10-111
PMCID: PMC3024993  PMID: 21192809

Results 1-8 (8)