Biomedical subjects

Nicole L Glazer

Publications and source records attributed to Nicole L Glazer.

4 recordsLinked to original sources

PubMed2006

Risk of new-onset atrial fibrillation in relation to body mass index.

BACKGROUND: Obesity is associated with increased risk of atrial fibrillation (AF), but it is unknown whether the association differs by duration or persistence of AF. It is also unknown to what extent cardiovascular risk factors may mediate this association. METHODS: This population-based case-control study included 425 subjects with new-onset AF and 707 controls. The AF cases were identified through International Classification of Diseases, Ninth Revision codes for inpatient and outpatient visits and verified by medical record review. Medical records provided data on height, weight, and cardiovascular risk factors. RESULTS: On average, AF risk was 3% higher (95% confidence interval [CI], 1%-5%) per unit increment in body mass index (BMI) (calculated as weight in kilograms divided by height in meters squared). For sustained AF (duration > or =6 months), risk was higher by 7% (95% CI, 3%-11%) per unit BMI increment; for intermittent AF (duration > or =8 days or recurrent), 4% (95% CI, 1%-6%); and for transitory AF (duration <8 days), 1% (95% CI, -1% to +4%). Compared with those with normal BMI, the odds ratios for overweight and obese subjects were as follows: overweight, 0.97 (95% CI, 0.68-1.38); obese class 1, 1.18 (95% CI, 0.80-1.73); obese class 2, 1.34 (95% CI, 0.82-2.18); and obese class 3, 2.31 (95% CI, 1.36-3.91) (P = .002 for trend). When diabetes mellitus, a possible mediator, was added to the model, the odds ratio per unit increment of BMI decreased from 1.034 to 1.028. Adjustment for other cardiovascular risk factors including hyperlipidemia and blood pressure did not attenuate the BMI-AF association. CONCLUSIONS: The association with BMI was stronger for sustained AF than for transitory or intermittent AF. The obesity-AF association appears to be partially mediated by diabetes mellitus but minimally through other cardiovascular risk factors.

Adult↗

PubMed2005

Risk of myocardial infarction attributable to elevated levels of total cholesterol among hypertensives.

BACKGROUND: Although cholesterol is an important risk factor for coronary heart disease (CHD) among hypertensives, the burden of CHD among hypertensives that may be due to elevated cholesterol has not been well documented. This study aimed to estimate the proportion of incident myocardial infarction (MI) among hypertensives that may be attributable to elevated total cholesterol, and to investigate how well the National Cholesterol Education Program Adult Treatment Panel III (ATP III) classification method represents risk of MI among hypertensives. METHODS: A population-based, case-control study of patients aged 30 to 79 years enrolled in a health maintenance organization, treated pharmacologically for hypertension, and who were not using lipid-lowering medication. Cases were diagnosed with an incident fatal or nonfatal MI between 1986 and 2000 (n = 1535). Controls were randomly sampled and frequency-matched to cases by sex, 10-year age category, and year of event (n = 3743). Subjects' most recent total cholesterol values were categorized according to ATP III guidelines. RESULTS: Overall, 31% (95% confidence interval: 23-39) of incident MIs among hypertensives could be explained by total cholesterol level above the optimal level of 200 mg/dL. Among participants in the highest ATP III risk stratum, 41% (95% confidence interval: 9-62) of the incident MIs were attributable to total cholesterol levels >160 mg/dL, but total cholesterol >or=200 mg/dL accounted for the majority of these excess events. CONCLUSIONS: The ATP III risk stratification approach improves detection of the CHD burden due to elevated total cholesterol among hypertensives at highest risk. A strategy to improve cholesterol control in hypertensive patients might prevent a substantial part of the burden of morbidity and mortality from MI.

Adult↗

PubMed2004

Weight change and the risk of gestational diabetes in obese women.

BACKGROUND: Obesity is an established risk factor for gestational diabetes. It is not known whether this risk might be reduced through weight loss between pregnancies. We sought to determine whether weight loss between pregnancies reduced the risk of gestational diabetes among obese women. METHODS: We conducted a population-based cohort study of 4102 women with 2 or more singleton live births in Washington State between 1992 and 1998. All subjects were nondiabetic and obese (at least 200 lbs) at their first birth during these years. Weight change was calculated as the difference between prepregnancy weight for the 2 pregnancies. We estimated relative risks of gestational diabetes at the subsequent delivery through stratified analyses and Mantel-Haenszel estimates. RESULTS: Thirty-two percent of women lost weight between pregnancies, with a mean weight loss of 23 lbs. Women who lost at least 10 lbs between pregnancies had a decreased risk of gestational diabetes relative to women whose weight changed by less than 10 lbs (relative risk = 0.63; 95% confidence interval = 0.38-1.02, adjusted for age and weight gain during each pregnancy). Of the 61% of women who gained weight between pregnancies, the mean weight gain was 22 lbs. Women who gained at least 10 lbs had an increased risk of gestational diabetes (1.47; 1.05-2.04). CONCLUSIONS: Even moderate changes in prepregnancy weight can apparently affect the risk of gestational diabetes among obese women. This may offer further motivation for interventions aimed at reducing obesity among women of reproductive age.

Cohort Studies↗

PubMed2004

Microenvironmental VEGF concentration, not total dose, determines a threshold between normal and aberrant angiogenesis.

Use of long-term constitutive expression of VEGF for therapeutic angiogenesis may be limited by the growth of abnormal blood vessels and hemangiomas. We investigated the relationship between VEGF dosage and the morphology and function of newly formed blood vessels by implanting retrovirally transduced myoblasts that constitutively express VEGF164 into muscles of adult mice. Reducing VEGF dosage by decreasing the total number of VEGF myoblasts implanted did not prevent vascular abnormalities. However, when clonal populations of myoblasts homogeneously expressing different levels of VEGF were implanted, a threshold between normal and aberrant angiogenesis was found. Clonal myoblasts that expressed low to medium levels of VEGF induced growth of stable, pericyte-coated capillaries of uniform size that were not leaky and became VEGF independent, as shown by treatment with the potent VEGF blocker VEGF-TrapR1R2. In contrast, clones that expressed high levels of VEGF induced hemangiomas. Remarkably, when different clonal populations were mixed, even a small proportion of cells with high production of VEGF was sufficient to cause hemangioma growth. These results show for the first time to our knowledge that the key determinant of whether VEGF-induced angiogenesis is normal or aberrant is the microenvironmental amount of growth factor secreted, rather than the overall dose. Long-term continuous delivery of VEGF, when maintained below a threshold microenvironmental level, can lead to normal angiogenesis without other exogenous growth factors.

Animals↗