The Impact of a Health Promotion Educational Program on Cardiovascular Risk Factors for HIV Infected Women on Antiretroviral Therapy

Background: Concerning trends in weight gain from 2000-2009 exist in the Dallas Heart Study (DHS), a probability-based sample of Dallas County residents aged 30-65. However, the impact of significant weight gain (≥ 5% increase in body weight) on cardiovascular risk factors (CVRF) in this contemporary, multi-ethnic population is not known. Methods: We measured weight, LDL-c, blood pressure (SBP and DBP), and fasting glucose (FG) in 2,022 DHS participants (58% female) at study entry in 2000 and in 2009. Using logistic regression stratified by sex and race/ethnicity, we determined the age-adjusted odds of worsening CVRF (any increase in LDL-c, SBP, DBP or FG) for people who gained significant weight compared to those who did not. Results: Among women, 43% (N=500) gained significant weight, compared to 42% of men (N=355). Despite similar average weight gain (9.7±5.8 kg for women vs. 10±5.6 kg for men, p=0.4), women who gained significant weight had almost twice as large an increase in LDL-c (14±34 vs. 8±39 mg/dl, p=0.01) and SBP (12±18 vs. 6±19 mmHg, p<0.001) compared with men who gained significant weight. Increases in DBP (5±10 vs. 4±11 mmHg, p=0.05) and FG (4±29 vs. 2±32 mg/dl, p=0.30) were not significantly different between men and women. Among those with significant weight gain who were not on medications, SBP and LDL-c increases were higher in women compared with men (p<0.05). Differences in the amount of weight gained stratified by race and sex were modest (Table). Black women who gained significant weight were likely to have a worsening of all CVRF, while Hispanic women had the highest likelihood of having an increase in SBP associated with weight gain. In contrast, significant weight gain among men was not associated with worsening CVRF. Conclusions: Significant weight gain was associated with a deleterious impact on CVRF among women but not men. Disparate effects of weight gain between men and women highlight the importance of targeting aggressive weight control interventions toward women to help prevent adverse cardiac outcomes.

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Letter to the Editor in Response to the Article “Effectiveness on major cardiovascular risk factors of an educational program to promote a Mediterranean type of diet among the employees of the company FCA Italia S.p.A”

Diabetes Research and Clinical Practice ◽

10.1016/j.diabres.2021.109072 ◽

2021 ◽

pp. 109072

Author(s):

Shanpin Fanchiang ◽

Matthew F. Bouchonville

Keyword(s):

Risk Factors ◽

Cardiovascular Risk ◽

Cardiovascular Risk Factors ◽

Educational Program ◽

Letter To The Editor

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Abstract 11505: Arterial Inflammation in HIV-Infected Patients Assessed by 18F-Fluorodeoxyglucose Positron Emission Tomography

Circulation ◽

10.1161/circ.130.suppl_2.11505 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Rasmus S Ripa ◽

Andreas Knudsen ◽

Anne Mette F Hag ◽

Annika Loft ◽

Eric von Benzon ◽

...

Keyword(s):

Risk Factors ◽

Cardiovascular Disease ◽

Cardiovascular Risk ◽

Antiretroviral Therapy ◽

Cardiovascular Risk Factors ◽

Abdominal Aorta ◽

Viral Suppression ◽

Intima Media Thickness ◽

Carotid Intima Media Thickness ◽

Arterial Inflammation

Introduction: HIV-infected patients are at increased risk of myocardial infarction and arterial inflammation has been suggested as an explanation. Vascular inflammation can be assessed in vivo by 18F-fluorodeoxyglucose (FDG) PET. Hypothesis: Well-treated HIV-infected patients without known cardiovascular disease will have increased uptake of FDG in different arterial regions as compared to healthy controls. Methods: We prospectively included 26 HIV-infected patients on stable antiretroviral therapy and 25 healthy volunteers. All underwent whole-body PET/CT 3 hours after injection of FDG. FDG uptake was assessed (SUV) in the carotid arteries, the ascending, descending, and abdominal aorta. Carotid intima-media thickness was determined by ultrasound. Soluble biomarkers of endothelial dysfunction and inflammation were measured by ELISA. Known cardiovascular risk factors were recorded for all included. Results: The HIV-infected patients were on stable antiretroviral therapy with full viral suppression. The HIV-infected group was older (50 vs 41 yrs; p = 0.01), had higher blood pressure and total cholesterol, and accordingly a higher Framingham risk score. FDG uptake was similar in the two groups quantified as SUVmax (figure) in the carotid region (1.67 ± 0.04 vs. 1.67 ± 0.04, p = 0.98), the ascending aorta (1.84 ± 0.06 vs. 1.97 ± 0.06, p = 0.15), the descending aorta (1.89 ± 0.08 vs. 1.93 ± 0.08, p = 0.70), and the abdominal aorta (1.70 ± 0.06 vs. 1.65 ± 0.06, p = 0.56) even when adjusting for differences in risk profile. No significant correlations between SUV, carotid intima-media thickness, known cardiovascular risk factors and soluble biomarkers were found. Conclusions: We found no evidence of increased arterial inflammation among HIV-infected patients with full viral suppression compared to controls. This may challenge the idea of chronic inflammation as the cause of cardiovascular disease among optimally treated HIV-infected patients.

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Factor XIII Val34Leu polymorphism and the risk of myocardial infarction under the age of 36 years

Thrombosis and Haemostasis ◽

10.1160/th07-12-0755 ◽

2008 ◽

Vol 99 (06) ◽

pp. 1085-1089 ◽

Cited By ~ 15

Author(s):

Marianna Politou ◽

Christoforos Komporozos ◽

Demosthenes Panagiotakos ◽

Chrisoula Belessi ◽

Anthi Travlou ◽

...

Keyword(s):

Risk Factors ◽

Myocardial Infarction ◽

Cardiovascular Risk ◽

Cardiovascular Risk Factors ◽

Factor Xiii ◽

Control Group ◽

Lower Prevalence ◽

Premature Coronary Heart Disease ◽

Acute Mi ◽

The Impact

SummaryThere are limited and controversial data regarding the impact of factor XIII (FXIII) Val34Leu polymorphism in the pathogenesis of premature myocardial infarction (MI). We examined whether FXIII Val34Leu polymorphism is associated with the development of early MI.We recruited 159 consecutive patients who had survived their first acute MI under the age of 36 years (mean age=32.1 ± 3.6 years, 138 were men). The control group consisted of 121 healthy individuals matched with cases for age and sex, without a family history of premature coronary heart disease (CHD). FXIII Val34Leu polymorphism was tested with polymerase chain reaction and reverse hybridization. There was a lower prevalence of carriers of the Leu34 allele in patients than in controls (30.2 vs. 47.1%, p=0.006). FXIII Val34Leu polymorphism was associated with lower risk for acute MI after adjusting for major cardiovascular risk factors (odds ratio [OR] = 0.51, 95% confidence interval [CI] 0.27–0.95, p=0.03). Subgroup analysis according to angiographic findings (“normal” coronary arteries [n=29] or significant CHD [n=130]) showed that only patients with MI and significant CHD had lower prevalence of carriers of the Leu34 allele compared to controls after adjusting for major cardiovascular risk factors (OR = 0.42, 95% CI 0.22–0.83, p=0.01). Our data indicate that FXIII Val34Leu polymorphism has a protective effect against the development of MI under the age of 36 years, particularly in the setting of significant CHD.

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