Publications by authors named "Barry E Hurwitz"

34 Publications

Predicting cardiovascular risk using a novel risk score in young and middle-age adults with HIV: associations with biomarkers and carotid atherosclerotic plaque.

Int J STD AIDS 2021 Nov 2:9564624211050335. Epub 2021 Nov 2.

Department of Psychiatry and Behavioral Sciences, 12235University of Miami Miller School of Medicine, Miami, FL, USA.

Background: Traditional risk factors associated with cardiovascular disease (CVD) include older age, smoking, poor diet, lack of exercise, obesity, high blood pressure, high cholesterol, and family history. Young-to-middle age adults (YMAA) are less often identified as being at risk of CVD, but traditional risk scores primarily target older adults and do not accurately estimate risk among YMAA.

Methods: This study examined biomarkers associated with CVD risk in YMAA in the context of HIV and cocaine use; risk was assessed by two methods: (1) a relative cardiovascular (CV) risk score that includes several factors and (2) carotid atherosclerotic plaque. Associations between CVD risk (CV risk score and carotid atherosclerotic plaque) and proinflammatory cytokines, markers of immune activation, HIV status, and cocaine use were examined. Participants ( = 506) included people with and without HIV and people who use or do not use cocaine.

Results: Participants' mean age was 36 (SD = 9.53); half (51%) were men. Cocaine use and C-reactive protein were associated with greater relative CV risk scores, but no associations between biomarkers and CV risk emerged. Age and CV risk scores were associated with carotid atherosclerotic plaque, but biomarkers were not. HIV was not associated with CV risk scores or carotid atherosclerotic plaque.

Conclusions: Among YMAA, CV risk scores may help providers identify lifestyle changes needed among those at risk for CVD before more advanced risk (e.g., atherosclerotic plaque) is identified. Implications are discussed.
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http://dx.doi.org/10.1177/09564624211050335DOI Listing
November 2021

Systemic Inflammation and Cognitive Decrements in Patients with Stage B Heart Failure.

Psychosom Med 2021 Oct 12. Epub 2021 Oct 12.

College of Behavioral and Community Sciences, University of South Florida, Tampa, FL, USA Department of Psychiatry, University of California School of Medicine, San Diego, CA, USA Department of Family Medicine and Public Health, University of California School of Medicine, San Diego, CA, USA Division of Cardiology, University of Miami Miller School of Medicine, Miami, FL, USA Behavioral Medicine Research Center, University of Miami, Miami, Florida, USA; Department of Psychology, University of Miami, Coral Gables, Florida, USA; Division of Endocrinology, Diabetes and Metabolism, Miller School of Medicine, University of Miami, Miami, Florida, USA Department of Medicine, University of California School of Medicine, San Diego, CA, USA Department of Public Health Sciences, University of Miami Miller School of Medicine, Miami, FL, USA.

Objective: To investigate the role of systemic inflammation in reduced cognitive functioning in patients with early-stage heart failure (HF), while taking associations with other cardiovascular risk factors into account.

Methods: Patients with stage B HF (n = 270; mean age 66.1 ± 10.1) were examined cross-sectionally for relationships among cardiovascular disease (CVD) and psychological risk factors, c-reactive protein (CRP) and Montreal Cognitive Assessment (MoCA) scores. A subsample (n = 83), at high-risk for stage C HF (B-type natriuretic peptide (BNP) levels >65 pg/mL) were followed for 12-months for relationships between CRP levels and cognitive function.

Results: Baseline smoking (c2 = 6.33), unmarried (c2 = 12.0), hypertension (c2 = 5.72), greater body mass index (d = .45), and physical fatigue (d = .25) were related to higher CRP levels (p's < .05). Cross-sectionally, CRP levels were negatively related to MoCA scores, beyond CVD (DR2 = .022, b = -.170, p < .010) and psychological risk factors (DR2 = .016, b = .145, p < .027) and related to MCI criteria (odds ratio = 1.35, 95% CI 1.00 - 1.81, p = .046). Across 12-months, BNP high-risk patients with CRP levels ≥3 mg/L had lower MoCA scores (23.6; 95% CI 22.4 - 24.8) than patients with CRP levels <3 mg/L (25.4; 95% CI 24.4 - 26.5) (p = .024).

Conclusion: Patients with stage B HF and heightened CRP levels had greater cognitive impairment at baseline and follow-up, independent of CVD and potentially psychological risk factors. Low-grade systemic inflammation may be one mechanism involved in cognitive dysfunction at early stages of HF.
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http://dx.doi.org/10.1097/PSY.0000000000001033DOI Listing
October 2021

Associations between physical activity, sedentary behaviour and left ventricular structure and function from the Echocardiographic Study of Latinos (ECHO-SOL).

Open Heart 2021 07;8(2)

Department of Medicine, Epidemiology & Population Health, Albert Einstein College of Medicine Department of Neurology, Bronx, New York, USA.

Objective: The cross-sectional association between accelerometer-measured physical activity (PA), sedentary behaviour (SB) and cardiac structure and function is less well described. This study's primary aim was to compare echocardiographic measures of cardiac structure and function with accelerometer measured PA and SB.

Methods: Participants included 1206 self-identified Hispanic/Latino men and women, age 45-74 years, from the Echocardiographic Study of Latinos. Standard echocardiographic measures included M-mode, two-dimensional, spectral, tissue Doppler and myocardial strain. Participants wore an Actical accelerometer at the hip for 1 week.

Results: The mean±SE age for the cohort was 56±0.4 years, 57% were women. Average moderate to vigorous PA (MVPA) was 21±1.1 min/day, light PA was 217±4.2 min/day and SB was 737±8.1 min/day. Both higher levels of light PA and MVPA (min/day) were associated with lower left ventricular (LV) mass index (LVMI)/end-diastolic volume and a lower E/e' ratio. Higher levels of MVPA (min/day) were associated with better right ventricular systolic function. Higher levels of SB were associated with increased LVMI. In a multivariable linear regression model adjusted for demographics and cardiovascular disease modifiable factors, every 10 additional min/day of light PA was associated with a 0.03 mL/m increase in left atrial volume index (LAVI) (p<0.01) and a 0.004 cm increase in tricuspid annular plane systolic excursion (p<0.01); every 10 additional min/day of MVPA was associated with a 0.18 mL/m increase in LAVI (p<0.01) and a 0.24% improvement in global circumferential strain (p<0.01).

Conclusions: Our findings highlight the potential positive association between the MVPA and light PA on cardiac structure and function.
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http://dx.doi.org/10.1136/openhrt-2021-001647DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8311330PMC
July 2021

Occupational Exposures and Cardiac Structure and Function: ECHO-SOL (Echocardiographic Study of Latinos).

J Am Heart Assoc 2020 09 26;9(17):e016122. Epub 2020 Aug 26.

Department of Medicine Albert Einstein College of Medicine Bronx NY.

Background Our objective was to determine associations of occupational exposures with cardiac structure and function in Hispanic/Latino adults. Methods and Results Employed participants were included (n=782; 52% women, mean age 52.9 years). Occupational exposures to burning wood, vehicle exhaust, solvents, pesticides, and metals at the current and longest-held job were assessed by questionnaire. Survey multivariable linear regression analyses were used to model the relationship of each self-reported exposure with echocardiographic measures of cardiac structure and function. Exposure to burning wood at the current job was associated with decreased left ventricular (LV) ejection fraction (-3.1%; standard error [SE], 1.0 [=0.002]). When the analysis was restricted to exposure at the longest-held job, occupational exposure to burning wood was associated with increased LV diastolic volume (6.7 mL; SE, 1.6 [<0.0001]), decreased LV ejection fraction (-2.7%; SE, 0.6 [<0.0001]), worse LV global longitudinal strain (1.0%; SE, 0.3 [=0.0009]), and decreased right ventricular fractional area change (-0.02; SE, 0.004 [<0.001]). Exposure to pesticides was associated with worse average global longitudinal strain (0.8%; SE, 0.2 [<0.0001]). Exposure to metals was associated with worse global longitudinal strain in the 2-chamber view (1.0%; SE, 0.5 [=0.04]), increased stroke volume (3.6 mL; SE, 1.6 [=0.03]), and increased LV mass indexed to BSA (9.2 g/m; SE, 3.8 [=0.01]) or height (4.4 g/m; SE, 1.9 [=0.02]). Conclusions Occupational exposures to burning wood, vehicle exhaust, pesticides, and metals were associated with abnormal parameters of LV and right ventricular systolic function. Reducing exposures to toxic chemicals and particulates in the workplace is a potential opportunity to prevent cardiovascular disease in populations at risk.
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http://dx.doi.org/10.1161/JAHA.120.016122DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7660755PMC
September 2020

Association Between Sleep Disordered Breathing and Left Ventricular Function: A Cross-Sectional Analysis of the ECHO-SOL Ancillary Study.

Circ Cardiovasc Imaging 2020 05 15;13(5):e009074. Epub 2020 May 15.

Departments of Medicine and Epidemiology & Population Health, Albert Einstein College of Medicine (C.J.R.).

Background: Prior studies have found that sleep-disordered breathing (SDB) is common among those with left ventricular (LV) dysfunction and heart failure. Few epidemiological studies have examined this association, especially in US Hispanic/Latinos, who may be at elevated risk of SDB and heart failure.

Methods: We examined associations between SDB and LV diastolic and systolic function using data from 1506 adults aged 18 to 64 years in the Hispanic Community Health Study/Study of Latinos ECHO-SOL Ancillary Study (2011-2014). Home sleep testing was used to measure the apnea-hypopnea index, a measure of SDB severity. Echocardiography was performed a median of 2.1 years later to quantify LV diastolic function, systolic function, and structure. Multivariable linear regression was used to model the association between apnea-hypopnea index and echocardiographic measures while accounting for the complex survey design, demographics, body mass, and time between sleep and echocardiographic measurements.

Results: Each 10-unit increase in apnea-hypopnea index was associated with 0.2 (95% CI, 0.1-0.3) lower E', 0.3 (0.1-0.5) greater E/E' ratio, and 1.07-fold (1.03-1.11) higher prevalence of diastolic dysfunction as well as 1.3 (0.3-2.4) g/m greater LV mass index. These associations persisted after adjustment for hypertension and diabetes mellitus. In contrast, no association was identified between SDB severity and subclinical markers of LV systolic function.

Conclusions: Greater SDB severity was associated with LV hypertrophy and subclinical markers of LV diastolic dysfunction. These findings suggest SDB in Hispanic/Latino men and women may contribute to the burden of heart failure in this population.
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http://dx.doi.org/10.1161/CIRCIMAGING.119.009074DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8117672PMC
May 2020

Early Insights into COVID-19 in Persons Living with HIV and Cardiovascular Manifestations.

J AIDS HIV Treat 2020 ;2(2):68-74

Department of Medicine, Division of Cardiovascular Disease, University of Miami Miller School of Medicine, Miami, Florida, USA.

Persons living with HIV-1 (PLHIV) are at increased risk of cardiovascular complications in part due to the persistent inflammatory state despite viral suppression. SARS-CoV-2, the virus causing COVID-19, was declared a pandemic virus in March 2020, and caused over 30 million cases and 900,000 deaths worldwide to date. Individuals with COVID-19 are manifesting acute cardiovascular complications because of the inflammatory response associated with SARS-CoV-2 infection. It is not yet known whether having COVID-19 in the context of ongoing HIV-1 infection results in worse cardiovascular complications than in PLHIV who have not had COVID-19 infection. In this review, the potential for exacerbated cardiovascular manifestations in persons coinfected with HIV-1 and COVID-19 is considered.
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http://dx.doi.org/10.33696/aids.2.010DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7971556PMC
January 2020

HIV and carotid atherosclerosis: a mediational model.

AIDS Care 2020 07 23;32(7):907-911. Epub 2019 Sep 23.

Department of Psychiatry and Behavioral Sciences, University of Miami Miller School of Medicine, Miami, FL, USA.

Cardiovascular disease (CVD) is the leading cause of death in the US and is a significant contributor to morbidity and mortality for people living with HIV (PLWH). This study examined the association between HIV infection, cocaine usage, and inflammatory markers, and their combined association with carotid atherosclerosis among young and middle-aged adults with HIV. Participants ( = 494) were enrolled based on HIV status and cocaine use. Blood pressure, body mass index (BMI), and cocaine use were assessed. Cytokines and growth factors, IL-1a, IL-6, TNFα and VEGF, and immune activation markers, sCD14 and sCD163 were measured. Participant age was 36.2 years (SD = 9.5); 50% were male, 49% female and 1% transgender; 39% were HIV-positive, 50% were current or past smokers, and 39% endorsed cocaine use. A path analysis showed an indirect effect of HIV serostatus on the presence of carotid atherosclerotic plaques (= 0.048, 0.024, .043), when controlling age, BMI, smoking, and cocaine use. This effect was mediated by inflammatory markers and changes in blood pressure. Findings point to putative underlying mechanisms leading to atherosclerosis among PLWH.
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http://dx.doi.org/10.1080/09540121.2019.1668527DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7085952PMC
July 2020

Gender Identity, Hormone Therapy, and Cardiovascular Disease Risk.

Curr Probl Cardiol 2020 May 20;45(5):100396. Epub 2018 Sep 20.

Transgender individuals represent a medically underserved and under researched population. There is a growing number of studies illustrating the importance of hormone therapy treatments in transgender men and women to assist ameliorating gender dysphoria and promoting well-being. However, the cardiovascular effects of these hormones are controversial. Large longitudinal epidemiological studies of cardiovascular event outcomes in these populations do not exist. In addition, studies of cardiovascular complications of transgender hormone therapy are limited in number and complicated by poor control of medication regimen, presence of gender confirming surgery, use of prescribed medications for prevailing conditions, and alcohol, smoking or illicit substance use, and comorbidities, such as HIV infection. The following provides an overview of current guidelines for hormone therapy regimens used by transgender individuals, as well as what is known about the use of exogenous hormones on the cardiovascular system and cardiovascular disease risk. Several gaps in our understanding of the cardiovascular effects of endogenous and exogenous hormones in treated transgender individuals are identified, which provide direction for future study.
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http://dx.doi.org/10.1016/j.cpcardiol.2018.09.003DOI Listing
May 2020

Cardiac structure and function with and without metabolic syndrome: the Echocardiographic Study of Latinos (Echo-SOL).

BMJ Open Diabetes Res Care 2018 13;6(1):e000484. Epub 2018 Aug 13.

Department of Epidemiology and Prevention, Wake Forest School of Medicine, Winston-Salem, North Carolina, USA.

Objective: We assessed the hypothesis that metabolic syndrome is associated with adverse changes in cardiac structure and function in participants of the Echocardiographic Study of Latinos (Echo-SOL).

Methods: Non-diabetic Echo-SOL participants were included in this cross-sectional analysis. Metabolic syndrome was defined according to the American Heart Association/National Heart, Lung, and Blood Institute 2009 Joint Scientific Statement. Survey multivariable linear regression analyses using sampling weights were used adjusting for multiple potential confounding variables. Additional analysis was stratified according to the presence/absence of obesity (body mass index (BMI) ≥25 kg/m) and the presence/absence of metabolic syndrome.

Results: Within Echo-SOL, 1260 individuals met inclusion criteria (59% female; mean age 55.2 years). Compared with individuals without metabolic syndrome, those with metabolic syndrome had lower medial and lateral E' velocities (-0.4 cm/s, (SE 0.1), p=0.0002; -0.5 cm/s (0.2), p=0.02, respectively), greater E/E' (0.5(0.2), p=0.01) and worse two-chamber left ventricular longitudinal strain (0.9%(0.3), p=0.009), after adjusting for potential confounding variables. Increased left ventricular mass index (9.8 g/m (1.9), p<0.0001 and 7.5 g/m (1.7), p<0.0001), left ventricular end-diastolic volume (11.1 mL (3.0), p=0.0003 and 13.3 mL (2.7), p<0.0001), left ventricular end-systolic volume (5.0 mL (1.4), p=0.0004 and 5.7 mL (1.3) p<0.0001) and left ventricular stroke volume (10.2 mL (1.8), p<0.0001 and 13.0 mL (2.0), p<0.0001) were observed in obese individuals with and without metabolic syndrome compared with individuals with normal weight without metabolic syndrome. In sensitivity analyses, individuals with normal weight (BMI <25 kg/m) and metabolic syndrome had worse left ventricular global longitudinal strain (2.1%(0.7), p=0.002) and reduced left ventricular ejection fraction (-3.5%(1.4), p=0.007) compared with normal-weight individuals without metabolic syndrome.

Conclusions: In a sample of US Hispanics/Latinos metabolic syndrome was associated with worse left ventricular systolic and diastolic function. Adverse changes in left ventricular size and function were observed in obese individuals with and without metabolic syndrome but decreased left ventricular function was also present in normal-weight individuals with metabolic syndrome.
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http://dx.doi.org/10.1136/bmjdrc-2017-000484DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6091897PMC
August 2018

Sleeping oxygen saturation, rapid eye movement sleep, and the adaptation of postprandial metabolic function in insulin sensitive and resistant individuals without diabetes.

Physiol Behav 2018 07 12;191:123-130. Epub 2018 Apr 12.

Behavioral Medicine Research Center, University of Miami, Miami, FL, USA; Department of Psychology, University of Miami, Coral Gables, FL, USA; Division of Endocrinology, Diabetes and Metabolism, Miller School of Medicine, University of Miami, Miami, FL, USA. Electronic address:

Aims: Sleeping oxygen saturation (SaO) and sleep stage duration have been linked with prediabetic alterations but the pathogenic pathways are not well understood. This study of insulin sensitive and resistant adults examined the effect on postprandial metabolic regulation of repeated mixed-meal challenges of different carbohydrate loading. The aim was to examine whether the relationship between lower sleeping oxygen saturation (SaO) and poorer fasting and postprandial metabolic function may be linked with reduced slow wave sleep (SWS) and rapid eye movement (REM) duration, independent of age, sex and total adiposity.

Methods: The 24 men and women, aged 25-54 years, had no diabetes or other diagnosed conditions, were evaluated with polysomnography to derive indices of SaO and sleep architecture. In addition, an OGTT and two 14-h serial mixed-meal tests were administered over 3 successive in-patient days. The carbohydrate content of the mixed-meals was manipulated to compare a standard-load day with a double-load day (300 vs. 600 kcal/meal). Quantitative modeling was applied to derive β-cell glucose sensitivity (β-GS), early insulin secretion rate sensitivity (ESRS), and total postprandial insulinemia (AUC).

Results: Analyses showed that, for the 14-h tests, the SaO relationship with metabolic outcomes was associated significantly with percent time spent in REM but not SWS, independent of age, sex and total adiposity. Specifically, indirect pathways indicated that lower SaO was related to shorter REM duration, and shorter REM was respectively associated with higher β-GS, ESRS, and AUC for the 300- and 600-load days (300 kcal/meal: β = -8.68, p < .03, β = -8.54, p < .002, and β = -10.06, p < .008; 600 kcal/meal: β = -11.45, p < .003, β = -11.44, p < .001, and β = -11.00, p < .03).

Conclusion: Sleeping oxygen desaturation and diminished REM duration are associated with a metabolic pattern that reflects a compensatory adaptation of postprandial insulin metabolism accompanying preclinical diabetic risk.
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http://dx.doi.org/10.1016/j.physbeh.2018.04.009DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5975635PMC
July 2018

GLP-1 response to sequential mixed meals: influence of insulin resistance.

Clin Sci (Lond) 2017 Dec 4;131(24):2901-2910. Epub 2017 Dec 4.

CNR Institute of Clinical Physiology, Pisa, Italy

Previous work has shown that potentiation of insulin release is impaired in non-diabetic insulin resistance; we tested the hypothesis that this defect may be related to altered glucagon-like peptide-1 (GLP-1) release. On consecutive days, 82 non-diabetic individuals, classified as insulin sensitive (IS, =41) or insulin resistant (IR, =41) by the euglycaemic clamp, were given two sequential mixed meals with standard (75 g, LCD) or double (150 g, HCD) carbohydrate content. Plasma glucose, insulin, C-peptide, non-esterified fatty acids (NEFA) and GLP-1 concentrations were measured; β-cell function (glucose sensitivity and potentiation) was resolved by mathematical modelling. Fasting GLP-1 levels were higher in IR than IS (by 15%, =0.006), and reciprocally related to insulin sensitivity after adjustment for sex, age, fat mass, fasting glucose or insulin concentrations. Mean postprandial GLP-1 responses were tightly correlated with fasting GLP-1, were higher for the second than the first meal, and higher in IR than IS subjects but only with LCD. In contrast, incremental GLP-1 responses were higher during (i) the second than the first meal, (ii) on HCD than LCD, and (iii) significantly smaller in IR than IS independently of meal and load. Potentiation of insulin release was markedly reduced in IR vs IS across meal and carbohydrate loading. In the whole dataset, incremental GLP-1 was directly related to potentiation, and both were inversely related to mean NEFA concentrations. We conclude that (a) raised GLP-1 tone may be inherently linked with a reduced GLP-1 response and (b) defective post-meal GLP-1 response may be one mechanism for impaired potentiation of insulin release in insulin resistance.
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http://dx.doi.org/10.1042/CS20171409DOI Listing
December 2017

Current assessment of heart rate variability and QTc interval length in HIV/AIDS.

Curr Opin HIV AIDS 2017 Nov;12(6):528-533

aDepartment of Health Psychology, University of Miami, Coral Gables, Florida bBehavioral Medicine Research Center cDivision of Endocrinology, Diabetes and Metabolism, Miller School of Medicine, University of Miami, Miami, Florida, USA.

Purpose Of Review: The increasing prevalence of cardiovascular disease comorbidity in persons infected with the HIV has become a global concern. The electrocardiogram (ECG) is increasingly being utilized to provide clinically relevant information regarding cardiac arrhythmias and cardio-autonomic dysfunction. The purpose of this review is to summarize the latest research comparing QT and R-to-R interval length as a function of HIV+ status or antiretroviral therapy (ART) regimen.

Recent Findings: Prolongation of the corrected QTc interval may be acquired in HIV+ ART-naive individuals, exacerbated by various classes of ART drugs, and is generally predictive of lethal cardiac arrhythmias, with effects observed from childhood to adulthood. Recent literature also suggests the trend of lower heart rate variability in HIV is indicative of cardiorespiratory and inflammatory-immune dysfunction.

Summary: These emergent studies support the clinical relevance of the ECG across the age and HIV disease spectrum. Furthermore, the reported findings have implications for the management of cardiovascular and chronic inflammatory disease comorbidity in persons living with HIV.
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http://dx.doi.org/10.1097/COH.0000000000000408DOI Listing
November 2017

Higher number of live births is associated with left ventricular diastolic dysfunction and adverse cardiac remodelling among US Hispanic/Latina women: results from the Echocardiographic Study of Latinos.

Open Heart 2017;4(1):e000530. Epub 2017 May 8.

Wake Forest School of Medicine, Winston-Salem, North Carolina, USA.

Introduction: Female sex is a risk factor for heart failure with preserved ejection fraction (HFpEF). Previous literature suggests that some diastolic dysfunction (DD) develops during pregnancy and may persist postdelivery. Our objective was to examine the relationship between parity and cardiac structure and function in a population-based cohort.

Methods: Participants included 1172 Hispanic/Latina women, aged ≥45 years, enrolled in the Echocardiographic Study of Latinos from four US communities (Bronx, Miami, San Diego and Chicago). Standard echocardiographic techniques were used to measure cardiac volumes, left ventricular mass, systolic and diastolic function. Using sampling weights and survey statistics, multivariable linear and logistic regression models were constructed adjusting for age, body mass index, diabetes or prediabetes, systolic blood pressure, use of antihypertensive medications, smoking, total cholesterol and high-density lipoprotein cholesterol.

Results: In the target population, 5.0% were nulliparous (no live births) and 10.5% were grand multiparous (≥5 live births). Among the nulliparous women, 46% had DD as compared with 51%-58% of women with 1-4 live births and 81% of women with ≥5 live births (p<0.01). In full multivariate models, higher parity was significantly associated with greater left ventricular end-systolic volumes, end-diastolic volumes, left atrial volume indices and presence of DD (all p<0.01) but was not associated with ejection fraction. The log odds for having any grade of DD in grand-multiparous women was over three times that seen in nulliparous women (OR=3.4, 95% CI 1.5 to 7.9, p<0.01) in models further adjusted for income and education.

Conclusions: Higher parity is associated with increased cardiac mass, volumes and the presence of DD. Further studies are needed to elucidate this apparent deleterious relation and whether parity can help explain the increased risk of HFpEF in women.
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http://dx.doi.org/10.1136/openhrt-2016-000530DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5471863PMC
May 2017

Association of Albuminuria With Cardiac Dysfunction in US Hispanics/Latinos.

Am J Cardiol 2017 06 29;119(12):2073-2080. Epub 2017 Mar 29.

Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York; Department of Medicine, Albert Einstein College of Medicine, Bronx, New York.

Higher urine albumin-to-creatinine ratio (UACR) has been associated with cardiac dysfunction in the general population. We assessed the association of UACR with cardiac structure and function in the Echocardiographic Study of Latinos (Echo-SOL), an ancillary study of the Hispanic Community Health Study/Study of Latinos across 4 US sites. Echo-SOL participants underwent standard 2-dimensional echocardiography, including speckle-tracking strain analysis. UACR was categorized as normal and high-normal (based on the midpoint of values below microalbuminuria), microalbuminuria (≥17 mg/g for men; ≥25 mg/g for women), and macroalbuminuria (≥250 mg/g; ≥355 mg/g). Simultaneous assessments were made of left ventricular (LV) mass index and hypertrophy and measures of LV systolic and diastolic dysfunction. We assessed the association of UACR with subclinical cardiac measures, adjusting for sociodemographic and cardiometabolic factors. Among 1,815 participants (median age 54, women 65%), 42% had normal UACR, 43% high-normal UACR, 13% microalbuminuria, and 2% macroalbuminuria. Prevalence of LV hypertrophy was 13%, LV systolic dysfunction (ejection fraction <50%) 3%, and diastolic dysfunction 53%. After covariate adjustment, both micro- and macroalbuminuria were significantly associated with a twofold increase in LV hypertrophy. Microalbuminuria but not macroalbuminuria was associated with worse global longitudinal strain. Elevated UACR, even at high-normal levels, was significantly associated with greater diastolic dysfunction. In conclusion, elevated UACR was associated with LV hypertrophy and diastolic dysfunction in the largest known population sample of US Hispanic/Latinos. Screening and detection of even high-normal UACR could be of value to guide cardiovascular disease prevention efforts among Hispanic/Latino Americans.
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http://dx.doi.org/10.1016/j.amjcard.2017.03.039DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5609841PMC
June 2017

Change in urinary cortisol excretion mediates the effect of angry/hostile mood on 9 month diastolic blood pressure in HIV+ adults.

J Behav Med 2017 Aug 2;40(4):620-630. Epub 2017 Feb 2.

Department of Psychology, University of Miami, Coral Gables, FL, USA.

Cardiovascular disease is a growing concern in HIV disease management and nearly 1 out of 3 persons living with the virus is hypertensive. Biobehavioral factors such as anger, hostility, and HPA axis reactivity are emperically linked to blood pressure regulation. Whether HPA axis or mood disturbance increases risk for hypertension remains unclear in HIV disease. The aim of this study was to determine whether 9-month change in angry/hostile mood predicts alterations in systolic (SBP) or diastolic blood pressure (DBP), and whether this change is mediated by 24-h urinary cortisol (CORT) output. Sixty-one HIV positive adults, aged 41.1 ± 8.6 years, assigned to the control condition of a stress management intervention provided blood samples, 24-h urine specimens, blood pressure in-office, and self-reported mood at baseline and a 9-month follow-up. CORT was tested as a mediator in two separate models controlling for baseline BP, CD4 count, HIV-1 viral load, protease inhibitor use, body mass index, smoking status, and family history of cardiometabolic disease. Increase in angry/hostile mood was associated with greater SBP (β = 0.33, CI 0.09, 0.56, p = 0.01) and DBP (β = 0.39, CI 0.16, 0.62, p < 0.001) at follow-up. CORT partially mediated the effect of angry/hostile mood on DBP (β = 0.28, CI 0.03, 0.54, p = 0.03). Change in CORT was not related to SBP (β = 0.12, CI -0.20, 0.44, p = 0.46). The final mediation model accounted for 41.2% of the variance in 9-month DBP. Angry or hostile mood may contribute to increased risk for hypertension in persons treated for HIV via disturbance of the HPA-axis.
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http://dx.doi.org/10.1007/s10865-017-9827-1DOI Listing
August 2017

Airway and Pulmonary β-Adrenergic Vasodilatory Function in Current Smokers and Never Smokers.

Chest 2017 03 21;151(3):650-657. Epub 2016 Dec 21.

Division of Pulmonary, Critical Care, and Sleep Medicine, Miller School of Medicine, University of Miami, Coral Gables, FL.

Background: Cigarette smoking has been associated with diminished vasodilatory function in the airway circulation. It is possible that cigarette smoking similarly affects the pulmonary circulation before resting pulmonary circulatory abnormalities become manifested. The aim of this study was to compare the acute effect of inhaled albuterol on airway and pulmonary hemodynamic function as an index of β-adrenoceptor-mediated vasodilation in smokers and never smokers.

Methods: In 30 adults, airway and pulmonary vascular function was assessed before and 15 min after albuterol inhalation (270 μg). From mean systemic arterial pressure, cardiac output, airway blood flow, and mean pulmonary arterial pressure, airway vascular resistance (AVR) and pulmonary vascular resistance (PVR) were derived.

Results: Albuterol induced a substantial drop in mean (± SE) PVR (-67.2% ± 5%), with no difference between groups. In contrast, the albuterol-induced decrease in AVR was significantly greater in never smokers than in smokers (-28.6% ± 3% vs -3.1% ± 6%; P < .02).

Conclusions: These results are consistent with a dysfunction in a β-adrenergic signaling pathway mediating vasorelaxation in the airway circulation of current smokers. The vasodilatory deficit in the airway circulation but not in the pulmonary circulation could be related to local differences in the impact of cigarette smoke on the vascular endothelium.
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http://dx.doi.org/10.1016/j.chest.2016.12.008DOI Listing
March 2017

Association of Impaired Glucose Regulation and Insulin Resistance With Cardiac Structure and Function: Results From ECHO-SOL (Echocardiographic Study of Latinos).

Circ Cardiovasc Imaging 2016 Oct;9(10)

From the Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY (R.T.D., A.T.); Department of Family Medicine and Public Health (M.A.A.) and Graduate School of Public Health (G.A.T.), University of California, San Diego; Department of Biostatistics, University of North Carolina at Chapel Hill (J.C., M.E.Y.); Department of Epidemiology and Population Health, Albert Einstein College of Medicine, New York, NY (R.C.K.); Department of Medicine, University of Illinois, Champaign (A.A.D.); Department of Psychology, Behavioral Medicine Research Center, University of Miami, Coral Gables, FL (B.E.H.); Wake Forest School of Medicine, Wake Forest University, Winston-Salem, NC (J.C.N., K.S., C.J.R.); and Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL (S.J.S.).

Background: We examined the relationship between glucose homeostasis and comprehensive measures of cardiac structure and function among a representative sample of US Hispanics.

Methods And Results: ECHO-SOL (Echocardiographic Study of Latinos), an echocardiographic ancillary study of the HCHS/SOL (Hispanic Community Health Study/Study of Latinos), enrolled 1818 Hispanic/Latino men (43%) and women (57%) aged ≥45 years (mean=56). Glucose intolerance was defined as follows: (1) prediabetes: hemoglobin (HbA1c) ≥5.7 and <6.5% and (2) diabetes mellitus: fasting plasma glucose ≥126 mg/dL, 2-hour postload glucose ≥200 mg/dL, HbA1c ≥6.5%, or hypoglycemic agent use. Uncontrolled diabetes mellitus was defined as HbA1c ≥7.0%. Insulin resistance was defined using the homeostatic model assessment for insulin resistance. Echocardiography examinations assessed left ventricular structure and systolic/diastolic function. Multivariable linear and logistic regression models were used. Prediabetes prevalence was 42%, and diabetes mellitus prevalence was 28% (47% uncontrolled). Glucose intolerance was associated with increased left ventricular posterior wall and interventricular septal and relative wall thicknesses (all P<0.05), reduced ejection fraction (P<0.01), reduced stroke and end-diastolic volumes (both P<0.001), decreased peak E' velocity (lateral and septal P<0.001), and increased E/E' ratio (lateral and septal P<0.01). The odds ratios (95% confidence intervals) for diastolic dysfunction among individuals with prediabetes and diabetes mellitus (versus diabetes mellitus free) were 1.36 (0.96-1.9) and 1.90 (1.3-2.8), respectively(P=0.006). Results were consistent for uncontrolled diabetes mellitus versus diabetes mellitus. Homeostatic model assessment for insulin resistance was associated with increased E/E' (P<0.001), and greater relative wall thickness and septal thickness (both P<0.05); lower stroke volume (P<0.0001); and lower peak lateral and septal E' velocities (both P<0.01).

Conclusions: Glucose intolerance and insulin resistance are associated with unfavorable cardiac structure and function, particularly worsened measures of diastolic function, even before the development of diabetes mellitus.
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http://dx.doi.org/10.1161/CIRCIMAGING.116.005032DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5111817PMC
October 2016

Comparison of Echocardiographic Measures in a Hispanic/Latino Population With the 2005 and 2015 American Society of Echocardiography Reference Limits (The Echocardiographic Study of Latinos).

Circ Cardiovasc Imaging 2016 Jan;9(1)

From the Departments of Internal Medicine (W.T.Q., J.A.L., A.D., C.J.R.) and Public Health Sciences (K.S., C.J.R.), Wake Forest School of Medicine, Winston-Salem, NC; San Diego School of Medicine, University of California (M.A.A.); Department of Biostatistics, Gillings School of Global Public Health, University of North Carolina, Chapel Hill (J.C., F.G.); Department of Psychology, University of Miami, FL (B.E.H.); Department of Medicine - Cardiology, Feinberg School of Medicine, Northwestern University, Chicago, IL (S.J.S.); Department of Medicine, University of Arizona, Tucson (A.A.D.); and Department of Medicine, Division of Cardiology, Albert Einstein College of Medicine, Bronx, NY (D.M.S.).

Background: Reference limits for echocardiographic quantification of cardiac chambers in Hispanics are not well studied.

Methods And Results: We examined the reference values of left atrium and left ventricle (LV) structure in a large ethnically diverse Hispanic cohort. Two-dimensional transthoracic echocardiography was performed in 1818 participants of the Echocardiographic Study of Latinos (ECHO-SOL). Individuals with body mass index ≥30 kg/m(2), hypertension, diabetes mellitus, coronary artery disease, and atrial fibrillation were excluded leaving 525 participants defined as healthy reference cohort. We estimated 95th weighted percentiles of LV end systolic volume, LV end diastolic volume, relative wall and septal thickness, LV mass, and left atrial volume. We then used upper reference limits of the 2005 and 2015 American Society of Echocardiography (ASE) and 95th percentile of reference cohort to classify the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) target population into abnormal and normal. Reference limits were also calculated for each of 6 Hispanic origins. Using ASE 2015 defined reference values, we categorized 7%, 21%, 57%, and 17% of men and 18%, 29%, 60%, and 26% of women as having abnormal LV mass index, relative, septal, and posterior wall thickness, respectively. Conversely, 10% and 11% of men and 4% and 2% of women were classified as having abnormal end-diastolic volume and internal diameter by ASE 2015 cutoffs, respectively. Similar differences were found when we used 2005 ASE cutoffs. Several differences were noted in distribution of cardiac structure and volumes among various Hispanic/Latino origins. Cubans had highest values of echocardiographic measures, and Central Americans had the lowest.

Conclusions: This is the first large study that provides normal reference values for cardiac structure. It further demonstrates that a considerable segment of Hispanic/Latinos residing in the United States may be classified as having abnormal measures of cardiac chambers when 2015 and 2005 ASE reference cutoffs are used.
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http://dx.doi.org/10.1161/CIRCIMAGING.115.003597DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4696402PMC
January 2016

Allogeneic Mesenchymal Stem Cells Restore Endothelial Function in Heart Failure by Stimulating Endothelial Progenitor Cells.

EBioMedicine 2015 May 28;2(5):467-75. Epub 2015 Mar 28.

Interdisciplinary Stem Cell Institute, University of Miami Miller School of Medicine, FL, USA.

Background: Endothelial dysfunction, characterized by diminished endothelial progenitor cell (EPC) function and flow-mediated vasodilation (FMD), is a clinically significant feature of heart failure (HF). Mesenchymal stem cells (MSCs), which have pro-angiogenic properties, have the potential to restore endothelial function. Accordingly, we tested the hypothesis that MSCs increase EPC function and restore flow-mediated vasodilation (FMD).

Methods: Idiopathic dilated and ischemic cardiomyopathy patients were randomly assigned to receive autologous (n = 7) or allogeneic (n = 15) MSCs. We assessed EPC-colony forming units (EPC-CFUs), FMD, and circulating levels of vascular endothelial growth factor (VEGF) in patients before and three months after MSC transendocardial injection (n = 22) and in healthy controls (n = 10).

Findings: EPC-colony forming units (CFUs) were markedly reduced in HF compared to healthy controls (4 ± 3 vs. 25 ± 16 CFUs, P < 0.0001). Similarly, FMD% was impaired in HF (5.6 ± 3.2% vs. 9.0 ± 3.3%, P = 0.01). Allogeneic, but not autologous, MSCs improved endothelial function three months after treatment (Δ10 ± 5 vs. Δ1 ± 3 CFUs, P = 0.0067; Δ3.7 ± 3% vs. Δ-0.46 ± 3% FMD, P = 0.005). Patients who received allogeneic MSCs had a reduction in serum VEGF levels three months after treatment, while patients who received autologous MSCs had an increase (P = 0.0012), and these changes correlated with the change in EPC-CFUs (P < 0.0001). Lastly, human umbilical vein endothelial cells (HUVECs) with impaired vasculogenesis due to pharmacologic nitric oxide synthase inhibition, were rescued by allogeneic MSC conditioned medium (P = 0.006).

Interpretation: These findings reveal a novel mechanism whereby allogeneic, but not autologous, MSC administration results in the proliferation of functional EPCs and improvement in vascular reactivity, which in turn restores endothelial function towards normal in patients with HF. These findings have significant clinical and biological implications for the use of MSCs in HF and other disorders associated with endothelial dysfunction.
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http://dx.doi.org/10.1016/j.ebiom.2015.03.020DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4485912PMC
May 2015

Adaptation of β-Cell and Endothelial Function to Carbohydrate Loading: Influence of Insulin Resistance.

Diabetes 2015 Jul 9;64(7):2550-9. Epub 2015 Mar 9.

Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy National Research Council Institute of Clinical Physiology, Pisa, Italy

High-carbohydrate diets have been associated with β-cell strain, dyslipidemia, and endothelial dysfunction. We examined how β-cell and endothelial function adapt to carbohydrate overloading and the influence of insulin resistance. On sequential days in randomized order, nondiabetic subjects (classified as insulin-sensitive [IS] [n = 64] or insulin-resistant [IR] [n = 79] by euglycemic clamp) received four mixed meals over 14 h with either standard (300 kcal) or double carbohydrate content. β-Cell function was reconstructed by mathematical modeling; brachial artery flow-mediated dilation (FMD) was measured before and after each meal. Compared with IS, IR subjects showed higher glycemia and insulin hypersecretion due to greater β-cell glucose and rate sensitivity; potentiation of insulin secretion, however, was impaired. Circulating free fatty acids (FFAs) were less suppressed in IR than IS subjects. Baseline FMD was reduced in IR, and postprandial FMD attenuation occurred after each meal, particularly with high carbohydrate, similarly in IR and IS. Throughout the two study days, higher FFA levels were significantly associated with lower (incretin-induced) potentiation and impaired FMD. In nondiabetic individuals, enhanced glucose sensitivity and potentiation upregulate the insulin secretory response to carbohydrate overloading. With insulin resistance, this adaptation is impaired. Defective suppression of endogenous FFA is one common link between impaired potentiation and vascular endothelial dysfunction.
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http://dx.doi.org/10.2337/db15-0106DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4477346PMC
July 2015

The ABCs of Trait Anger, Psychological Distress, and Disease Severity in HIV.

Ann Behav Med 2015 Jun;49(3):420-33

Department of Psychology, University of Miami, Coral Gables, FL, 33124, USA,

Background: Trait anger consists of affective, behavioral, and cognitive (ABC) dimensions and may increase vulnerability for interpersonal conflict, diminished social support, and greater psychological distress. The concurrent influence of anger and psychosocial dysfunction on Human Immunodeficiency Virus (HIV) disease severity is unknown.

Purpose: The purpose of this study was to examine plausible psychosocial avenues (e.g., coping, social support, psychological distress), whereby trait anger may indirectly influence HIV disease status.

Methods: Three hundred seventy-seven HIV seropositive adults, aged 18-55 years (58% AIDS-defined), completed a battery of psychosocial surveys and provided a fasting blood sample for HIV-1 viral load and T lymphocyte count assay.

Results: A second-order factor model confirmed higher levels of the multidimensional anger trait, which was directly associated with elevated psychological distress and avoidant coping (p<.001) and indirectly associated with greater HIV disease severity (p<.01) (comparative fit index (CFI)=0.90, root-mean-square error of approximation (RMSEA)=0.06, standardized root-mean-square residual (SRMR)=0.06).

Conclusion: The model supports a role for the ABC components of anger, which may negatively influence immune function through various psychosocial mechanisms; however, longitudinal study is needed to elucidate these effects.
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http://dx.doi.org/10.1007/s12160-014-9667-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4623323PMC
June 2015

Airway vascular endothelial function in healthy smokers without systemic endothelial dysfunction.

Chest 2013 Jun;143(6):1733-1739

Division of Pulmonary, Critical Care and Sleep Medicine, University of Miami Miller School of Medicine, Miami, FL.

Background: Cigarette smoking can lead to systemic endothelial dysfunction. Since the airway circulation is exposed to a high concentration of cigarette smoke constituents, we reasoned that airway vascular endothelial dysfunction could be present in healthy smokers without systemic endothelial dysfunction.

Objectives: The purpose of this study was to compare airway and systemic endothelial function and measure markers of systemic inflammation in lung-healthy current smokers. Since endothelial dysfunction in smokers has been related to systemic inflammation, we also investigated its response to an inhaled glucocorticosteroid (ICS).

Methods: Fifteen healthy, current smokers and 17 healthy, lifetime nonsmokers were enrolled. Smokers were randomly assigned to 3-week treatments with inhaled fluticasone propionate or placebo in a crossover design. Vascular endothelial function was assessed in the airway by the airway blood-flow response to inhaled albuterol (ΔQaw) and in the extrapulmonary circulation by brachial arterial flow-mediated vasodilation (FMD). Venous blood was collected for C-reactive protein and IL-6.

Results: Baseline parameters did not differ between groups except for ΔQaw, which was greater in nonsmokers (45% ± 12%) than smokers (1% ± 12%) (P = .001). In the smokers, ICS treatment increased Qaw to 41% ± 7% (P < .001), but had no effect on FMD or inflammatory markers. There was an inverse relationship between baseline and ICS-induced changes in ΔQaw.

Conclusions: Healthy smokers with no signs of systemic inflammation or endothelial dysfunction display impaired airway vascular endothelial function, possibly preceding systemic endothelial dysfunction. Airway endothelial function was restored with an ICS, and the response was directly related to the severity of endothelial dysfunction.
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http://dx.doi.org/10.1378/chest.12-1033DOI Listing
June 2013

Sleep Debt and Postprandial Metabolic Function in Subclinical Cardiometabolic Pathophysiology.

Authors:
Barry E Hurwitz

Endocrinol Metab Syndr 2012 Jun;1(3)

Behavioral Medicine Research Center, University of Miami, Miami, USA.

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http://dx.doi.org/10.4172/2161-1017.1000e107DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4189802PMC
June 2012

Central obesity and insulin resistance in the cardiometabolic syndrome: pathways to preclinical cardiovascular structure and function.

J Cardiometab Syndr 2009 ;4(2):63-71

Behavioral Medicine Research Center, University of Miami, Miami, FL 33136, USA.

The cardiometabolic syndrome (CMS) has been an organizing conceptual framework for subclinical cardiovascular pathophysiology. Using cross-sectional data from 338 healthy men and women aged 18 to 55 years, the study examined the role of central adiposity and insulin sensitivity and assessed potential relationships with other metabolic indices (insulin sensitivity, glucose tolerance, fibrinolysis, lipidemia, endothelial function, and inflammation) and measures of cardiac structure and function (cardiac mass, compliance and contractility, myocardial oxygen demand, and blood pressure). Structural equation modeling analyses, which controlled for sex, age, and race, demonstrated good fit to the data. The derived relationships provided a physiologically consistent model of CMS, with an initiating role for central adiposity and insulin resistance. The model accounted for 30% and 82% of the variance in diastolic blood pressure and myocardial oxygen demand, respectively. The findings suggest predominant pathways through which subclinical metabolic processes may exert pathogenic impact on the heart and vasculature.
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http://dx.doi.org/10.1111/j.1559-4572.2008.00038.xDOI Listing
September 2009

Long-term oral contraceptive treatment, metabolic syndrome and measures of cardiovascular risk in pre-menopausal women: National Health and Nutrition Examination Survey 1999-2004.

Gynecol Endocrinol 2009 Jul;25(7):441-9

Behavioral Medicine Research Centre, University of Miami, Clinical Research Building #777, 1120 NW 14th Street, Miami, FL 33136, USA.

Aim: Differences in subclinical cardiometabolic measures were examined as a function of oral contraceptive pills (OCP) treatment duration to compare never-treated women with four OCP-treatment groups (<1, 1-5, 5-10 and >10 years).

Methods: The NHANES (1999-2004) database was used to evaluate 2089 healthy, pre-menopausal women, aged 18-55 years, with or without OCP history, no other hormonal treatment or history of systemic conditions. Outcome measures included body mass, central obesity, blood pressure, glycemia, insulinemia, lipid profile and inflammation. Analyses evaluated differences in prevalence of Metabolic Syndrome (MetS), constituent MetS and other clinical risk criteria, as well as outcome magnitudes. Analyses controlled for demographic and health-related variables, and study-eligible conditions.

Results: Relative to other groups, women with >10 years OCP-use, and to some extent those with 5-10 years treatment, displayed no differences in prevalence of MetS and most risk criteria. Further analysis showed that, relative to women treated for <5 years, those with more prolonged OCP treatment displayed lower body mass and fasting glycemia with higher HDL-c levels, but more elevated LDL-c and total cholesterol.

Conclusions: The findings of both beneficial and detrimental subclinical cardiometabolic differences with more long-term OCP-treatment reinforces the need to monitor changes in these factors within the context of the treated patient's risk-benefit profile. However, because the magnitude of these differences was small, relative to normative ranges, it may be concluded that OCPs, as used in recent decades, are unlikely to markedly affect cardiometabolic risk.
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http://dx.doi.org/10.1080/09513590902770149DOI Listing
July 2009

Chronic fatigue syndrome: illness severity, sedentary lifestyle, blood volume and evidence of diminished cardiac function.

Clin Sci (Lond) 2009 Oct 19;118(2):125-35. Epub 2009 Oct 19.

Behavioral Medicine Research Center, University of Miami, Miami, FL 33136, USA.

The study examined whether deficits in cardiac output and blood volume in a CFS (chronic fatigue syndrome) cohort were present and linked to illness severity and sedentary lifestyle. Follow-up analyses assessed whether differences in cardiac output levels between CFS and control groups were corrected by controlling for cardiac contractility and TBV (total blood volume). The 146 participants were subdivided into two CFS groups based on symptom severity data, severe (n=30) and non-severe (n=26), and two healthy non-CFS control groups based on physical activity, sedentary (n=58) and non-sedentary (n=32). Controls were matched to CFS participants using age, gender, ethnicity and body mass. Echocardiographic measures indicated that the severe CFS participants had 10.2% lower cardiac volume (i.e. stroke index and end-diastolic volume) and 25.1% lower contractility (velocity of circumferential shortening corrected by heart rate) than the control groups. Dual tag blood volume assessments indicated that the CFS groups had lower TBV, PV (plasma volume) and RBCV (red blood cell volume) than control groups. Of the CFS subjects with a TBV deficit (i.e. > or = 8% below ideal levels), the mean+/-S.D. percentage deficit in TBV, PV and RBCV were -15.4+/-4.0, -13.2+/-5.0 and -19.1+/-6.3% respectively. Lower cardiac volume levels in CFS were substantially corrected by controlling for prevailing TBV deficits, but were not affected by controlling for cardiac contractility levels. Analyses indicated that the TBV deficit explained 91-94% of the group differences in cardiac volume indices. Group differences in cardiac structure were offsetting and, hence, no differences emerged for left ventricular mass index. Therefore the findings indicate that lower cardiac volume levels, displayed primarily by subjects with severe CFS, were not linked to diminished cardiac contractility levels, but were probably a consequence of a co-morbid hypovolaemic condition. Further study is needed to address the extent to which the cardiac and blood volume alterations in CFS have physiological and clinical significance.
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http://dx.doi.org/10.1042/CS20090055DOI Listing
October 2009

Psychological distress, killer lymphocytes and disease severity in HIV/AIDS.

Brain Behav Immun 2008 Aug 5;22(6):901-11. Epub 2008 Mar 5.

Department of Psychology, University of Miami, Miami, FL 33136, USA.

Immunocellular mechanisms that account for the association between psychosocial risk factors and increased susceptibility to faster progression of HIV/AIDS are largely unknown. This study used structural equation modeling to test the hypothesis that enumerative and functional alterations in killer lymphocytes mediate the relationship between higher levels of psychological distress (defined by perceived stress, anxiety and depressive symptoms) and greater HIV disease severity (defined by HIV-1 viral load and T-helper (CD4(+)) cell count), independent of standard demographic and various HIV-related covariates. Participants were 200 HIV-1 seropositive adults on combination antiretroviral therapy (ages 20-55 years; 67% men; 62% black; 84% AIDS). The data fit a psychoimmune model in which the significant relationship between higher distress levels and greater disease severity was mediated by diminished natural killer (NK) cell count and cytotoxic function, as well as increased cytotoxic (CD8(+)) T-cell activation. Overall the findings indicated that the psychoimmune model accounted for 67% of the variation in HIV disease severity. In contrast, the data did not support a reverse directionality mediation model, where greater HIV disease severity predicted greater distress as a function of killer lymphocyte status. In sum, the psychoimmune associations of the final model are physiologically consistent and suggest that distress-related alterations in killer lymphocyte immunity may play a role in the biobehavioral mechanisms linked with HIV-1 pathogenesis.
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http://dx.doi.org/10.1016/j.bbi.2008.01.001DOI Listing
August 2008

Suppression of human immunodeficiency virus type 1 viral load with selenium supplementation: a randomized controlled trial.

Arch Intern Med 2007 Jan;167(2):148-54

Behavioral Medicine Research Center, University of Miami, c/o VA Medical Center, FL 33125, USA.

Background: Despite findings that selenium supplementation may improve immune functioning, definitive evidence of its impact on human immunodeficiency virus (HIV) disease severity is lacking.

Methods: High selenium yeast supplementation (200 mug/d) was evaluated in a double-blind, randomized, placebo-controlled trial. Intention-to-treat analyses assessed the effect on HIV-1 viral load and CD4 count after 9 months of treatment. Unless otherwise indicated, values are presented as mean +/- SD.

Results: Of the 450 HIV-1-seropositive men and women who underwent screening, 262 initiated treatment and 174 completed the 9-month follow-up assessment. Mean adherence to study treatment was good (73.0% +/- 24.7%) with no related adverse events. The intention-to-treat analyses indicated that the mean change (Delta) in serum selenium concentration increased significantly in the selenium-treated group and not the placebo-treated group (Delta = 32.2 +/- 24.5 vs 0.5 +/- 8.8 microg/L; P<.001), and greater levels predicted decreased HIV-1 viral load (P<.02), which predicted increased CD4 count (P<.04). Findings remained significant after covarying age, sex, ethnicity, income, education, current and past cocaine and other drug use, HIV symptom classification, antiretroviral medication regimen and adherence, time since HIV diagnosis, and hepatitis C virus coinfection. Follow-up analyses evaluating treatment effectiveness indicated that the nonresponding selenium-treated subjects whose serum selenium change was less than or equal to 26.1 microg/L displayed poor treatment adherence (56.8% +/- 29.8%), HIV-1 viral load elevation (Delta = +0.29 +/- 1.1 log(10) units), and decreased CD4 count (Delta = -25.8 +/- 147.4 cells/microL). In contrast, selenium-treated subjects whose serum selenium increase was greater than 26.1 microg/L evidenced excellent treatment adherence (86.2% +/- 13.0%), no change in HIV-1 viral load (Delta = -0.04 +/- 0.7 log(10) units), and an increase in CD4 count (Delta = +27.9 +/- 150.2 cells/microL).

Conclusions: Daily selenium supplementation can suppress the progression of HIV-1 viral burden and provide indirect improvement of CD4 count. The results support the use of selenium as a simple, inexpensive, and safe adjunct therapy in HIV spectrum disease. Trial Registration isrctn.org Identifier: ISRCTN22553118.
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http://dx.doi.org/10.1001/archinte.167.2.148DOI Listing
January 2007
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