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1.  The Association of HIV Infection with Left Ventricular Mass/Hypertrophy 
Left ventricular hypertrophy (LVH) is an independent predictor of major cardiovascular events. Cardiovascular risk is increased among human immunodeficiency virus (HIV)-infected patients. To assess LV mass/hypertrophy in HIV infection, 654 women enrolled in the Women's Interagency HIV Study underwent transthoracic echocardiography. There were 454 HIV-infected and 200 uninfected women, mean age 40.8 ± 9.3 years. LV mass/height2.7 was similar between the HIV-infected and the HIV-uninfected groups (41.4 ± 11.1 vs. 39.9 ± 10.3 g/h2.7; p = 0.37). The prevalence of LVH was similar between the two groups (LVH by LV mass/height2.7 criteria 15.0% vs. 13.0%, p = 0.29). Relative wall thickness (RWT), defined as the ratio of LV wall thickness to cavity diameter, was also similar between the HIV-infected and HIV-uninfected groups (0.36 ± 0.05 vs. 0.37 ± 0.06, p = 0.16). On multiple linear regression analysis adjusting for age, W/H ratio, triceps skinfold thickness, systolic/diastolic BP, diabetes, hypertension and dyslipidemia; HIV status (b = 2.08, p = 0.02, CI 0.27–3.88); weight (b per kg = 0.15, p < 0.01, CI 0.08–0.22); and smoking duration (b per one-year increase = 0.08, p = 0.03, CI 0.01–0.16) were independent correlates of LV mass/height2.7 (Model R2 = 0.20, p < 0.001). Weight (aOR = 1.04, CI 1.01–1.06) and smoking duration (aOR = 1.03, CI 1.01–1.06) were independent correlates of LVH. Being HIV negative, increased age, increased triceps skinfold thickness, and higher W/H ratio were independent correlates of higher RWT. Among HIV-infected women, higher LV mass was not associated with a history of AIDS-defining illness, nadir CD4+ count <200 cells/μl, or with the duration of highly active antiretroviral therapy (HAART). Women taking NRTIs had higher LV mass. Higher RWT was associated with current CD4+ count. In conclusion, HIV infection is associated with greater LV mass but not with a higher prevalence of LVH. Among HIV-infected women, RWT, but not LV mass, is associated with the degree of immunosuppression.
PMCID: PMC2801578  PMID: 19397399
2.  Natural History of Concentric Left Ventricular Geometry in Community-Dwelling Older Adults without Heart Failure during Seven Years of Follow-up 
The American journal of cardiology  2010;107(2):321-324.
The presence of concentric left ventricular (LV) geometry has important pathophysiologic and prognostic implications. However, little is known about its natural history in older adults. Of the 5795 community-dwelling adults, ≥65 years, in the Cardiovascular Health Study, 1871 without baseline heart failure had data on baseline and 7-year echocardiography. Of these 343 (18%) had baseline concentric LV geometry (concentric remodeling, 83% and concentric LV hypertrophy, 17%) and are the focus of the current study. LV geometry at year 7 was categorized into 4 groups based on LV hypertrophy (LVH; LV mass indexed for height >51 g/m2.7) and relative wall thickness (RWT): eccentric hypertrophy (RWT ≤0.42 with LVH), concentric hypertrophy (RWT >0.42 with LVH), concentric remodeling (RWT >0.42 without LVH), and normal (RWT ≤0.42 without LVH). At year 7, LV geometry normalized in 57%, remained unchanged in 35%, and transitioned to eccentric hypertrophy in 7% of participants. Incident eccentric hypertrophy occurred in 4% and 25% of those with baseline concentric remodeling and concentric hypertrophy respectively, and was associated with increased LV end-diastolic volume and decreased LV ejection fraction at year-7. Prior myocardial infarction and baseline above-median LV mass (>39 g/m2.7) and RWT (>0.46) had significant unadjusted associations with incident eccentric LV hypertrophy; however, only LV mass >39 g/m2.7 (odds ratio, 17.52; 95% CI, 3.91–78.47; p<0.001) and prior myocardial infarction (odds ratio, 4.73; 95% CI, 1.16–19.32; p=0.031) had significant independent associations. In conclusion, in community-dwelling older adults with concentric LV geometry, transition to eccentric hypertrophy was uncommon but structurally maladaptive.
PMCID: PMC3022324  PMID: 21129719
concentric left ventricular remodeling; concentric left ventricular hypertrophy; eccentric left ventricular hypertrophy
3.  Increased relative wall thickness is a marker of subclinical cardiac target-organ damage in African diabetic patients 
Cardiovascular Journal of Africa  2012;23(8):435-441.
To assess the prevalence and covariates of abnormal left ventricular (LV) geometry in diabetic outpatients attending Muhimbili National Hospital in Dar es Salaam, Tanzania.
Echocardiography was performed in 61 type 1 and 123 type 2 diabetes patients. LV hypertrophy was taken as LV mass/height2.7 > 49.2 g/m2.7 in men and > 46.7 g/m2.7 in women. Relative wall thickness (RWT) was calculated as the ratio of LV posterior wall thickness to end-diastolic radius and considered increased if ≥ 0.43. LV geometry was defined from LV mass index and RWT in combination.
The most common abnormal LV geometries were concentric remodelling in type 1 (30%) and concentric hypertrophy in type 2 (36.7%) diabetes patients. Overall, increased RWT was present in 58% of the patients. In multivariate analyses, higher RWT was independently associated with hypertension, longer isovolumic relaxation time, lower stress-corrected midwall shortening and circumferential end-systolic stress, both in type 1 (multiple R2 = 0.73) and type 2 diabetes patients (multiple R2 = 0.66), both p < 0.001. These associations were independent of gender, LV hypertrophy or renal dysfunction.
Increased RWT is common among diabetic sub-Saharan Africans and is associated with hypertension and LV dysfunction.
PMCID: PMC3721891  PMID: 22447437
left ventricular geometry; African diabetes; relative wall thickness
4.  Left ventricular hypertrophy and geometry in type 2 diabetes patients with chronic kidney disease. An echocardiographic study 
We assessed left ventricular structural alterations associated with chronic kidney disease (CKD) in Congolese patients with type 2 diabetes.
This was a cross-sectional study of a case series. We obtained anthropometric, clinical, biological and echocardiographic measurements in 60 consecutive type 2 diabetes patients (37 females, 62%) aged 20 years or older from the diabetes outpatient clinic, University of Kinshasa Hospital, DRC. We computed creatinine clearance rate according to the MDRD equation and categorised patients into mild (CrCl > 60 ml/min per 1.73 m2), moderate (CrCl 30–60 ml/min per 1.73 m2) and severe CKD (< 30 ml/min per 1.73 m2). Left ventricular hypertrophy (LVH) was indicated by a LV mass index (LVMI) > 51 g/m2.7 and LV geometry was defined as normal, or with concentric remodelling, eccentric or concentric hypertrophy, using relative wall thickness (RWT) and LVMI.
Compared to patients with normal kidney function, CKD patients had higher uric acid levels (450 ± 166 vs 306 ± 107 μmol/l; p ≤ 0.001), a greater proportion of LVH (37 vs 14%; p ≤ 0.05) and longstanding diabetes (13 ± 8 vs 8 ± 6 years; p ≤ 0.001). Their left ventricular internal diameter, diastolic (LVIDD) was (47.00 ± 6.00 vs 43.00 ± 7.00 mm; p ≤ 0.001), LVMI was (47 ± 19 vs 36.00 ± 15 g/m2.7; p ≤ 0.05) and proportions of concentric (22 vs 11%; p ≤ 0.05) or eccentric (15 vs 3%; p ≤ 0.05) LVH were also greater. Severe CKD was associated with increased interventricular septum, diastolic (IVSD) (12.30 ± 3.08 vs 9.45 ± 1.94 mm; p ≤ 0.05), posterior wall thickness, diastolic (PWTD) (11.61 ± 2.78 vs 9.52 ± 1.77 mm; p ≤ 0.01), relative wall thickness (RWT) (0.52 ± 0.17 vs 0.40 ± 0.07; p ≤ 0.01) rate of LVH (50 vs 30%; p ≤ 0.05), and elevated proportions of concentric remodelling (25 vs 15%; p ≤ 0.05) and concentric LVH (42 vs 10%; p ≤ 0.05) in comparison with patients with moderate CKD. In multivariable adjusted analysis, hyperuricaemia emerged as the only predictor of the presence of LVH in patients with CKD (adjusted OR 9.10; 95% CI: 2.40–33.73).
In keeping with a higher rate of cardiovascular events usually reported in patients with impaired renal function, CKD patients exhibited LVH and abnormal LV geometry.
PMCID: PMC3721939  PMID: 22447475
type 2 diabetes; chronic kidney disease; left ventricular hypertrophy; prevalence; predictors
5.  Severe aortic stenosis without left ventricular hypertrophy: prevalence, predictors, and short-term follow up after aortic valve replacement. 
Heart  1996;76(3):250-255.
OBJECTIVES: The purpose of the present study in patients with severe aortic stenosis was to assess the prevalence of absent left ventricular hypertrophy (LVH) (determined according to mass criteria), to identify predictors of absent LVH, and to assess short-term left ventricular adaptation and prognosis after aortic valve replacement. METHODS: Left ventricular mass (LVM) was determined by echocardiography in 109 men and 101 women with severe aortic stenosis (mean pressure gradient < or = 50 mm Hg). LVH was defined as LVM > or = 109 g/m2 in women and LVM > or = 134 g/m2 in men. RESULTS: One hundred and eighty nine patients showed LVH (group 1) (90%; mean (SD) age 65 (14) years), and 21 showed no LVH (group 2) (10%, age 57 (21) years P = 0.02 for difference in age). Twelve (6%) of those without LVH had increased relative wall thickness (that is, > or = 0.45 with LV concentric remodelling) and nine (4%) showed no macroscopically detectable hypertrophic adaptation. The following variables were associated with the absence of LVH: low body surface area, low body mass index, and increased cardiac index. 76/210 patients were followed up a mean of six months after aortic valve replacement. The frequency of adequate ventricular adaptation to the decreased afterload after aortic valve replacement was higher in patients with LVH than in those without. Mortality six months after aortic valve replacement was lower, but not significantly, in patients with LVH (7.6%) than in those without LVH (12.5%, P = 0.10). CONCLUSIONS: A tenth of patients with severe aortic stenosis did not develop LVH according to mass criteria; 4% of the patients did not have any macroscopic signs of myocardial adaptation to the pressure overload despite longstanding disease. Small body size was independently associated with lack of LVH according to mass criteria. Six months after aortic valve replacement, ventricular adaptation was more often adequate in patients with LVH than in those without.
PMCID: PMC484516  PMID: 8868985
6.  Prevalence and risk factors of abnormal left ventricular geometrical patterns in untreated hypertensive patients 
The various prevalence of LVH and abnormal LV geometry have been reported in different populations. So far, only a few reports are available on the prevalence of LV geometric patterns in a large Chinese untreated hypertensive population.
A total of 9,286 subjects (5167 men and 4119 women) completed the survey and 1641 untreated hypertensive patients (1044 males and 597 females) enrolled in the present study. The LV geometry was classified into four patterns: normal; abnormal,defined as concentric remodeling;concentric or eccentric hypertrophy based on the values of left ventricular mass index (LVMI) and relative wall thickness (RWT). Logistic regression model was applied to determine the odds ratio (OR) and 95% confidence intervals (CI) of the risk factors of left ventricular hypertrophy.
The prevalence of LVH was 20.2% in untreated hypertensive patients, much higher in women (30.8%) than in men (14.2%) (P < 0.01). The prevalence of LV geometrical patterns was 34.9%, 11.1%, 9.1% for concentric remodeling, concentric and eccentric hypertrophy,respectively. After adjustment by using Logistic regression model, the risk factors for LVH and abnormal LV geometry were age, female, systolic blood pressure, and body mass index. And low high density lipoprotein maybe a positive factor.
The prevalence of LVH and abnormal LV geometric patterns was higher in women than in men and increased with age. It is crucial to improve the awareness rate of hypertension and control the risk factors of CV complications in untreated hypertensive population.
PMCID: PMC4192326  PMID: 25280487
Left ventricular hypertrophy; Left ventricular geometry; Risk factors; Untreated hypertension
7.  Effectiveness of the Standard WHO Recommended Retreatment Regimen (Category II) for Tuberculosis in Kampala, Uganda: A Prospective Cohort Study 
PLoS Medicine  2011;8(3):e1000427.
Prospective evaluation of the effectiveness of the WHO-recommended standardized retreatment regimen for tuberculosis by Edward Jones-López and colleagues reveals an unacceptable proportion of unsuccessful outcomes.
Each year, 10%–20% of patients with tuberculosis (TB) in low- and middle-income countries present with previously treated TB and are empirically started on a World Health Organization (WHO)-recommended standardized retreatment regimen. The effectiveness of this retreatment regimen has not been systematically evaluated.
Methods and Findings
From July 2003 to January 2007, we enrolled smear-positive, pulmonary TB patients into a prospective cohort to study treatment outcomes and mortality during and after treatment with the standardized retreatment regimen. Median time of follow-up was 21 months (interquartile range 12–33 months). A total of 29/148 (20%) HIV-uninfected and 37/140 (26%) HIV-infected patients had an unsuccessful treatment outcome. In a multiple logistic regression analysis to adjust for confounding, factors associated with an unsuccessful treatment outcome were poor adherence (adjusted odds ratio [aOR] associated with missing half or more of scheduled doses 2.39; 95% confidence interval (CI) 1.10–5.22), HIV infection (2.16; 1.01–4.61), age (aOR for 10-year increase 1.59; 1.13–2.25), and duration of TB symptoms (aOR for 1-month increase 1.12; 1.04–1.20). All patients with multidrug-resistant TB had an unsuccessful treatment outcome. HIV-infected individuals were more likely to die than HIV-uninfected individuals (p<0.0001). Multidrug-resistant TB at enrolment was the only common risk factor for death during follow-up for both HIV-infected (adjusted hazard ratio [aHR] 17.9; 6.0–53.4) and HIV-uninfected (14.7; 4.1–52.2) individuals. Other risk factors for death during follow-up among HIV-infected patients were CD4<50 cells/ml and no antiretroviral treatment (aHR 7.4, compared to patients with CD4≥200; 3.0–18.8) and Karnofsky score <70 (2.1; 1.1–4.1); and among HIV-uninfected patients were poor adherence (missing half or more of doses) (3.5; 1.1–10.6) and duration of TB symptoms (aHR for a 1-month increase 1.9; 1.0–3.5).
The recommended regimen for retreatment TB in Uganda yields an unacceptable proportion of unsuccessful outcomes. There is a need to evaluate new treatment strategies in these patients.
Please see later in the article for the Editors' Summary
Editors' Summary
One-third of the world's population is currently infected with Mycobacterium tuberculosis, the bacterium that causes tuberculosis (TB), and 5%–10% of HIV-uninfected individuals will go on to develop disease and become infectious. The risk of progression from infection to disease in HIV infected is much higher. If left untreated, each person with active TB may infect 10 to 15 people every year, reinforcing the public health priority of controlling TB through adequate treatment. Patients with a previous history of TB treatment are a major concern for TB programs throughout the world because these patients are at a much higher risk of harboring a form of TB that is resistant to the drugs most frequently used, resulting in poorer treatment outcomes and significantly complicating current management strategies. More then 1 million people in over 90 countries need to be “re-treated” after failing, interrupting, or relapsing from previous TB treatment.
Every year, 10%–20% of people with TB in low- and middle-income countries are started on a standardized five-drug retreatment regimen as recommended by the World Health Organization (WHO). Yet, unlike treatment regimens for newly diagnosed TB patients, the recommended retreatment regimen (also known as the category II regimen) has never been properly evaluated in randomized clinical trials or prospective cohort studies. Rather, this regimen was recommended by experts before the current situation of widespread drug-resistant TB and HIV infection.
Why Was This Study Done?
WHO surveillance data suggest that the retreatment regimen is successful in about 70% of patients, but retrospective studies that have evaluated the regimen's efficacy showed variable treatment responses with success rates ranging from 26% to 92%. However, these studies have generally only assessed outcomes at the completion of the retreatment regimen, and few have examined the risk of TB recurrence, especially in people who are also infected with HIV and so are more likely to experience TB recurrence—an issue of particular concern in sub-Saharan Africa. Therefore, in this study based in Kampala, Uganda, the researchers conducted a prospective cohort study to assess treatment and survival outcomes in patients previously treated for TB and to identify factors associated with poor outcomes. Given the overwhelming contribution of HIV infection to death, the researchers categorized their survival analysis by HIV status.
What Did the Researchers Do and Find?
The researchers recruited consecutive smear-positive TB patients who were admitted to Mulago Hospital, Kampala, Uganda, for the retreatment of TB with the standard retreatment regimen between July 2003 and January 2007. Eligible patients received daily directly observed therapy and after hospital discharge, were seen every month during their 8-month TB-retreatment course. Home health visitors assessed treatment adherence through treatment card review, monthly pill counts, and patient self-report. After the completion of the retreatment regimen, patients were evaluated for TB recurrence every 3 months for a median of 21 months. The researchers then used a statistical model to identify treatment outcomes and mortality HIV-uninfected and HIV-infected patients.
The researchers found that 29/148 (20%) of HIV-uninfected and 37/140 (26%) of HIV-infected patients had an unsuccessful treatment outcome. Factors associated with an unsuccessful treatment outcome were poor adherence, HIV infection, increasing age, and duration of TB symptoms. All patients with multidrug resistant TB, a form of TB that is resistant to the two most important drugs used to treat TB, had an unsuccessful treatment outcome. In addition, HIV-infected subjects were more likely to die than HIV-uninfected subjects (p<0.0001), and having multidrug resistant TB at enrollment was the only common risk factor for death during follow-up for both HIV-infected and HIV uninfected patients. Other risk factors for death among HIV-infected patients were CD4<50 cells/ml and no antiretroviral therapy treatment and among HIV-uninfected patients were poor adherence and duration of TB symptoms.
What Do These Findings Mean?
The researchers found that although 70%–80% of patients had a successful treatment outcome on completion of antituberculous therapy (a result that compares well with retrospective studies), the standard retreatment regimen had low treatment response rates and was associated with poor long-term outcomes in certain subgroups of patients, particularly those with multidrug resistant TB and HIV.
These findings indicate that the standard retreatment approach to TB as implemented in low- and middle-income settings is inadequate and stress the importance of a new, more effective, strategies. Improved access to rapid diagnostics for TB drug-resistance, second-line TB treatment, and antiretroviral therapy is urgently needed, along with a strong evidence base to guide clinicians and policy makers on how best to use these tools.
Additional Information
Please access these Web sites via the online version of this summary at
The World Health Organization has information on TB, TB retreatment, and multidrug-resistant TB
WHO also provides information on TB/HIV coinfection
The Stop TB Partnership provides information on the global plan to stop TB
PMCID: PMC3058098  PMID: 21423586
8.  Relations of Biomarkers Representing Distinct Biological Pathways to Left Ventricular Geometry 
Circulation  2008;118(22):2252-2258.
Several biological pathways are activated concomitantly during left ventricular (LV) remodeling. However, the relative contribution of circulating biomarkers representing these distinct pathways to LV geometry is unclear.
Methods and Results
We evaluated 2119 Framingham Offspring Study participants (mean age 57 years; 57% women) who underwent measurements of biomarkers of inflammation (C-reactive protein, CRP), hemostasis (fibrinogen; plasminogen activator inhibitor 1, PAI-1), neurohormonal activation (B-type natriuretic peptide, BNP); renin-angiotensin-aldosterone system ([RAAS], aldosterone and renin modeled as a ratio, ARR), and echocardiography at a routine examination. LV geometry was defined based on sex-specific distributions of LV mass (LVM) and relative wall thickness (RWT): normal (LVM and RWT<80th percentile), concentric remodeling (LVM
Modeled individually, CRP, fibrinogen, PAI-1 and ARR were related to LV geometry (p<0.01). In multivariable analyses, the biomarker panel was significantly related to altered LV geometry (p<0.0001). Upon backwards elimination, logARR alone was significantly and positively associated with eccentric (odds ratio [OR] per standard deviation (SD) increment 1.20; 95% CI 1.05-1.37) and concentric LV hypertrophy (OR per SD increment 1.29; 95% CI 1.06-1.58).
Our cross-sectional observations on a large community-based sample identified ARR as a key correlate of concentric and eccentric LV hypertrophy, consistent with a major role for RAAS in LV remodeling.
PMCID: PMC2747641  PMID: 19001021
epidemiology; ventricular hypertrophy; biomarkers; ventricular remodeling; renin angiotensin system; aldosterone; c-reactive protein; PAI-1; fibrinogen
PLoS ONE  2012;7(10):e46534.
Growth differentiation factor-15 (GDF-15) has been identified as an endogenous anti-hypertrophy effect. However, the association of plasma GDF-15 levels with left ventricular hypertrophy (LVH) in hypertension is poorly understood. We investigate the effect of plasma GDF-15 levels on left ventricular hypertrophy (LVH) in hypertension. We measured the plasma levels of GDF-15 in 299 untreated hypertensive patients which consisted of 99 with LVH and 200 without LVH using immunoradiometric assay. All subjects were examined by the ultrasonic cardiograph to determine Left ventricular (LV) internal diameters, septal thickness, and posterior wall thickness. The associations of GDF-15 with left ventricular mass index (LVMI), LV end-systolic and –diastolic diameters, LV wall thickness, and LV ejection fraction were evaluated. We found that plasma GDF-15 levels in hypertensive patients with LVH [median 1101, 25th–75th percentiles (879–1344) ng/L] were higher than that in hypertensive patients without LVH [median 516, 25th–75th percentiles (344–640) ng/L] (P<0.001). After adjustment for traditional covariates, plasma GDF-15 levels were independently related to LVMI (R2 = 0.53; β = 0.624, P<0.001), LV interventricular septal thickness (R2 = 0.23; β = 0.087, P<0.01) and LV posterior wall thickness (R2 = 0.26; β = 0.103, P<0.05). Our cross-sectional data on a hospital-based sample indicate that plasma GDF-15 levels are associated with LVH in hypertensive patients.
PMCID: PMC3469555  PMID: 23071585
BMC Medical Imaging  2006;6:10.
Left ventricular hypertrophy (LVH) is a well known independent risk factor for cardiovascular events. It has been shown that combination of left ventricular mass (LVM) and relative wall thickness (RWT) can be used to identify different forms of left ventricular (LV) geometry. Prospective studies have shown that LV geometric patterns have prognostic implications, with the worst prognosis associated with concentric hypertrophy. The methods for the normalization or indexation of LVM have also recently been shown to confer some prognostic value especially in obese population. We sought to determine the prevalence of echocardiographic lLVH using eight different and published cut-off or threshold values in hypertensive subjects seen in a developing country's tertiary centre.
Echocardiography was performed in four hundred and eighty consecutive hypertensive subjects attending the cardiology clinic of the University college Hospital Ibadan, Nigeria over a two-year period.
Complete data was obtained in 457 (95.2%) of the 480 subjects (48.6% women). The prevalence of LVH ranged between 30.9–56.0%. The highest prevalence was when LVM was indexed to the power of 2.7 with a partition value of 49.2 g/ht2.7 in men and 46.7 g/ht2.7 in women. The lowest prevalence was observed when LVM was indexed to body surface area (BSA) and a partition value of 125 g/m2 was used for both sexes. Abnormal LV geometry was present in 61.1%–74.0% of our subjects and commoner in women.
The prevalence of LVH hypertensive patients is strongly dependent on the cut-off value used to define it. Large-scale prospective study will be needed to determine the prognostic implications of the different LV geometry in native Africans.
PMCID: PMC1564011  PMID: 16939651
Hypertensive left ventricular mass (LVM) is expected to decrease during antihypertensive therapy, based on results of clinical trials.
Methods and Results
We assessed 4‐year change of echocardiographic LVM in 851 hypertensive free‐living participants of the Strong Heart Study (57% women, 81% treated). Variations of 5% or more of the initial systolic blood pressure (SBP) and LVM were categorized for analysis. At baseline, 23% of men and 36% of women exhibited LV hypertrophy (LVH, P<0.0001). At the follow‐up, 3% of men and 10% of women had regression of LVH (P<0.0001 between genders); 14% of men and 15% of women, free of baseline LVH, developed LVH. There was an increase in LVM over time, more in men than in women (P<0.001). Participants whose LVM did not decrease had similar baseline SBP and diastolic BP, but higher body mass index (BMI), waist/hip ratio, heart rate (all P<0.008), and urinary albumin/creatinine excretion (P<0.001) than those whose LVM decreased. After adjusting for field center, initial LVM index, target BP, and kinship degree, lack of decrease in LVM was predicted by higher baseline BMI and urinary albumin/creatinine excretion, independently of classes of antihypertensive medications, and significant effects of older age, male gender, and percentage increase in BP over time. Similar findings were obtained in the subpopulation (n=526) with normal BP at follow‐up.
In a free‐living population, higher BMI is associated with less reduction of hypertensive LVH; lack of reduction of LVM is independent of BP control and of types of antihypertensive treatment, but is associated with renal damage.
PMCID: PMC3698775  PMID: 23744404
antihypertensive therapy; blood pressure; obesity; proteinuria; ventricular hypertrophy
Journal of hypertension  2010;28(9):1959-1967.
Cardiac computed tomography (CT) is a state-of-the-art technology that provides an accurate noninvasive method to quantify left ventricular mass for analysis of left ventricular hypertrophy (LVH). We aimed to examine seven ECG-based LVH criteria against two CT indexation criteria for LVH: a CT-specific body surface area cutoff and the obesity-independent height2.7 criteria.
In 333 patients (mean age 53 ± 12 years, 61% men), 64-slice contrast-enhanced CT was performed and 12-lead surface ECG within 24 h. Left ventricular mass was measured at end-diastole. Using both CT indexation criteria, the cohort was subdivided into patients with LVH and without LVH. The seven ECG criteria for LVH were the Cornell voltage index, Cornell voltage duration product, Cornell/strain index, Sokolow–Lyon index, Romhilt–Estes scores at least 4 and at least 5, and Gubner–Ungerleider.
The ECG parameters had high specificities (85–97%) and variable low sensitivities (4–43%) when compared to either CT criteria of LVH. The three Cornell-based methods performed the best (test-positive likelihood ratio: 4.5–6.7), followed by the Sokolow–Lyon and Romhilt–Estes scores (test-positive likelihood ratio: 2.3–4.0). With the exception of the Gubner–Ungerleider criterion, the other six ECG criteria were associated with at least one of the CT-based LVH (adjusted odds ratio 2.4–9.5) and had incremental predictive value beyond that of hypertension history.
Using cardiac CT as a gold standard for LVH assessment, ECG criteria for LVH have high specificities with the three Cornell-based criteria providing the best test performance for identifying patients with LVH.
PMCID: PMC3218429  PMID: 20498615
computed tomography; electrocardiography; left ventricular hypertrophy; left ventricular mass
HIV medicine  2010;11(9):573-583.
To describe growth and body composition changes in HIV+ children after initiating or changing ART and correlate these with viral, immune and treatment parameters.
Ninety-seven prepubertal HIV+ children were observed over 48 weeks upon beginning or changing ART. Anthropometry and BIA were compared to NHANES to generate z-scores and HIV-exposed, uninfected children from WITS. Multivariate analysis evaluated associations between growth and body composition and disease parameters.
All baseline lean and fat mass measures were below those of controls from NHANES. Weight, height and FFM index (FFM/height2) z-scores increased over time (p=0.004, 0.037 and 0.027) and waist/height ratio z-score decreased (p=0.045), but BMI and % body fat z-scores did not change. Measures did not increase more than in uninfected WITS controls. In multivariate analysis, baseline height, mid-thigh circumference and FFM z-scores related to CD4% (p=0.029, p=0.008 and 0.020) and change in FFM and FFM index z-scores to CD4% increase (p=0.010 and 0.011). Compared to WITS controls, baseline difference in height and mid-thigh muscle circumference were also associated with CD4%. Case-control differences in change in both subscapular skinfold (SSF) thickness and the SSF/triceps skinfold ratio were inversely associated with viral suppression. No measures related to ART class(es) at baseline or over time.
In these HIV+ children, beginning or changing ART was associated with improved growth and lean body mass, as indicated by FFM index. Height and LBM relate to CD4% at baseline and over time. Altered fat distribution and greater central adiposity are associated with detectable virus but not ART class(es) received.
PMCID: PMC3075205  PMID: 20345880
Growth; body composition; HIV; children; fat redistribution; antiretroviral therapy; CD4; viral load
Heart  2002;87(3):270-275.
Background: Hypertrophic cardiomyopathy (HCM) is an inherited disease of the sarcomere characterised clinically by myocardial hypertrophy and its consequences. Phenotypic expression is heterogeneous even within families with the same aetiological mutation and may be influenced by additional genetic factors.
Objective: To determine the influence of genetic polymorphisms of the renin-angiotensin-aldosterone system (RAAS) on ECG and two dimensional echocardiographic left ventricular hypertrophy (LVH) in genetically identical patients with HCM.
Patients and methods: Polymorphisms of five RAAS components were determined in 26 gene carriers from a single family with HCM caused by a previously identified myosin binding protein C mutation. Genotypes associated with a higher activation status of the RAAS were labelled “pro-LVH genotypes”.
Results: There was a non-biased distribution of pro-LVH genotypes in the gene carriers. Those without pro-LVH genotypes did not manifest cardiac hypertrophy whereas gene carriers with pro-LVH genotypes did (mean (SD) left ventricular muscle mass 190 (48) v 320 (113), p = 0.002; interventricular septal thickness 11.5 (2.0) v 16.4 (6.7), p = 0.01; pathological ECG 0% (0 of 10) v 63% (10 of 16), respectively). Multivariate analysis controlling for age, sex, and hypertension confirmed an independent association between the presence of pro-LVH polymorphisms and left ventricular mass. When each polymorphism was assessed individually, carriers of each pro-LVH genotype had a significantly greater left ventricular mass than those with no pro-LVH mutation; these associations, with the exception of cardiac chymase A AA polymorphism (p = 0.06), remained significant in multivariate analysis.
Conclusion: Genetic polymorphisms of the RAAS influence penetrance and degree of LVH in 26 gene carriers from one family with HCM caused by a myosin binding protein C mutation.
PMCID: PMC1767035  PMID: 11847170
hypertrophic cardiomyopathy; polymorphisms; renin-angiotensin-aldosterone system
The American journal of cardiology  2013;112(8):1158-1164.
While concentric remodeling (CR) and concentric hypertrophy (CH) are common forms of left ventricular (LV) remodeling in heart failure with preserved ejection fraction (HFpEF), eccentric hypertrophy (EH) can also occur in these patients. However, clinical characteristics and outcomes of EH have not been well described in HFpEF. We prospectively studied 402 patients with HFpEF, divided into 4 groups based on LV structure: normal geometry (no LV hypertrophy [LVH] and relative wall thickness [RWT] < 0.42); CR (no LVH and RWT > 0.42); CH (LVH and RWT > 0.42); and EH (LVH and RWT < 0.42). We compared clinical, laboratory, echocardiographic, invasive hemodynamic, and outcome data among groups. Of 402 patients, 48 (12%) had EH. Compared to CH, patients with EH had lower systolic blood pressure and less renal impairment despite similar rates of hypertension. After adjustment for covariates, EH was associated with reduced LV contractility compared to CH (lower LVEF [β-coefficient = −3.2; 95% confidence interval (CI) −5.4, −1.1%] and ratio of systolic blood pressure to end-systolic volume [β-coefficient = −1.0; 95% CI −1.5, −0.5 mmHg/ml]). EH was also associated with increased LV compliance compared to CH (LV end-diastolic volume at an idealized LV end-diastolic pressure of 20 mmHg [EDV20] β-coefficient = 14.2;95% CI 9.4, 19.1 ml). Despite these differences, EH and CH had similarly elevated cardiac filling pressures and equivalent adverse outcomes. In conclusion, the presence of EH denotes a distinct subset of HFpEF that is pathophysiologically similar to HF with reduced EF (HFrEF), and may benefit from HFrEF therapy.
PMCID: PMC3788852  PMID: 23810323
heart failure with preserved ejection fraction; left ventricular hypertrophy; cardiac remodeling; echocardiography; outcomes
PLoS ONE  2015;10(3):e0120300.
Left ventricular hypertrophy (LVH) was suggested to be an important risk factor for hypertensive vascular complications. Previous studies had also shown that red cell distribution width (RDW) was associated with morbidity and mortality of cardiovascular disease. However, few have yet investigated possible association between RDW and LVH. The aim of the present study was to evaluate the relationship between LVH and RDW levels in hypertensive patients.
Physical examination, laboratory tests and echocardiography were conducted in 330 untreated newly diagnosed hypertensive patients attending the cardiology consultation unit at the Anzhen Hospital of Beijing. The multivariate logistic regression model was used to verify the independent association between RDW and LVH.
174 patients without LVH and 156 patients with LVH were rolled in the study. The patients with LVH had higher mean SBP, albumin to creatinine ratio, total cholesterol, RDW and fasting glucose compared with non-LVH group. The mean HDL-cholesterol level was significantly lower in patients with LVH than patients without LVH. The multiple logistic regression model suggested that patients with a higher RDW level were more likely to be LVH (OR=2.187, 95%CI: 1.447-3.307, P<0.001). Other predictive factors for LVH were mean SBP, serum creatinine, glucose level. The receiver operating characteristics (ROC) curves indicated area under the curve was 0.688(95%CI: 0.635-0.737, P<0.001) with a cut-off value of 12.9, the RDW predicted LVH status among hypertensive patients with a sensitivity of 72.4% and a specificity of 60.3%.
The higher RDW level was observed in the LVH group compared with the non-LVH group. RDW might be associated with LVH in hypertensive patients. These data highlight the role of RDW as a predictor of organ damage in essential hypertensive patients.
PMCID: PMC4368702  PMID: 25793884
PLoS ONE  2012;7(4):e35534.
Background and Aims
Electrocardiography (ECG) is the most widely used initial screening test for the assessment of left ventricular hypertrophy (LVH), an independent predictor of cardiovascular mortality in patients with end-stage renal disease (ESRD). However, traditional ECG criteria based only on voltage to detect LVH have limited clinical utility for the detection of LVH because of their poor sensitivity.
This prospective observational study was undertaken to compare the prognostic significance of commonly used ECG criteria for LVH, namely Sokolow-Lyon voltage (SV) or voltage-duration product (SP) and Cornell voltage (CV) or voltage-duration product (CP) criteria, and to investigate the association between echocardiographic LV mass index (LVMI) and ECG-LVH criteria in ESRD patients, who consecutively started maintenance hemodialysis (HD) between January 2006 and December 2008.
A total of 317 patients, who underwent both ECG and echocardiography, were included. Compared to SV and CV criteria, SP and CP criteria, respectively, correlated more closely with LVMI. In addition, CP criteria provided the highest positive predictive value for echocardiographic LVH. The 5-year cardiovascular survival rates were significantly lower in patients with ECG-LVH by each criterion. In multivariate analyses, echocardiographic LVH [adjusted hazard ratio (HR): 11.71; 95% confidence interval (CI): 1.57–87.18; P = 0.016] and ECG-LVH by SP (HR: 3.43; 95% CI: 1.32–8.92; P = 0.011) and CP (HR: 3.07; 95% CI: 1.16–8.11; P = 0.024) criteria, but not SV and CV criteria, were significantly associated with cardiovascular mortality.
The product of QRS voltage and duration is helpful in identifying the presence of LVH and predicting cardiovascular mortality in incident HD patients.
PMCID: PMC3328457  PMID: 22530043
PLoS Medicine  2012;9(6):e1001251.
In a prospective study, Craig Cohen and colleagues investigate the association between bacterial vaginosis and the risk of female-to-male HIV-1 transmission.
Bacterial vaginosis (BV), a disruption of the normal vaginal flora, has been associated with a 60% increased risk of HIV-1 acquisition in women and higher concentration of HIV-1 RNA in the genital tract of HIV-1–infected women. However, whether BV, which is present in up to half of African HIV-1–infected women, is associated with an increase in HIV-1 transmission to male partners has not been assessed in previous studies.
Methods and Findings
We assessed the association between BV on female-to-male HIV-1 transmission risk in a prospective study of 2,236 HIV-1–seropositive women and their HIV-1 uninfected male partners from seven African countries from a randomized placebo-controlled trial that enrolled heterosexual African adults who were seropositive for both HIV-1 and herpes simplex virus (HSV)-2, and their HIV-1–seronegative partners. Participants were followed for up to 24 months; every three months, vaginal swabs were obtained from female partners for Gram stain and male partners were tested for HIV-1. BV and normal vaginal flora were defined as a Nugent score of 7–10 and 0–3, respectively. To reduce misclassification, HIV-1 sequence analysis of viruses from seroconverters and their partners was performed to determine linkage of HIV-1 transmissions. Overall, 50 incident HIV-1 infections occurred in men in which the HIV-1–infected female partner had an evaluable vaginal Gram stain. HIV-1 incidence in men whose HIV-1–infected female partners had BV was 2.91 versus 0.76 per 100 person-years in men whose female partners had normal vaginal flora (hazard ratio 3.62, 95% CI 1.74–7.52). After controlling for sociodemographic factors, sexual behavior, male circumcision, sexually transmitted infections, pregnancy, and plasma HIV-1 RNA levels in female partners, BV was associated with a greater than 3-fold increased risk of female-to-male HIV-1 transmission (adjusted hazard ratio 3.17, 95% CI 1.37–7.33).
This study identified an association between BV and increased risk of HIV-1 transmission to male partners. Several limitations may affect the generalizability of our results including: all participants underwent couples HIV counseling and testing and enrolled in an HIV-1 prevention trial, and index participants had a baseline CD4 count ≥250 cells/mm3 and were HSV-2 seropositive. Given the high prevalence of BV and the association of BV with increased risk of both female HIV-1 acquisition and transmission found in our study, if this association proves to be causal, BV could be responsible for a substantial proportion of new HIV-1 infections in Africa. Normalization of vaginal flora in HIV-1–infected women could mitigate female-to-male HIV-1 transmission.
Trial Registration: NCT00194519
Please see later in the article for the Editors' Summary
Editors' Summary
Since the first reported case of AIDS in 1981, the number of people infected with HIV, the virus that causes AIDS, has risen steadily. By the end of 2010, 34 million people were living with HIV/AIDS. At the beginning of the epidemic more men than women were infected with HIV. Now, however, 50% of all adults infected with HIV are women and in sub-Saharan Africa, where two-thirds of HIV-positive people live, women account for 59% of people living with HIV. Moreover, among 15–24 year-olds, women are eight times more likely than men to be HIV-positive. This pattern of infection has developed because most people in sub-Saharan Africa contract HIV through unprotected heterosexual sex. The risk of HIV transmission for both men and women in Africa and elsewhere can be reduced by abstaining from sex, by only having one or a few partners, by always using condoms, and by male circumcision. In addition, several studies suggest that antiretroviral therapy (ART) greatly reduces HIV transmission.
Why Was This Study Done?
Unfortunately, in sub-Saharan Africa, only about a fifth of HIV-positive people are currently receiving ART, which means that there is an urgent need to find other effective ways to reduce HIV transmission in this region. In this prospective cohort study (a type of study that follows a group of people for some time to see which personal characteristics are associated with disease development), the researchers investigate whether bacterial vaginosis—a condition in which harmful bacteria disrupt the normal vaginal flora—increases the risk of female-to-male HIV transmission among African couples. Bacterial vaginosis, which is extremely common in sub-Saharan Africa, has been associated with an increased risk of HIV acquisition in women and induces viral replication and shedding in the vagina in HIV-positive women, which may mean that HIV-positive women with bacterial vaginosis are more likely to transmit HIV to their male partners than women without this condition. If this is the case, then interventions that reduce the incidence of bacterial vaginosis might be valuable HIV prevention strategies.
What Did the Researchers Do and Find?
The researchers analyzed data collected from 2,236 heterosexual African couples enrolled in a clinical trial (the Partners in Prevention HSV/HIV Transmission Study) whose primary aim was to investigate whether suppression of herpes simplex virus infection could prevent HIV transmission. In all the couples, the woman was HIV-positive and the man was initially HIV-negative. The female partners were examined every three months for the presence of bacterial vaginosis and the male partners were tested regularly for HIV infection. The researchers also determined whether the men who became HIV-positive were infected with the same HIV strain as their partner to check that their infection had been acquired from this partner. The HIV incidence in men whose partners had bacterial vaginosis was 2.9 per 100 person-years (that is, 2.9 out of every 100 men became HIV-positive per year) whereas the HIV incidence in men whose partners had a normal vaginal flora was 0.76 per 100 person-years. After controlling for factors that might affect the risk of HIV transmission such as male circumcision and viral levels in female partner's blood, the researchers estimated that bacterial vaginosis was associated with a 3.17-fold increased risk of female-to-male HIV transmission in their study population.
What Do These Findings Mean?
These findings suggest that HIV-positive African women with bacterial vaginosis are more than three times as likely to transmit HIV to their male partners as those with a normal vaginal flora. It is possible that some unknown characteristic of the men in this study might have increased both their own risk of HIV infection and their partner's risk of bacterial vaginosis. Nevertheless, because bacterial vaginosis is so common in Africa (half of the women in this study had bacterial vaginosis at least once during follow-up) and because this condition is associated with both female HIV acquisition and transmission, these findings suggest that bacterial vaginosis could be responsible for a substantial proportion of new HIV infections in Africa. Normalization of vaginal flora in HIV-infected women by frequent presumptive treatment with antimicrobials (treatment with a curative dose of antibiotics without testing for bacterial vaginosis) or possibly by treatment with probiotics (live “good” bacteria) might, therefore, reduce female-to-male HIV transmission in sub-Saharan Africa.
Additional Information
Please access these Web sites via the online version of this summary at
Information is available from the US National Institute of Allergy and infectious diseases on all aspects of HIV infection and AIDS and on bacterial vaginosis
The US Centers for Disease Control and Prevention has information on all aspects of HIV/AIDS, including specific information about HIV/AIDS and women; it also has information on bacterial vaginosis (in English and Spanish)
NAM/aidsmap provides basic information about HIV/AIDS, and summaries of recent research findings on HIV care and treatment, and information on bacterial vaginosis and HIV transmission (in several languages)
Information is available from Avert, an international AIDS nonprofit group on many aspects of HIV/AIDS, including detailed information on HIV and AIDS prevention, on women, HIV and AIDS and on HIV/AIDS in Africa (in English and Spanish); personal stories of women living with HIV are available; the website Healthtalkonline also provides personal stories about living with HIV
More information about the Partners in Prevention HSV/HIV Transmission Study is available
PMCID: PMC3383741  PMID: 22745608
BioMed Research International  2014;2014:603459.
Left ventricular hypertrophy (LVH) is frequently observed in chronic dialysis patients and is also highly prevalent in kidney transplant recipients. This study evaluates the impact of long-functioning hemodialysis vascular access on LVH in single center cohort of kidney transplant recipients. 162 patients at 8.7 ± 1.8 years after kidney transplantation were enrolled. Echocardiography, carotid ultrasound, and assessment of pulse wave velocity were performed. LVH was defined based on left ventricular mass (LVM) indexed for body surface area (BSA) and height2.7. There were 67 patients with and 95 without patent vascular access. Both study groups were comparable with respect to gender, age, duration of dialysis therapy, and time after transplantation, kidney graft function, and cardiovascular comorbidities. Patients with patent vascular access were characterized by significantly elevated LVM and significantly greater percentage of LVH, based on LVMI/BSA (66.7 versus 48.4%, P = 0.02). OR for LVH in patients with patent vascular access was 2.39 (1.19–4.76), P = 0.01. Regression analyses confirmed an independent contribution of patent vascular access to higher LVM and increased prevalence of LVH. We concluded that long-lasting patent hemodialysis vascular access after kidney transplantation is associated with the increased prevalence of LVH in kidney transplant recipients.
PMCID: PMC3925527  PMID: 24616896
Left ventricular hypertrophy (LVH) is prevalent in patients with type 2 diabetes mellitus (T2DM). Recent studies show that an increase in albumin-adjusted serum calcium level is associated with an elevated risk of T2DM. We speculate that increased serum calcium levels in T2DM patients are related to LVH prevalence.
In this echocardiographic study, 833 normocalcemia and normophosphatemia patients with T2DM were enrolled. The associations between serum calcium and metabolic parameters, left ventricular mass index (LVMI), as well as the rate of LVH were examined using bivariate linear correlation, multivariate linear regression and logistic regression, respectively. The predictive performance of serum calcium for LVH was evaluated using the area under the receiver operating characteristic curve (AUC).
Patients with LVH have significantly higher serum calcium than those without LVH. Serum calcium was positively associated with total cholesterol, triglycerides, low-density lipoprotein cholesterol, serum uric acid, HOMA-IR and fasting plasma glucose. Multivariate linear regression analysis demonstrated that serum calcium was independently associated with LVMI (p < 0.001). In comparison with patients in the lowest serum calcium quartile, the odds ratio (OR) for LVH in patients in the highest quartile was 2.909 (95% CI 1.792-4.720; p < 0.001). When serum calcium was analyzed as a continuous variable, per 1 mg/dl increase, the OR (95% CI) for LVH was [2.400 (1.552-3.713); p < 0.001]. Serum calcium can predict LVH (AUC = 0.617; 95% CI (0.577-0.656); p < 0.001).
Albumin-adjusted serum calcium is associated with an increased risk of LVH in patients with T2DM.
PMCID: PMC4422420  PMID: 25924883
Calcium; Left ventricular hypertrophy; Type 2 diabetes
BMC Research Notes  2014;7:45.
Left ventricular hypertrophy (LVH) is an independent cardiovascular risk factor in patients with essential hypertension. The main objective of this study was to assess the echocardiographic prevalence of left ventricular hypertrophy in patients with hypertension, its risk factors and effect of antihypertensive drugs on its prevalence.
A hospital based cross sectional study was conducted on 200 hypertensive patients on treatment in southwest Ethiopia. A pretested structured questionnaire was used to collect data from participants and their clinical records. Blood pressure and anthropometric measurements were taken according to recommended standards. Left ventricular mass was measured by transthoracic echocardiography. Associations between categorical variables were assessed using chi-square test and odds ratio with 95% confidence interval. Logistic regression model was done to identify risks factors of LVH. P values of < 0.05 were considered as statistically significant.
The mean age, systolic blood pressure, diastolic blood pressure and body mass index were 55.7 ± 11.3 years, 139.2 ± 7.7 mmHg, 89.2 ± 5.7 mmHg and 24.2 ± 3.4 Kg/m2 respectively. The overall prevalence of LVH among these study subjects was 52%. Age ≥50 years (OR: 3.49, 95% CI 1.33-9.14, P = 0.011), female gender (OR: 7.69, 95% CI 3.23-20.0, P < 0.001), systolic blood pressure ≥140 mmHg (OR: 2.85, 95% CI 1.27-6.41, P = 0.011), and duration of hypertension (OR: 3.59, 95% CI 1.47-8.76, P = 0.005) were independent predictors of left ventricular hypertrophy. Angiotensin converting enzyme (ACE) inhibitors were the only antihypertensive drugs associated with lower risk of left ventricular hypertrophy (OR: 0.08, 95% CI 0.03-0.19, p < 0.001).
Left ventricular hypertrophy was found to be highly prevalent in hypertensive patients in Ethiopia. ACE inhibitors were the only antihypertensive drugs associated with reduced risk of LVH. We thus recommend strategies to early detect and treat hypertension and to timely screen for LVH among patients with hypertension. Multicenter prospective studies in Africa settings would be ideal to identify the best antihypertensive agents in black Africans.
PMCID: PMC3900673  PMID: 24444396
Hypertension; Left ventricular hypertrophy; Cardiovascular disease; Angiotensin converting enzyme inhibitors; Ethiopia; Africa
American journal of hypertension  2010;23(7):767-774.
African-Americans with hypertension are susceptible to left ventricular hypertrophy (LVH). Serum osteoprotegerin level has been reported to be associated with LVH. We investigated the association of osteoprotegerin with LV mass (LVM) in 898 African-Americans with hypertension (mean age 65 years, 71% women).
Osteoprotegerin levels were measured in serum by an immunoassay and log-transformed for analyses. LVM index (LVMi; LVM/height2.7) was estimated using M-mode echocardiography. Linear regression analyses using generalized estimating equations were used to assess the association of osteoprotegerin with LVMi.
Serum osteoprotegerin was correlated with LVMi (r = 0.21; P < 0.0001), an estimated increase in LVMi of 5.05 (95% confidence interval 2.93, 7.17) g/m2.7 in the highest compared to the lowest osteoprotegerin quartile. This association remained statistically significant after adjustment for conventional cardiovascular risk factors (age, sex, body mass index (BMI), history of smoking, diabetes, systolic blood pressure (BP), total and high-density lipoprotein cholesterol), estimated renal function, history of myocardial infarction and stroke, lifestyle factors (physical activity score, years of education, amount of alcohol consumption), medications (aspirin, antihypertensives, statins, estrogens), and C-reactive protein (CRP) (P = 0.02). Additionally, osteoprotegerin was correlated with early/atrial (E/A) ratio (r = −0.16; P < 0.0001), LV mean wall thickness (r = 0.17; P < 0.0001) and relative wall thickness (r = 0.14; P < 0.0001) but not ejection fraction (r = 0.04; P = 0.24) or internal end-diastolic dimension (r = 0.02; P = 0.60).
In African-Americans with hypertension, a higher serum osteoprotegerin level is weakly but independently associated with a higher LVM.
PMCID: PMC2901868  PMID: 20339356
African-American; biomarker; blood pressure; cardiology; echocardiography; epidemiology; hypertension; hypertrophy; osteoprotegerin
To examine the prevalence of left ventricular hypertrophy (LVH) and LV remodeling patterns within Hispanic subgroups compared with non-Hispanic whites in the Multi-Ethnic Study of Atherosclerosis.
Hispanics are the largest and fastest growing ethnic minority in the United States but there are no data on LVH and LV geometry among Hispanic subgroups.
Cardiac magnetic resonance imaging was performed in 4309 men and women aged 45 to 84 years without clinical cardiovascular disease. Hispanics were categorized into subgroups based on self-reported ancestry. LVH was defined as the upper 95th percentile of indexed LV mass in a reference normotensive, non-diabetic, non-obese population, and LV remodeling according to the presence/absence of LVH and abnormal/normal LV mass to LV end-diastolic volume ratio.
Among Hispanic participants, 574 were of Mexican, 329 were of Caribbean, and 161 were of Central/South American origin. On unadjusted analysis, only Caribbean-origin Hispanics (PR 1.2 [95% CI, 1.03–1.4]) had greater prevalence of hypertension than non-Hispanic whites. Hispanic subgroups were more likely to have LVH than non-Hispanic whites after adjustment for hypertension and other covariates (Caribbean-origin Hispanics: OR 1.8 [95% CI 1.1–3.0]; Mexican-origin Hispanics: OR 2.2 [95% CI 1.4–3.3]; Central/South Americans: OR 1.5 [95% CI 0.7–3.1]). All Hispanic subgroups also had a higher prevalence of concentric and eccentric hypertrophy compared to non-Hispanic whites (P<0.001).
Caribbean-origin Hispanics had a higher prevalence of LVH and abnormal LV remodeling compared to non-Hispanic whites. A higher prevalence of LVH and abnormal LV remodeling was also observed among Mexican-origin Hispanics despite a lower prevalence of hypertension. Differences among Hispanic subgroups regarding LVH and LV remodeling should be taken into account when evaluating cardiovascular risk in this population.
PMCID: PMC2849669  PMID: 20117402
hypertension; hypertrophy; remodeling; epidemiology; Hispanics; magnetic resonance imaging
PLoS Medicine  2014;11(2):e1001608.
Alison Drake and colleagues conduct a systematic review and meta-analysis to estimate maternal HIV incidence during pregnancy and the postpartum period and to compare mother-to-child HIV transmission risk among women with incident versus chronic infection.
Please see later in the article for the Editors' Summary
Women may have persistent risk of HIV acquisition during pregnancy and postpartum. Estimating risk of HIV during these periods is important to inform optimal prevention approaches. We performed a systematic review and meta-analysis to estimate maternal HIV incidence during pregnancy/postpartum and to compare mother-to-child HIV transmission (MTCT) risk among women with incident versus chronic infection.
Methods and Findings
We searched PubMed, Embase, and AIDS-related conference abstracts between January 1, 1980, and October 31, 2013, for articles and abstracts describing HIV acquisition during pregnancy/postpartum. The inclusion criterion was studies with data on recent HIV during pregnancy/postpartum. Random effects models were constructed to pool HIV incidence rates, cumulative HIV incidence, hazard ratios (HRs), or odds ratios (ORs) summarizing the association between pregnancy/postpartum status and HIV incidence, and MTCT risk and rates. Overall, 1,176 studies met the search criteria, of which 78 met the inclusion criterion, and 47 contributed data. Using data from 19 cohorts representing 22,803 total person-years, the pooled HIV incidence rate during pregnancy/postpartum was 3.8/100 person-years (95% CI 3.0–4.6): 4.7/100 person-years during pregnancy and 2.9/100 person-years postpartum (p = 0.18). Pooled cumulative HIV incidence was significantly higher in African than non-African countries (3.6% versus 0.3%, respectively; p<0.001). Risk of HIV was not significantly higher among pregnant (HR 1.3, 95% CI 0.5–2.1) or postpartum women (HR 1.1, 95% CI 0.6–1.6) than among non-pregnant/non-postpartum women in five studies with available data. In African cohorts, MTCT risk was significantly higher among women with incident versus chronic HIV infection in the postpartum period (OR 2.9, 95% CI 2.2–3.9) or in pregnancy/postpartum periods combined (OR 2.3, 95% CI 1.2–4.4). However, the small number of studies limited power to detect associations and sources of heterogeneity.
Pregnancy and the postpartum period are times of persistent HIV risk, at rates similar to “high risk” cohorts. MTCT risk was elevated among women with incident infections. Detection and prevention of incident HIV in pregnancy/postpartum should be prioritized, and is critical to decrease MTCT.
Please see later in the article for the Editors' Summary
Editors' Summary
Worldwide, about 3.4 million children younger than 15 years old (mostly living in sub-Saharan Africa) are infected with HIV, the virus that causes AIDS by gradually destroying immune system cells, thereby leaving infected individuals susceptible to other serious infections. In 2012 alone, 230,000 children (more than 700 every day) were newly infected with HIV. Most HIV infections among children are the result of mother-to-child HIV transmission (MTCT) during pregnancy, delivery, or breastfeeding. The rate of MTCT (and deaths among HIV-positive pregnant women from complications related to HIV infection) can be greatly reduced by testing women for HIV infection during pregnancy (antenatal HIV testing), treating HIV-positive women with antiretroviral drugs (ARVs, powerful drugs that control HIV replication and allow the immune system to recover) during pregnancy, delivery, and breastfeeding, and giving ARVs to their newborn babies.
Why Was This Study Done?
The World Health Organization and the Joint United Nations Programme on HIV/AIDS (UNAIDS) have developed a global plan that aims to move towards eliminating new HIV infections among children by 2015 and towards keeping their mothers alive. To ensure the plan's success, the incidence of HIV (the number of new infections) among women and the rate of MTCT must be reduced by increasing ARV uptake by mothers and their infants for the prevention of MTCT. However, the risk of HIV infection among pregnant women and among women who have recently given birth (postpartum women) is poorly understood because, although guidelines recommend repeat HIV testing during late pregnancy or at delivery in settings where HIV infection is common, pregnant women are often tested only once for HIV infection. The lack of retesting represents a missed opportunity to identify pregnant and postpartum women who have recently acquired HIV and to prevent MTCT by initiating ARV therapy. In this systematic review (a study that uses predefined criteria to identify all the research on a given topic) and meta-analysis (a study that uses statistical methods to combine the results of several studies), the researchers estimate maternal HIV incidence during pregnancy and the postpartum period, and compare the risk of MTCT among women with incident (new) and chronic (long-standing) HIV infection.
What Did the Researchers Do and Find?
The researchers identified 47 studies (35 undertaken in Africa) that examined recent HIV acquisition by women during pregnancy and the 12-month postpartum period. They used random effects statistical models to estimate the pooled HIV incidence rate and cumulative HIV incidence (the number of new infections per number of people at risk), and the association between pregnancy/postpartum status and HIV incidence and MTCT risk and rates. The pooled HIV incidence rate among pregnant/postpartum women estimated from 19 studies (all from sub-Saharan Africa) that reported HIV incidence rates was 3.8/100 person-years. The pooled cumulative HIV incidence was significantly higher in African countries than in non-African countries (3.6% and 0.3%, respectively; a “significant” difference is one that is unlikely to arise by chance). In the five studies that provided suitable data, the risk of HIV acquisition was similar in pregnant, postpartum, and non-pregnant/non-postpartum women. Finally, among African women, the risk of MTCT was 2.9-fold higher during the postpartum period among those who had recently acquired HIV than among those with chronic HIV infection, and 2.3-fold higher during the pregnancy/postpartum periods combined.
What Do These Findings Mean?
These results suggest that women living in regions where HIV infection is common are at high risk of acquiring HIV infection during pregnancy and the postpartum period and that mothers who acquire HIV during pregnancy or postpartum are more likely to pass the infection on to their offspring than mothers with chronic HIV infections. However, the small number of studies included in this meta-analysis and the use of heterogeneous research methodologies in these studies may limit the accuracy of these findings. Nevertheless, these findings have important implications for the global plan to eliminate HIV infections in children. First, they suggest that women living in regions where HIV infection is common should be offered repeat HIV testing (using sensitive methods to enhance early detection of infection) during pregnancy and in the postpartum period to detect incident HIV infections, and should be promptly referred to HIV care and treatment. Second, they suggest that prevention of HIV transmission during pregnancy and postpartum should be prioritized, for example, by counseling women about the need to use condoms to prevent transmission during this period of their lives.
Additional Information
Please access these websites via the online version of this summary at
Information is available from the US National Institute of Allergy and Infectious Diseases on HIV infection and AIDS
NAM/aidsmap provides basic information about HIV/AIDS and summaries of recent research findings on HIV care and treatment
Information is available from Avert, an international AIDS charity, on many aspects of HIV/AIDS, including information on children and HIV/AIDS and on the prevention of mother-to-child transmission of HIV (in English and Spanish)
The 2013 UNAIDS World AIDS Day Report provides information about the AIDS epidemic and efforts to halt it; the 2013 UNAIDS Progress Report on the Global Plan provides information on progress towards eliminating new HIV infections among children; the UNAIDS Believe it. Do it website provides information about the campaign to support the UNAIDS global plan
Personal stories about living with HIV/AIDS, including stories from young people infected with HIV, are available through Avert, NAM/aidsmap, and Healthtalkonline
PMCID: PMC3934828  PMID: 24586123
PLoS Clinical Trials  2007;2(2):e10.
Assess efficacy of intermittent intravaginal metronidazole gel treatment in reducing frequency of bacterial vaginosis (BV).
Randomized, double-masked, placebo-controlled phase 3 trial.
Postnatal and family planning clinics of the Queen Elizabeth Central Hospital and two health centers in Blantyre, Malawi.
Nonpregnant HIV-uninfected and -infected women.
Intravaginal metronidazole treatment and placebo gels provided at baseline and every 3 mo for 1 y.
Outcome measures:
Primary: Cross-sectional and longitudinal comparisons of BV frequency at baseline, 1 mo after product dispensation (post-treatment evaluation [PTE]), and every quarterly visit. Secondary: Effect of treatment on BV clearance and recurrence.
Baseline: 842 HIV-uninfected and 844 HIV-infected women were enrolled. The frequency of BV at baseline in treatment and placebo arms, respectively, was 45.9% and 46.8% among HIV-uninfected women, and 60.5% and 56.9% among HIV-infected women. Primary outcomes: At the PTEs the prevalence of BV was consistently lower in treatment than placebo arms irrespective of HIV status. The differences were statistically significant mainly in HIV-uninfected women. Prevalence of BV was also reduced over time in both treatment and placebo arms. In a multivariable analysis that controlled for other covariates, the effect of intravaginal metronidazole treatment gel compared with placebo was not substantial: adjusted relative risk (RR) 0.90, 95% confidence interval (CI) 0.83–0.97 in HIV-uninfected women and adjusted RR 0.95, 95% CI 0.89–1.01 in HIV-infected women. Secondary outcomes: Intravaginal metronidazole treatment gel significantly increased BV clearance (adjusted hazard ratio [HR] 1.34, 95% CI 1.07–1.67 among HIV-uninfected women and adjusted HR 1.29, 95% CI 1.06–1.58 among HIV-infected women) but was not associated with decreased BV recurrence. Safety: No serious adverse events were related to use of intravaginal gels.
Intermittent microbicide treatment with intravaginal gels is an innovative approach that can reduce the frequency of vaginal infections such as BV.
Editorial Commentary
Background: Bacterial vaginosis (BV) results from a change in the normal balance of bacteria in the vaginal tract, and is very common. In pregnant women, it is associated with poorer outcomes in pregnancy, and is also linked with HIV transmission (although it is not certain that BV actually increases the chance of getting HIV—just because these two occur together it does not necessarily follow that one causes the other). BV can be treated with metronidazole tablets, although these can cause gut symptoms and should not be taken repeatedly. The researchers wanted to carry out a multiclinic–based trial to find out whether a metronidazole gel applied intermittently to the vagina (for five nights every three months) would reduce the frequency of BV among women in Malawi. HIV-infected and HIV-uninfected women, recruited from postnatal and family planning clinics, were randomized to receive either metronidazole gels, or equivalent placebo gels, every three months and were then followed up for 12 months. The primary outcome for the trial was the proportion of women with BV at each quarterly follow-up visit, and the researchers intended to compare this outcome between treatment arms at each visit and also to look at the overall changes over time among women receiving either metronidazole or placebo, looking separately at HIV-infected and HIV-uninfected women.
What this trial shows: In total 1,686 women took part in the trial (842 not infected with HIV, and 844 infected with HIV). The proportion of HIV-uninfected women with BV dropped by around 20% over the course of the trial, both in women using metronidazole and in those using placebo. However, when comparing the proportion of HIV-uninfected women with BV between the two arms of the trial, there did not seem to be a consistent effect: differences were statistically significant at some time points and not others. Among HIV-infected women, there was also a drop over the course of the trial in the proportion of women with BV, irrespective of whether they used metronidazole or placebo. Again, when comparing the rate of BV among HIV-infected women between study arms (metronidazole versus placebo), the researchers did not see a consistent trend; differences were statistically significant at some time points but not others. Overall, when comparing metronidazole and placebo in an analysis that controlled for other factors, the metronidazole gel seemed to show a small effect in reduction of BV among HIV-uninfected women, but no obvious effect among HIV-infected women.
Strengths and limitations: Strengths in the design of this trial include the sample size, which was appropriate to detect an important effect of the metronidazole gel (versus placebo) had one existed, and the randomization and blinding procedures, which were designed to minimize the chance that the trialists or women being enrolled could anticipate to which arm of the trial they might be assigned. A key limitation of this study, as the researchers acknowledge, is the absence of a “no treatment” study arm. The frequency of BV dropped over the course of the trial in women using the placebo gel, raising the possibility that the placebo actually has some effect on bacteria in the vagina. However, a trial with a “no treatment” arm would pose its own problems, since trialists and participants would then not be fully blinded as to their treatment status.
Contribution to the evidence: This trial adds data on the efficacy of metronidazole gel when used intermittently, and among women in the community who may or may not actually have BV. Previous studies have evaluated treatment with metronidazole among women who already have symptoms or a diagnosis of BV. The findings of this trial rule out a substantial effect of metronidazole gel, as compared to placebo gel, in reducing the frequency of BV in this setting.
PMCID: PMC1851729  PMID: 17318258

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