Prevalence of Triple-Negative Breast Cancer in India: Systematic Review and Meta-Analysis

Purpose There is considerable variation in prevalence rates of triple-negative breast cancer (TNBC) reported by various studies from India. We performed a systematic review and literature-based meta-analysis of these studies. Methods We searched databases of Medline, Scopus, EMBASE, and Web of Science for studies that reported on the prevalence of TNBC in India that were published between January 1, 1999, and December 31, 2015. We extracted relevant information from each study by using a standardized form. We pooled study-specific estimates by using random-effects meta-analysis to provide summary estimates. We explored sources of heterogeneity by using subgroup analyses and metaregression. Results Data were obtained from 17 studies that involved 7,237 patients with breast cancer. Overall combined prevalence of TNBC was 31% (95% CI, 27% to 35%). There was substantial heterogeneity across the studies (I2 of 91% [95% CI, 88% to 94%]; P \u3c .001) that was not explained by available study level characteristics, including study location, definition of human epidermal growth factor receptor 2 or estrogen receptor, mean age of participants, proportion of patients with premenopausal cancer, grade 3 disease, or tumor size \u3e 5 cm. Overall combined prevalence of hormone receptor–positive and human epidermal growth factor receptor 2–positive breast cancer was 48% (95% CI, 42% to 54%) and 27% (95% CI, 24% to 31%), respectively. There was no evidence of publication bias. Conclusion Prevalence of TNBC in India is considerably higher compared with that seen in Western populations. As many as as one in three women with breast cancer could have triple-negative disease. This finding has significant clinical relevance as it may contribute to poor outcomes in patients with breast cancer in India. Additional research is needed to understand the determinants of TNBC in India

Coronary artery calcification and plaque characteristics in people living with HIV: A systematic review and meta-analysis

Background Studies have reported that people living with HIV have higher burden of subclinical cardiovascular disease, but the data are not adequately synthesized. We performed meta-analyses of studies of coronary artery calcium and coronary plaque in people living with HIV. Methods and Results We performed systematic search in electronic databases, and data were abstracted in standardized forms. Study-specific estimates were pooled using meta-analysis. 43 reports representing 27 unique studies and involving 10 867 participants (6699 HIV positive, 4168 HIV negative, mean age 52 years, 86% men, 32% Black) were included. The HIV-positive participants were younger (mean age 49 versus 57 years) and had lower Framingham Risk Score (mean score 6 versus 18) compared with the HIV-negative participants. The pooled estimate of percentage with coronary artery calcium \u3e0 was 45% (95% CI, 43%-47%) for HIV-positive participants, and 52% (50%-53%) for HIV-negative participants. This difference was no longer significant after adjusting for difference in Framingham Risk Score between the 2 groups. The odds ratio of coronary artery calcium progression for HIV-positive versus -negative participants was 1.64 (95% CI, 0.91-2.37). The pooled estimate for prevalence of noncalcified plaque was 49% (95% CI, 47%-52%) versus 20% (95% CI, 17%-23%) for HIV-positive versus HIV-negative participants, respectively. Odds ratio for noncalcified plaque for HIV-positive versus -negative participants was 1.23 (95% CI, 1.08-1.38). There was significant heterogeneity that was only partially explained by available study-level characteristics. Conclusions People living with HIV have higher prevalence of noncalcified coronary plaques and similar prevalence of coronary artery calcium, compared with HIV-negative individuals. Future studies on coronary artery calcium and plaque progression can further elucidate subclinical atherosclerosis in people living with HIV

Lipoprotein(a) and the risk of vascular disease

Background: Lipoprotein(a) [Lp(a)] is composed of a low density-lipoprotein (LDL) particle and a glycoprotein molecule known as apolipoprotein(a) [apo(a)]. Apo(a) exists in several differently-sized isoforms and is responsible for the unique properties of Lp(a). Although Lp(a) has been known for the past 40 years its relationship with coronary heart disease (CHD) has not been characterized in sufficient detail. Whether Lp(a) causes CHD is not clear. Furthermore, the role of apo(a) isoform variation and other sources of Lp(a) heterogeneity (e.g., level of oxidized phospholipids) in Lp(a)-disease association has not been determined. Objectives: To characterize in detail the association of circulating Lp(a) levels with the risk CHD To assess the nature of Lp(a)-CHD association using an integrative genetic study To explore the role of Lp(a) heterogeneity in its association with CHD Data sources: 1. The Emerging Risk Factors Collaboration (ERFC) database (36 studies, 127,000 participants) 2. The European Prospective Investigation of Cancer – Norfolk (EPIC-Norfolk) study (2200CHD cases, 2200 controls) 3. The Pakistani Risk of Myocardial Infarction Study (PROMIS) (1800 MI cases and 1800 controls) 4. Systematic quantitative reviews of published epidemiological studies Results: ERFC data - Analyses of cross-sectional data on up to 127,000 participants (predominantly of European descent) demonstrated that Lp(a) is generally not strongly correlated with known CHD risk factors. Weakly positive correlations were observed with LDL-cholesterol, apolipoprotein B100 and fibrinogen. Levels were over 2-fold higher in Blacks compared to Whites. Analyses of available data on repeat measurements in 6600 participants demonstrated that Lp(a) values have very high long-term within-person consistency (regression dilution ratio ~ 0.9). Outcome data involved 9300 incident CHD events, 1900 ischaemic strokes and 8100 nonvascular deaths. The risk ratio for CHD per 1SD higher Lp(a) concentration, adjusted for age, sex, lipids and other conventional vascular risk factors, was 1.13 (95% CI, 1.09-1.18). The corresponding risk ratios for ischaemic stroke and nonvascular death were 1.10 (1.02 – 1.18) and 1.01 (0.98-1.05), respectively. Data were too limited to assess association in nonwhites. PROMIS data – the adjusted odds ratio for MI in South Asians was comparable to that of Europeans. EPIC-Norfolk genetic data - The odds ratio for CHD per 1-SD higher Lp(a) concentration, after adjustment for cardiovascular risk factors, was 1.37 (1.20-1.56). Tagging SNPs rs10455872 and rs11751605 (minor allele frequency: 8% and 18%, respectively) were associated with 207% (95% CI, 188 - 227%) and 38% (31 - 46%) higher Lp(a) concentrations per copy of minor allele, respectively. These SNPs accounted for 35% and 5% of the variation in circulating Lp(a) levels, respectively, and were associated with an odds ratio for CHD of 1.34 (1.14-1.58) and 1.17 (1.04-1.33), respectively. The observed SNP-CHD associations were consistent with expected odds ratios corresponding to the Lp(a) effect of the SNPs. Systematic reviews – meta-analysis of published data from 40 studies (11,300 cases, 47,000 controls) demonstrated that people with smaller apo(a) isoforms have about a 2-fold higher risk of CHD or ischemic stroke than those with larger isoforms. Meta-analysis of published data from 10 studies (1500 cases, 10,200 controls) showed that people in the top third of baseline distribution of oxidized LDL levels have a 1.8-fold higher risk of CHD than those in bottom third. EPIC-Norfolk biomarker data – Levels of oxidized phospholipids were strongly correlated with Lp(a) concentration (r = 0.7, p-value < 0.0001). One SD higher concentration of oxidized phospholipids was associated with an adjusted odds ratio for CHD of 1.31 (1.15-1.49). The risk ratio was no longer significant after adjustment for Lp(a) concentration (1.08; 95% CI, 0.91-1.29). Conclusion: Lp(a) concentration is specifically, continuously and independently associated with the risk of ischaemic vascular outcomes. Available evidence supports the causal role of the particle in CHD. Lp(a) appears to induce vascular damage through causal mechanisms that involve apo(a) isoforms and oxidized phospholipids. A comprehensive study of markers of Lp(a) heterogeneity should help to understand the full impact of Lp(a) on cardiovascular diseases. In addition, further study is needed in nonwhites to assess the relevance of the factor to vascular disease risk in these populations.EThOS - Electronic Theses Online ServiceGates Cambridge Trust, Overseas Research StudentshipGBUnited Kingdo

Particulate matter 2.5, metropolitan status, and heart failure outcomes in US counties: A nationwide ecologic analysis.

The relationship between particulate matter with a diameter of 2.5 micrometers or less (PM2.5) and heart failure (HF) hospitalizations and mortality in the US is unclear. Prior studies are limited to studying the effects of daily PM2.5 exposure on HF hospitalizations in specific geographic regions. Because PM2.5 can vary by geography, this study examines the effects of annual ambient PM2.5 exposure on HF hospitalizations and mortality at a county-level across the US. A cross-sectional analysis of county-level ambient PM2.5 concentration, HF hospitalizations, and HF mortality across 3135 US counties nationwide was performed, adjusting for county-level demographics, socioeconomic factors, comorbidities, and healthcare-associated behaviors. There was a moderate correlation between county PM2.5 and HF hospitalization among Medicare beneficiaries (r = 0.41) and a weak correlation between county PM2.5 and HF mortality (r = 0.08) (p-values < 0.01). After adjustment for various county level covariates, every 1 ug/m3 increase in annual PM2.5 concentration was associated with an increase of 0.51 HF Hospitalizations/1,000 Medicare Beneficiaries and 0.74 HF deaths/100,000 residents (p-values < 0.05). In addition, the relationship between PM2.5 and HF hospitalizations was similar when factoring in metropolitan status of the counties. In conclusion, increased ambient PM2.5 concentration level was associated with increased incidence of HF hospitalizations and mortality at the county level across the US. This calls for future studies exploring policies that reduce ambient particulate matter pollution and their downstream effects on potentially improving HF outcomes

Epidemiology of prediabetes and diabetes in Namibia, Africa: a multilevel analysis.

BACKGROUND Diabetes is a leading cause of progressive morbidity and early mortality worldwide. Little is known on the burden of diabetes and pre-diabetes in Namibia, a Sub-Saharan African (SSA) country that is undergoing a demographic transition. METHODS We estimated the prevalence and correlates of diabetes (defined as fasting [capillary] blood glucose [FBG] >126 mg/dL) and prediabetes (defined by World Health Organization [WHO] and American Diabetes Association [ADA] criteria [FBG 110-125 mg/dL and 100-125 mg/dL, respectively]) in a random sample of 3278 participants aged 35-64 from the 2013 Namibia Demographic and Health Survey. RESULTS The prevalence of diabetes was 5.1% (95% Confidence Interval [CI]: 4.2-6.2), with no evidence of gender differences (p=0.45). The prevalence of prediabetes was 6.8% (5.8-8.0) and 20.1% (18.4-21.9) using WHO and ADA criteria, respectively. Male sex, older age, higher body mass index (BMI) and occupation independently increased the odds of diabetes in Namibia, while higher BMI was associated with the higher odds of prediabetes and residing in household categorized as middle wealth index were associated with lower odds of prediabetes (Adjusted odds ratio [aOR] = 0.71; 95% Credible Interval [CrI] = 0.46-0.99). There was significant clustering of prediabetes and diabetes at the community-level. CONCLUSIONS One in five adult Namibians has prediabetes by ADA criteria. Resources should be invested at the community level to promote efforts to prevent progression of this disease and its complications. This article is protected by copyright. All rights reserved

Electromagnetic Interference from Left Ventricular Assist Device (LVAD) Inhibiting the Pacing Function of an Implantable Cardioverter-Defibrillator (ICD) Device

There is an increasing prevalence of patients with concomitant implantable cardioverter-defibrillators (ICDs) and left ventricular devices (LVADs). The potential for negative interactions between these continually evolving technologies is a valid concern. Previously reported interactions include inappropriate ICD therapy and interference with ICD telemetry function. Understanding the nature of such interactions and developing a comprehensive strategy to approach such situations are important. In this report, we describe a case of electromagnetic interference from LVAD inhibiting the pacing function of an ICD that was corrected by reprograming the device. We would encourage investigators to review patients with ICD and LVAD in their institutions in order to help assess the frequency and nature of these and other interactions

Association of cumulative social risk with mortality and adverse cardiovascular disease outcomes

Abstract Background Quantifying the cumulative effect of social risk factors on cardiovascular disease (CVD) risk can help to better understand the sources of disparities in health outcomes. Method and results Data from the Heart Strategies Concentrating on Risk Evaluation (HeartSCORE) study were used to create an index of cumulative social risk (CSR) and quantify its association with incident CVD and all-cause mortality. CSR was defined by assigning a score of 1 for the presence of each of 4 social factors: i) racial minority status (Black race), ii) single living status, iii) low income, and iv) low educational level. Hazard ratios (HRs) were computed using Cox-regression models, adjusted for CVD risk factors. Over a median follow-up period of 8.3 years, 127 incident events were observed. The incidence of the primary outcome for subgroups of participants with 0, 1, and ≥2 CSR scores was 5.31 (95% CI, 3.40–7.22), 10.32 (7.16–13.49) and 17.80 (12.94–22.67) per 1000 person-years, respectively. Individuals with CSR score of 1 had an adjusted HR of 1.85 (1.15–2.97) for incident primary outcomes, compared to those with score of 0. The corresponding HR for individuals with CSR score of 2 or more was 2.58 (1.60–4.17). Conclusion An accumulation of social risk factors independently increased the likelihood of CVD events and deaths in a cohort of White and Black individuals

Prevalence of hypertension in older people in Africa: a systematic review and meta-analysis

Objective: The prevalence of hypertension in older people living on the African continent has not been comprehensively assessed. We aimed to provide accurate estimates of hypertension prevalence and variations by major predictive characteristics in this population to assist prevention and monitoring efforts. Methods: For this systematic review and meta-analysis, we searched major electronic databases for population-based studies on hypertension prevalence reported from 1 January 2000 to 5 March 2016. Two independent reviewers undertook quality assessment and data extraction. We stabilized the variance of study-specific prevalence with the Freeman-Tukey single arcsine transformation before pooling the data with random-effects models. Results: From the 2864 citations identified via searches, 91 studies providing 156 separate data contributions involving 54 198 individuals met the inclusion criteria. The overall prevalence of hypertension was 55.2% (95% confidence interval 53.1–57.4). Prevalence was higher in urban compared with rural settings [59.0% (55.3–62.6) vs. 48.0% (43.8–52.3), P 94%, P < 0.001) and no evidence of publication bias. Conclusion: Our findings highlight the need to implement timely and aggressive strategies for prevention, detection, and control of hypertension among older people in Afric