Effect of Walnut-Enriched Restructured Meat in the Antioxidant Status of Overweight/Obese Senior Subjects with at Least One Extra CHD-Risk Factor

2007 ◽  
Vol 26 (3) ◽  
pp. 225-232 ◽  
Author(s):  
Amaia Canales ◽  
Juana Benedí ◽  
Meritxell Nus ◽  
Josana Librelotto ◽  
Jose M Sánchez-Montero ◽  
...  
Keyword(s):  
Risk Factor ◽  
Antioxidant Status ◽  
Chd Risk ◽  
Restructured Meat

Cardiovascular Risk in Perimenopausal Women

2019 ◽  
Vol 17 (6) ◽  
pp. 591-594 ◽  
Author(s):  
John C. Stevenson ◽  
Sophia Tsiligiannis ◽  
Nick Panay
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Ovarian Function ◽  
Density Lipoprotein ◽  
Premenopausal Women ◽  
Therapeutic Interventions ◽  
Additional Risk Factor ◽  
Chd Risk ◽  
Perimenopausal Women ◽  
Chd Risk Factors

Cardiovascular disease, and particularly coronary heart disease (CHD), has a low incidence in premenopausal women. Loss of ovarian hormones during the perimenopause and menopause leads to a sharp increase in incidence. Although most CHD risk factors are common to both men and women, the menopause is a unique additional risk factor for women. Sex steroids have profound effects on many CHD risk factors. Their loss leads to adverse changes in lipids and lipoproteins, with increases being seen in low density lipoprotein (LDL) cholesterol and triglycerides, and decreases in high density lipoprotein (HDL) cholesterol. There is a reduction in insulin secretion and elimination, but increases in insulin resistance eventually result in increasing circulating insulin levels. There are changes in body fat distribution with accumulation in central and visceral fat which links to the other adverse metabolic changes. There is an increase in the incidence of hypertension and of type 2 diabetes mellitus, both major risk factors for CHD. Oestrogens have potent effects on blood vessels and their loss leads to dysfunction of the vascular endothelium. All of these changes result from loss of ovarian function contributing to the increased development of CHD. Risk factor assessment in perimenopausal women is recommended, thereby permitting the timely introduction of lifestyle, hormonal and therapeutic interventions to modify or reverse these adverse changes.

Pitavastatin 4 mg vs. Pravastatin 40 mg in HIV Dyslipidemia: Post-Hoc Analysis of the INTREPID Trial Based on the Independent CHD Risk Factor of Age†

2014 ◽  
Vol 8 (3) ◽  
pp. 331-332 ◽  
Author(s):  
Craig A. Sponseller ◽  
Masaya Tanahashi ◽  
Hideki Suganami ◽  
Judith A. Aberg
Keyword(s):  
Risk Factor ◽  
Post Hoc Analysis ◽  
Chd Risk ◽  
Post Hoc

Longitudinal Evolution of Risk of Coronary Heart Disease in Systemic Lupus Erythematosus

2012 ◽  
Vol 39 (5) ◽  
pp. 968-973 ◽  
Author(s):  
IGOR KARP ◽  
MICHAL ABRAHAMOWICZ ◽  
PAUL R. FORTIN ◽  
LOUISE PILOTE ◽  
CAROLYN NEVILLE ◽  
...  
Keyword(s):  
Risk Factors ◽  
Systemic Lupus Erythematosus ◽  
Coronary Heart Disease ◽  
Risk Factor ◽  
Heart Disease ◽  
Blood Glucose ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Chd Risk ◽  
Over Time

Objective.To produce evidence on the longitudinal evolution of risk factors for coronary heart disease (CHD) in patients with systemic lupus erythematosus (SLE).Methods.Based on data for 115 patients from the Montreal General Hospital Lupus Clinic (1971–2003) and for 4367 control subjects from the Framingham Offspring Study (1971–1994), we investigated the temporal evolution of total serum cholesterol, systolic blood pressure (SBP), body mass index (BMI), blood glucose, and estimated risk for CHD (reflecting the balance of changes in different risk factors). In analyses limited to patients with SLE, we assessed the effect of SLE duration on each risk factor, adjusting for age, calendar time, sex, baseline level of the risk factor, and medication use. Next, we assessed how the adjusted difference in the values of the risk factors between SLE and controls changes over time.Results.Among patients with SLE, longer disease duration was independently associated with higher SBP and blood glucose levels. Compared with controls, these patients appeared to have accelerated rates of increase in total cholesterol, blood glucose, and overall estimated CHD risk. The rate of increase in BMI was lower in patients with SLE than in controls.Conclusion.Elevated CHD risk in patients with SLE appears to be at least partially mediated by accelerated increases in some CHD risk factors, longitudinal trajectories of which increasingly diverge over time from those of population controls.

scholarly journals Candidate Gene Genotypes, Along with Conventional Risk Factor Assessment, Improve Estimation of Coronary Heart Disease Risk in Healthy UK Men

2007 ◽  
Vol 53 (1) ◽  
pp. 8-16 ◽  
Author(s):  
Steve E Humphries ◽  
Jackie A Cooper ◽  
Philippa J Talmud ◽  
George J Miller
Keyword(s):  
Coronary Heart Disease ◽  
Risk Factor ◽  
Heart Disease ◽  
Disease Risk ◽  
Uncoupling Protein ◽  
False Positive Rate ◽  
Conventional Risk Factor ◽  
Risk Estimates ◽  
Chd Risk ◽  
Genotype Information

Abstract Background: One of the aims of cardiovascular genetics is to test the efficacy of the use of genetic information to predict cardiovascular risk. We therefore investigated whether inclusion of a set of common variants in candidate genes along with conventional risk factor (CRF) assessment enhanced coronary heart disease (CHD)-risk algorithms. Methods: We followed middle-aged men in the prospective Northwick Park Heart Study II (NPHSII) for 10.8 years and analyzed complete trait and genotype information available on 2057 men (183 CHD events). Results: Of the 12 genes previously associated with CHD risk, in stepwise multivariate risk analysis, uncoupling protein 2 (UCP2; P = 0.0001), apolipoprotein E (APOE; P = 0.0003), lipoprotein lipase (LPL; P = 0.007), and apolipoprotein AIV (APOA4; P = 0.04) remained in the model. Their combined area under the ROC curve (AROC) was 0.62 (0.58–0.66) [12.6% detection rate for a 5% false positive rate (DR5)]. The AROC for the CRFs age, triglyceride, cholesterol, systolic blood pressure, and smoking was 0.66 (0.61–0.70) (DR5 = 14.2%). Combining CRFs and genotypes significantly improved discrimination (P = 0.001). Inclusion of previously demonstrated interactions of smoking with LPL, interleukin-6 (IL6), and platelet/endothelial cell adhesion molecule (PECAM1) genotypes increased the AROC to 0.72 (0.68–0.76) for a DR5 of 19.1% (P = 0.01 vs CRF combined with genotypes). Conclusions: For a modest panel of selected genotypes, CHD-risk estimates incorporating CRFs and genotype–risk factor interactions were more effective than risk estimates that used CRFs alone.

Coronary Heart Disease (CHD) Risk Factor Knowledge in a Rural Population

2008 ◽  
Vol 17 ◽  
pp. S205
Author(s):  
Heather Pascoe ◽  
John Kotroulas ◽  
Alan Soward
Keyword(s):  
Coronary Heart Disease ◽  
Risk Factor ◽  
Heart Disease ◽  
Rural Population ◽  
Chd Risk

scholarly journals PETANDA KEBAHAYAAN (RISIKO) PENYAKIT JANTUNG KORONER TERKAIT LDL

2018 ◽  
Vol 14 (3) ◽  
pp. 102
Author(s):  
Adi Priyana .
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Density Lipoprotein ◽  
Control Group ◽  
Risk Marker ◽  
Conventional Risk Factor ◽  
Small Dense Ldl ◽  
Chd Risk ◽  
Chd Risk Factors ◽  
And Control

Atherosclerosis is the most common cause of coronary heart disease (CHD), and it is still the primary cause of death in Indonesia and most industrialized countries. The conventional risk factor for atherosclerosis and CHD are diabetes mellitus, hypertension, dyslipidemiaand smoking. On the other hand, Lp (a), homocystein and small dense LDL (sd-LDL) have been considered as novel risk factors for CHDLow of high density lipoprotein (HDL), high of low density cholesterol (LDL-c) and high homocystein as part of dyslipidemia, has beenconsidered as independent risk factor for CHD.The principal objective of the present study was to compare between HDL-c, Lp (a), andsd-LDL and homocystein as a risk marker of CHD. The study subject were divided into two groups, risk group consist of 94 subjects whohad > 2 CHD risk factors and control group recruited 49 subject who had no CHD risk factors. Both groups had fasted for 10-12 hourbefore their sera were collected. The sera were examined for HDL-c, Lp (a), sd-LDL and homocystein. Four alternative multivariate modelwere compared: sd-LDL, sd-LDL + HDL-c, sd-LDL, HDL-c + Lp (a) and sd-LDL, HDL-c + sd-LDL + Lp (a) + homocystein. Result of thistudy showed that the sd-LDL had the most significant and accurate as risk marker for CHD. Lp (a), HDL-c and homocystein were lessaccurate if used as risk marker for CHD compare with sd-LDL. Small dense LDL is an accurate risk marker for CHD. Further study musbe done using larger sample size of CHD subjects with similar age between risk and control groups.

Abstract P204: Coronary Heart Disease Risk Factors and Perceived Risk among Overweight and Obese Adults

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Christopher C Imes ◽  
Meghan Mattos ◽  
Yaguang Zheng ◽  
Lei Ye ◽  
Edvin Music ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Heart Disease ◽  
Weight Loss ◽  
Risk Factor ◽  
Heart Disease ◽  
Perceived Risk ◽  
Pearson Correlation ◽  
Obese Adults ◽  
Chd Risk ◽  
Chd Risk Factors

Background: Obesity is a known risk factor for coronary heart disease (CHD) and plays a role in other CHD risk factors including dyslipidemia, hypertension, and type 2 diabetes mellitus. With nearly two-thirds of the adult US population being overweight and obese, it is important to know how these individuals perceive their CHD risk. Objective: The purpose of this study was to examine the associations between self-reported CHD risk factors and perceived CHD risk among overweight and obese adults. Methods: Demographic data, CHD risk factors, and perceived lifetime CHD risk were collected via electronic surveys using REDCap, an Internet-based data capture tool, of overweight and obese adults enrolled in a Weight Loss Research Registry. CHD risk factors were assessed using an investigator-developed survey of self-reported diagnoses of hyperlipidemia, hypertension, and diabetes, family history of CHD, and current smoking status. A risk factor ranking was assigned to each participant ranging from 0 to 5, with one point given for each of the aforementioned risk factors. Perceived lifetime CHD risk was assessed using a visual analogue scale with a range of 0 (No Risk) to 100 (High Risk). Linear regression and Pearson Correlation were used to analyze the data. Results: The response rate was 44.7% (N = 151) from 338 eligible adults. Respondents were mostly female (91%), White (81.5%), 51.3±10.4 years old with 16.2±2.9 years of education, 65.6% had annual household incomes ≥ $50,000. Males reported a higher perceived risk compared to females (77.6±18.0 vs. 64.9 ±21.5, p=.03). There was no difference in perceived risk based on age, race, education, or income. The prevalence of reported risk factors in the sample was as follows: 49.6% (n=75) had at least one first degree-relative with CHD, 32.5% (n=49) had hypertension, 31.8% (n=48) had hyperlipidemia, 3.9% (n=6) had diabetes and 3.3% (n=5) reported currently smoking. Perceived CHD risk was associated with the number of CHD risk factors (p<.001). The mean perceived risk increased incrementally as the number of risk factors increased: 56.5±24.8 for 0 risk factors (n=46), 65.1±17.6 for 1 risk factor (n=53), 74.3±18.4 for 2 risk factors (n=30), 77.0±17.3 for 3 risk factors (n=19), and 79.7±20.5 for respondents (n=3) with 4 risk factors. No respondent reported 5 risk factors. Conclusions: In this sample, the number of self-reported CHD risk factor was associated with perceived CHD risk (r= .353, p<.001). Male respondents had a higher perceived risk compared to females (77.6±18.0 vs. 64.9±21.5); however, the percent of males in the Registry was significantly lower than females (9% vs. 91%) This might suggest that males may require a higher perceived risk before enrolling in a Registry for weight loss studies. For these respondents, awareness of CHD risk factors and their health implications could be a motivator for enrollment in the Registry.

Peripheral Blood Cytopenia and Subsequent Risk of Cardiovascular Disease and Mortality

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 5002-5002
Author(s):  
Radhika Gangaraju ◽  
Insu Koh ◽  
Marguerite R. Irvin ◽  
Leslie A. Lange ◽  
Damon E. Houghton ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Risk Factor ◽  
Mortality Risk ◽  
Peripheral Blood ◽  
Cvd Risk ◽  
Clonal Hematopoiesis ◽  
Chd Risk ◽  
Increased Risk ◽  
Cvd Mortality

INTRODUCTION: African-Americans (blacks) have higher risk of stroke and coronary heart disease (CHD) - collectively referred to here as cardiovascular disease (CVD), than Caucasian-Americans (whites). Though partly explained by traditional cardiovascular risk factors, half of the excess risk in blacks is not explained by known risk factors. Recent data suggest increased risk of CVD and mortality in individuals with clonal hematopoiesis, which often presents as cytopenia. Using peripheral blood cytopenia as a marker of clonal hematopoiesis, we examined the association between cytopenia and risk of CVD and mortality in blacks and whites. METHODS: The REasons for Geographic and Racial Differences in Stroke (REGARDS) cohort study enrolled 30,239 US black and white adults between 2003 and 2007 (41% black). Socio-demographics and medical history were obtained by telephone interview, and laboratory studies (including complete blood count [CBC]) and physical exam from an in-home visit at baseline. Participants or their proxies were contacted every 6 months to ascertain CVD events, hospitalizations or deaths, and medical records were reviewed to confirm these events. Cytopenia was defined using thresholds in Table 1 as presence of 2 or more of the following: i) hemoglobin in age-, sex-, and race-specific lowest 5th percentile; ii) white cell count in race-specific lowest 5th percentile; iii) platelet count in lowest 5th percentile, and iv) macrocytosis (MCV >98fL). Participants with pre-baseline history of stroke (for analyses including stroke or CVD mortality) or CHD (for analyses including CHD or CVD mortality) and those with missing CBC were excluded. Cox proportional hazards models were used to calculate hazard ratios (HRs) of incident CVD and mortality associated with cytopenia. Models adjusted for socio-demographics (Model 1), Framingham stroke or CHD risk factors (Model 2), and estimated glomerular filtration rate and C-reactive protein (Model 3) were used. Differences in the association of cytopenia with outcomes by race were tested using cross-product interaction terms, using a p of <0.1 for interaction. RESULTS: The study included 19,544 participants who were followed for a median of ~9 years. There were 798 (4.3% of those at risk) incident stroke cases and 727 (4.3%) incident CHD cases; 1033 (5.3%) died of CVD, and 3933 (20.1%) died of all-causes. Cytopenia was present in 378 (1.9%) participants, ranging from 0.9% to 3.5% in blacks, 1.4 to 3.9% in whites, 1.6 to 3.9% in men, and 0.9 to 1.8% in women, with increasing prevalence by age. There was no association between cytopenia and stroke or CHD risk in any model. However, cytopenia was associated with increased risk of all-cause mortality (HR=1.73, 95%CI: 1.34-2.22), and CVD mortality (HR=1.56, 95% CI: 1.11-2.19) in the extended risk factor Model 3 and also in CVD risk factor adjusted model (Model 2), with little evidence of confounding (Table 2). While the race by cytopenia interaction term was not significant in any model for incident CHD or mortality, the interaction for cytopenia by race for stroke was statistically significant (p-interaction=0.08) in Model 2. The HR of stroke for cytopenia in blacks was 0.86 (95%CI: 0.46-1.61), and for whites was 1.96 (95%CI: 1.0-3.82). CONCLUSION: In this large biracial cohort, cytopenia was associated with increased all-cause and CVD mortality. Cytopenia was a race-specific risk factor for stroke affecting white Americans but not black Americans. With growing knowledge on the role of clonal hematopoiesis in CVD risk and mortality, further work is needed to determine if our phenotype of cytopenia is accurate in classifying clonal hematopoiesis and for determining the mortality risk. Given these findings, assessing clonal hematopoiesis and outcomes related to clonal hematopoiesis in diverse populations is critical to understanding the interactions between somatic mutations in hematopoietic cells and CVD/mortality risk. Disclosures Safford: Amgen: Research Funding.

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