Search

Inflammatory illnesses, such as periodontitis and atherosclerotic coronary heart disease (ASCHD), trigger the production of pro-inflammatory mediators. The aim of this study was to assess the accuracy of using salivary interleukin-1β (IL-1β), interleukin-18 (IL-18), and gasdermin D (GSDMD) in discerning patients with periodontitis with and without ASCHD from healthy individuals, and to assess their correlation with clinical periodontal parameters and low-density lipoprotein (LDL) levels. The study involved 120 participants: 30 were healthy subjects (control group, C), 30 had generalized periodontitis (group P), 30 had ASCHD and clinically healthy periodontium (group AS-C), and 30 had ASCHD and generalized periodontitis (group AS-P). Saliva and blood samples were collected, and periodontal characteristics such as plaque index, bleeding on probing, probing pocket depth, and clinical attachment loss were examined. IL-1β, IL-18, and GSDMD levels from saliva were determined using ELISA. LDL levels were determined from the blood samples. Groups P, AS-C, and AS-P had higher levels of salivary IL-1β, IL-18, and GSDMD than group C. The receiver operating characteristic (ROC) curves of all biomarkers showed high diagnostic accuracy, with a significant positive correlation with the clinical parameters and LDL levels. The observed correlations between the studied pro-inflammatory mediators and disease severity suggest that these biomarkers could serve as indicators of disease progression in conditions such as periodontitis and ASCHD., Competing Interests: The authors declare no conflict of interest., (© 2024 by the authors.)

Numerous studies have established a link between gene variants within the inflammasome complex and the incidence of periodontitis and cardiovascular illness across various ethnic groups. This study investigated the association between PYCARD gene polymorphism and susceptibility to periodontal disease and coronary heart disease (CHD) and their correlation with clinical periodontal indices. A total of 120 participants were enrolled, categorized into four groups: 30 healthy controls (C), 30 patients with generalized periodontitis (P), 30 patients with atherosclerotic CHD but clinically healthy periodontium (AS-C), and 30 patients with both atherosclerotic CHD and generalized periodontitis (AS-P). We recorded demographic data, collected blood samples, and measured periodontal indices, including plaque index, clinical attachment loss, bleeding on probing, and pocket depth. The genomic variant of the PYCARD gene was analyzed using a conventional polymerase reaction. A significant prevalence of T and G allele mutations and a higher distribution of CT and TT genotypes in PYCARD C/T (rs8056505) and the AG genotype in PYCARD A/G (rs372507365) were observed in groups P, AS-P, and AS-C. These single nucleotide polymorphisms (SNPs) were also positively correlated with the severity of clinical periodontitis indices. Our findings suggest that the increased frequency of T and G alleles and the distribution of CT, TT, and AG genotypes in PYCARD SNPs are significantly associated with an elevated risk for periodontal disease and CHD. These SNPs may participate in the pathogenesis of these conditions. The study reinforces the potential role of these genetic markers as risk factors for both diseases in the Iraqi population., Competing Interests: The authors declare no conflict of interest., (© 2024 by the authors.)

• The southeast/south central region of the US is known as the "Stroke/Heart Attack Belt." • Little is known about EPA+DHA erythrocyte levels (Omega-3 Index) of people in this region. • We measured the Omega-3 Index in 2177 individuals participating in free health screens in 7 cities in this region. • Mean Omega-3 Index levels were 4.4%, which is lower than that of 2 comparator cohorts. • Low Omega-3 Index levels in this region correlates with a higher risk for disease. The Omega-3 Index (O3I; erythrocyte EPA+DHA as a percent of total fatty acids) is inversely related to risk for cardiovascular disease (CVD). The cardioprotective target O3I is 8%–12%. O3I levels in American regions with high CVD risk are poorly characterized. To determine the O3I in individuals participating in a Seafood Nutrition Partnership (SNP) survey in seven US cities in the CVD "belt." Fingerstick blood samples were analyzed for the O3I. The SNP cohort (n = 2177) had a mean (SD) O3I of 4.42% (1.12%). Only 1.2% were in the desirable range, whereas 42% had an undesirable (<4%) O3I. The mean (SD) O3I in a subset of 772 SNP subjects who were matched for age and sex with the Framingham study was 4.6% (1.2%) compared 5.3% (1.6%) in the Framingham cohort (p < 0.0001). Individuals in the CVD "belt" had relatively low O3I levels. Since in other settings, a low O3I is associated with increased risk for CVD, this may be one factor contributing to the higher risk for CVD in this region of the US. [ABSTRACT FROM AUTHOR]

Background: Previous studies suggested that vasomotor symptoms were associated with an increasing risk of coronary heart diseases (CHD) but not clear with menopausal symptoms other than vasomotor symptoms. Given the heterogeneity and interrelationship among menopausal symptoms, it is not easy to make causal inferences based on observational studies. We performed a Mendelian randomization (MR) to investigate the association of individual non-vasomotor menopausal symptoms and the risk of CHDs., Methods: A sample of 177,497 British women aged ≥51 years old (average age at menopause) without related cardiovascular diseases from the UK biobank is selected as our study population. Non-vasomotor menopausal symptoms, including anxiety, nervous, insomnia, urinary tract infection, fatigue, and vertigo, were selected as exposures based on the modified Kupperman index. Outcome variable is CHD., Results: In total, 54, 47, 24, 33, 22, and 81 instrumental variables were selected for anxiety, insomnia, fatigue, vertigo, urinary tract infection and nervous respectively. We conducted MR analyses of menopausal symptoms and CHD. Only insomnia symptoms increased the lifetime risk of CHD with OR 1.394 (p = 0.0003). There were no significant causal relationships with CHD and other menopausal symptoms. Insomnia near menopause age (45-50 years) does not increase the risk of CHD. However, postmenopausal (over 51) insomnia increases the risk of CHD., Conclusion: MR analyses support that among non-vasomotor menopausal symptoms, only insomnia symptoms may increase the lifetime risk of CHD. Insomnia at different ages near menopause has differential impacts on CHD risk., Competing Interests: The authors declare no competing interests., (© 2023 The Authors. Published by Elsevier Ltd.)

Background: Although homeostasis of the cardiovascular system is regulated by the cerebral cortex via the autonomic nervous system, the role of abnormal brain functional connectivity (FC) networks in patients with cardiac dysfunction remains unclear. Here, we report thalamus-based FC alterations and their relationship with clinical characteristics in patients with coronary heart disease (CHD)., Methods: We employed resting-state functional magnetic resonance imaging (rs-fMRI) to acquire imaging data in twenty-six patients with CHD alongside sixteen healthy controls (HCs). Next, we performed a thalamus-based FC analysis to profile abnormal FC patterns in the whole brain. Subsequently, the mean time series of the brain regions that survived in the FC analysis were used to determine correlations with clinical parameters in patients with CHD., Results: We found no statistically significant differences in demographic and clinical data between patients with CHD and HCs. Patients with CHD showed decreased FC patterns between bilateral thalami and left hemisphere, encompassing supplementary motor area, superior frontal gyrus, superior parietal gyrus, inferior parietal gyrus, middle cingulate cortex, lingual gyrus and calcarine sulcus., Conclusions: These findings not only have implications in clarifying the relationship between cerebral functional imbalance and cardiovascular system, but also provide valuable insights to guide future evaluation and management of cardiac autonomic regulation via the brain-heart axis., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 The Authors. Published by Elsevier Ltd.)

Stroke risk is currently estimated as part of the composite risk of cardiovascular disease (CVD). We investigated if composite-CVD risk prediction tools QRISK3 and Pooled Cohort Equations-PCE, derived from middle-aged adults, are as good as stroke-specific Framingham Stroke Risk Profile-FSRP and QStroke for capturing the true risk of stroke in older adults. External validation for 10y stroke outcomes was performed in men (60-79y) of the British Regional Heart Study. Discrimination and calibration were assessed in separate validation samples (FSRP n = 3762, QStroke n = 3376, QRISK3 n = 2669 and PCE n = 3047) with/without adjustment for competing risks. Sensitivity/specificity were examined using observed and clinically recommended thresholds. Performance of FSRP, QStroke and QRISK3 was further compared head-to-head in 2441 men free of a range of CVD, including across age-groups. Observed 10y risk (/1000PY) ranged from 6.8 (hard strokes) to 11 (strokes/transient ischemic attacks). All tools discriminated weakly, C-indices 0.63-0.66. FSRP and QStroke overestimated risk at higher predicted probabilities. QRISK3 and PCE showed reasonable calibration overall with minor mis-estimations across the risk range. Performance worsened on adjusting for competing non-stroke deaths. However, in men without CVD, QRISK3 displayed relatively better calibration for stroke events, even after adjustment for competing deaths, including in oldest men. All tools displayed similar sensitivity (63-73 %) and specificity (52-54 %) using observed risks as cut-offs. When QRISK3 and PCE were evaluated using thresholds for CVD prevention, sensitivity for stroke events was 99 %, with false positive rate 97 % suggesting existing intervention thresholds may need to be re-examined to reflect age-related stroke burden., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2022 The Author(s).)

Introduction: Oxidized LDL (oxLDL) is formed by the spontaneous reaction between aldehyde byproducts of lipid peroxidation and lysine residues of apolipoprotein B within LDL. Clinically, oxLDL is used as a marker of coronary artery disease and predictor of metabolic syndrome risk. Despite its popularity as a clinical marker, no systematic studies of oxLDL stability, in which serum or plasma has been pre-analytically exposed to an array of different time and temperature conditions, have been carried out., Objective: To systematically evaluate the stability of oxLDL in human serum samples exposed to thawed conditions (> -30 °C) for varying periods of time while monitoring a second protein/small molecule redox system as a positive control for non-enzymatic biomolecular activity., Methods: OxLDL was measured in serum samples, from 24 different humans, that had been pre-exposed to three different time courses at 23 °C, 4 °C and -20 °C using ELISA kits from Mercodia that employ the 4E6 mouse monoclonal antibody. A liquid chromatography/mass spectrometry-based marker of serum exposure to thawed conditions known as ΔS-Cys-Albumin was employed as a positive control., Results: OxLDL was stable in serum exposed to 23 °C for up to 48 h, 4 °C for 21 days, or -20 °C for 65 days. ΔS-Cys-Albumin changed dramatically during these time courses (p < 0.001)., Conclusions: OxLDL is remarkably stable ex vivo in human serum samples exposed to thawed conditions., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2022 THE AUTHORS.)

Background: We aimed to estimate the future burden of coronary heart disease (CHD) and stroke mortalities by sex and all 47 prefectures of Japan until 2040 while accounting for effects of age, period, and cohort and integrating them to be at the national level to account for regional differences among prefectures., Methods: We estimated future CHD and stroke mortality projections, developing Bayesian age-period-cohort (BAPC) models in population and the number of CHD and stroke by age, sex, and all 47 prefectures observed from 1995 to 2019; then applying these to official future population estimates until 2040. The present participants were all men and women aged over 30 years and were residents of Japan., Findings: In the BAPC models, the predicted number of national-level cardiovascular deaths from 2020 to 2040 would decrease (39,600 [95% credible interval: 32,200-47,900] to 36,200 [21,500-58,900] CHD deaths in men, and 27,400 [22,000-34,000] to 23,600 [12,700-43,800] in women; and 50,400 [41,900-60,200] to 40,800 [25,200-67,800] stroke deaths in men, and 52,200 [43,100-62,800] to 47,400 [26,800-87,200] in women)., Interpretation: After adjusting these factors, future CHD and stroke deaths will decline until 2040 at the national level and in most prefectures., Funding: This research was supported by the Intramural Research Fund of Cardiovascular Diseases of the National Cerebral and Cardiovascular Center (21-1-6, 21-6-8), JSPS KAKENHI Grant Number JP22K17821, and the Ministry of Health, Labour and Welfare Comprehensive Research on Life-Style Related (Diseases Cardiovascular Diseases and Diabetes Mellitus Program), Grant Number 22FA1015., Competing Interests: We have no conflicts of interest to declare., (© 2022 The Authors.)

Background: Contemporary prevalence, awareness, and control of severe hypercholesterolemia (SH) and familial hypercholesterolemia (FH) and the associated atherosclerotic cardiovascular disease risk in the US are unknown., Method: Using electronic health records, we assessed the burden of SH and FH in Olmsted County, Minnesota, US, between 2004 and 2015. We defined SH as low-density lipoprotein cholesterol (LDL-C) level ≥190 mg/dl without secondary causes of hypercholesterolemia and FH as a Dutch Lipid Clinic Network score ≥6. Controls were age- and sex-matched individuals with LDL-C level <190 mg/dl., Results: The age- and sex-adjusted point and period prevalence (age-recursive method) of SH was 4.44% and 8.95%, respectively; 1 in 21 had FH (∼1:233 adults), and 46.2% had a recorded diagnosis. Guideline recommended targets (LDL-C <100 mg/dl and <70 mg/dl in the primary and secondary prevention settings, respectively) were achieved in 33.1% and 21.2% of SH cases, with less women overall achieving the target than men (18.6% vs. 23.7%, p=0.022). After adjustment for conventional risk factors, the hazard ratio for incident coronary heart disease (CHD) in those with SH was 1.21 (1.05-1.39; p=0.010), in those with SH and a family history of CHD was 2.16 (1.57-2.96; p<0.001) and in those with FH was 4.61 (2.66-7.97; p<0.001). The association of SH with CHD was modified by age (p-interaction = 0.015), such that the risk was greater at younger ages., Conclusions: SH was prevalent and an independent risk factor for incident CHD. Awareness and control were low, highlighting a treatment gap (more prominent in women) that needs to be addressed., Competing Interests: We wish to confirm that there are no known conflicts of interest associated with this publication and there has been no significant financial support for this work that could have influenced its outcome. We confirm that the manuscript has been read and approved by all named authors and that there are no other persons who satisfied the criteria for authorship but are not listed. We further confirm that the order of authors listed in the manuscript has been approved by all of us. We further confirm that any aspect of the work covered in this manuscript that has involved either experimental animals or human patients has been conducted with the ethical approval of all relevant bodies and that such approvals are acknowledged within the manuscript., (© 2022 The Authors. Published by Elsevier B.V.)

Atherosclerotic cardiovascular disease (ASCVD) is epidemic throughout the world and is etiologic for such acute cardiovascular events as myocardial infarction, ischemic stroke, unstable angina, and death. ASCVD also impacts risk for dementia, chronic kidney disease peripheral arterial disease and mobility, impaired sexual response, and a host of other visceral impairments that adversely impact the quality and rate of progression of aging. The relationship between low-density lipoprotein cholesterol (LDL-C) and risk for ASCVD is one of the most highly established and investigated issues in the entirety of modern medicine. Elevated LDL-C is a necessary condition for atherogenesis induction. Basic scientific investigation, prospective longitudinal cohorts, and randomized clinical trials have all validated this association. Yet despite the enormous number of clinical trials which support the need for reducing the burden of atherogenic lipoprotein in blood, the percentage of high and very high-risk patients who achieve risk stratified LDL-C target reductions is low and has remained low for the last thirty years. Atherosclerosis is a preventable disease. As clinicians, the time has come for us to take primordial and primary prevention more serously. Despite a plethora of therapeutic approaches, the large majority of patients at risk for ASCVD are poorly or inadequately treated, leaving them vulnerable to disease progression, acute cardiovascular events, and poor aging due to loss of function in multiple visceral organs. Herein we discuss the need to greatly intensify efforts to reduce risk, decrease disease burden, and provide more comprehensive and earlier risk assessment to optimally prevent ASCVD and its complications. Evidence is presented to support that treatment should aim for far lower goals in cholesterol management, should take into account many more factors than commonly employed today and should begin significantly earlier in life., Competing Interests: Michael Makover: None. Michael Shapiro: Dr Shapiro has participated in the Scientific Advisory Boards for Amgen, Esperion, Novartis, and Novo Nordisk. Peter P. Toth: Dr. Toth is a member of the speakers bureau for Amarin, Amgen, Esperion, and Novo-Nordisk; he is a consultant to Amarin, Kowa, Merck, Novartis, and Resverlogix., (© 2022 The Authors. Published by Elsevier B.V.)

Background: The combined influence of traditional cardiovascular risk factors and socioeconomic status (SES) on premature CHD (<65 years) remains understudied., Methods: We used the National Health Interview Survey (NHIS) database (2012-2018) to examine the association of sociodemographic (income, education, insurance status) and cardiovascular risk profile (CRF: ranging from optimal (0-1 risk CV factor) to poor (≥4 risk CV factors)) with CHD in young (18- 44 years) and middle-aged (45-64 years) adults., Results: Among the 168,969 included adults (young: 46.6%), the prevalence of CHD was 3%, translating to 6.4 million young and middle-aged adults. Adults with low family income, lesser education and no insurance were more likely to have CHD. While majority of young adults (65%) had optimal CRF profile and only 4% had poor CRF profile, 26% of middle-aged adults carried poor CRF profile. When examined by income status, education, and insurance status, odds of CHD were increased with worsening CRF profile. In multivariate regressions, low income participants who had a poor CRF (reference: optimal CRF) had higher odds of CHD in both young (aOR: 9.12 [95% CI, 6.16-13.50]) and middle-aged adults (aOR: 8.22 [95% CI, 6.12-11.05]). Within participants with a high school education or lower, those with a poor CRF profile (reference: optimal CRF) had increased odds of CHD in young (aOR: 10.35 [95% CI, 6.66-16.11]) and middle-aged adults (aOR: 10.40 [95% CI, 7.91-13.66]). In the uninsured, those with a poor CRF profile (reference: optimal CRF) had an 8-9 fold increased odds of CHD in young (aOR: 7.65 [95% CI, 4.26-13.73]) and middle-aged adults (aOR: 9.34 [95% CI, 5.90-14.79])., Conclusions: In this national survey, individuals with poor CRF profile had higher odds of premature CHD than those with optimal profile, and burden of CHD increased with worsening of CRF profile., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2022 The Authors. Published by Elsevier B.V.)

Abstract: This study was designed to test the lipid-lowering and the antioxidative activities of green and black olive phenolic extracts. Wistar rats fed a standard laboratory diet or a cholesterol-rich diet for 16 weeks were used. The serum lipid levels, the malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) as well as that of catalase (CAT) were examined. The cholesterol-rich diet induced hypercholesterolemia that was manifested in the elevation of total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C). Administration of aqueous methanol and ethyl acetate extracts of green olives and ethyl acetate extract of black olives significantly lowered the serum levels of TC and LDL-C, while increasing the serum level of high density lipoprotein cholesterol (HDL-C). Furthermore, the content of MDA in liver, heart and kidney decreased significantly after oral administration of green and black olive extracts compared with those of rats fed a cholesterol-rich diet. In addition, olive extracts increased CAT and SOD activities in liver. These results suggested that the hypocholesterolemic effect of green and black olive extracts might be due to their abilities to lower serum cholesterol level as well as to slow down the lipid peroxidation process and to enhance the antioxidant enzyme activity. [Copyright &y& Elsevier]

The causal relation of total Homocysteine (tHcy) to coronary heart diseases (CHD) is unclear. In vitro studies suggest a proinflammatory effect. Among 32,826 women from the Nurses’ Health Study who provided blood samples in 1989–1990, 237 CHD events were documented during 8 years of follow-up. The cases (1:2) were matched to controls on age, smoking, and month of blood draw. Plasma tHcy was inversely associated with blood levels of folate (partial r = -0.3, P < 0.0001) and B12 (r = -0.2, P < 0.0001) and with dietary intake of folate (r = -0.1, P < 0.01) and B2 vitamin (r = -0.1, P = 0.01). tHcy was positively associated with soluble tumor necrosis receptor (sTNF-R) 1 and 2 (partial r = 0.2, P < 0.0001). In a multivariate model adjusted for age, smoking, BMI, parental history, hypertension, diabetes, postmenopausal hormone use, physical activity and alcohol intake, the relative risk of CHD between the extreme quartiles of tHcy was 1.66 (95% CI; 1.05–2.64, P trend = 0.02). The association was not appreciably attenuated after further adjustments for sTNF-R1, sTNF-R2, CRP, or Total Cholesterol:/HDL-c ratio. tHcy is an independent risk predictor of CHD and modestly associated with TNF-receptors. However, the inflammatory biomarkers measured could not explain its role in CHD. [Copyright &y& Elsevier]

Inflammation is a key feature of atherosclerosis and its clinical manifestations. The leukocyte count is a marker of inflammation that is widely available in clinical practice. This paper reviews the available epidemiologic evidence for a relationship between the leukocyte count and coronary heart disease (CHD). Numerous epidemiologic and clinical studies have shown leukocytosis to be an independent predictor of future cardiovascular events, both in healthy individuals free of CHD at baseline and in patients with stable angina, unstable angina, or a history of myocardial infarction. This relationship has been observed in prospective and retrospective cohort studies, as well as in case-control studies. It is strong, consistent, temporal, dose-dependent, and biologically plausible. The relationship persists after adjustment for multiple CHD risk factors, including smoking. Elevated differential cell counts, including eosinophil, neutrophil, and monocyte counts, also predict the future incidence of CHD. Leukocytosis affects CHD through multiple pathologic mechanisms that mediate inflammation, cause proteolytic and oxidative damage to the endothelial cells, plug the microvasculature, induce hypercoagulability, and promote infarct expansion. In summary, leukocytosis has been consistently shown to be an independent risk factor and prognostic indicator of future cardiovascular outcomes, regardless of disease status. The leukocyte count is inexpensive, reliable, easy to interpret, and ordered routinely in inpatient and outpatient settings. However, its diagnostic and prognostic utility in CHD is widely unappreciated. Further studies are needed to assess the true impact of leukocytosis on CHD, compare it with other inflammatory markers such as C-reactive protein and lipoprotein phospholipase A2 levels, and promote its use in CHD prediction. [Copyright &y& Elsevier]

This study sought to determine if an aggressive, focused low-density lipoprotein cholesterol (LDL-C)-lowering strategy was superior to usual care for coronary heart disease (CHD) patients enrolled in health maintenance organization or Veterans Administration settings.Statin therapy benefits are well established. No prospective, randomized studies have tested strategies to optimize these benefits in a “real-world” setting.A total of 2,442 CHD patients with hyperlipidemia were randomized to either an aggressive treatment arm using atorvastatin or usual care and followed for 51.5 months on average. Atorvastatin-group patients were titrated to LDL-C goals of <80 mg/dl (2.1 mmol/l) or a maximum atorvastatin dose of 80 mg/day. Usual-care patients received any treatment deemed appropriate by their regular physicians. End point assessments were complete in 958 atorvastatin-group and 941 usual-care patients. Partial assessments occurred in 259 patients in the atorvastatin group and 284 patients in the usual care group who did not complete four years of study participation because of adverse events, withdrawn consent, or follow-up loss. The primary efficacy parameter was time to first cardiovascular event.A total of 289 (23.7%) patients in the atorvastatin group compared with 333 (27.7%) patients in the usual care group experienced a primary outcome (hazard ratio, 0.83; 95% confidence interval 0.71 to 0.97, p = 0.02). This reduction in morbidity was largely due to fewer non-fatal myocardial infarctions (4.3% vs. 7.7%, p = 0.0002). Levels of LDL-C were reduced more (34.3% vs. 23.3%, p < 0.0001) and National Cholesterol Education Program goals (LDL-C <100 mg/dl) more likely met at end-of-study visits (72.4% vs. 40.0%) in patients receiving atorvastatin compared with those receiving usual care.An aggressive, focused statin therapy management strategy outperformed usual care in health maintenance organization and Veterans Administration clinic patients with CHD. [Copyright &y& Elsevier]

The oxidation of low-density lipoprotein (LDL) is centrally involved in the initiation and progression of atherosclerosis. High-density lipoprotein (HDL) paraoxonase 1 (PON1) retards the oxidation of LDL and is a major antiatherosclerotic component of HDL. The PON1 gene contains a number of functional polymorphisms in both the coding and the promoter regions, which affect either the level or the substrate specificity of PON1. Genetic case–control and prospective studies conducted to date have produced confusing results. Meta-analysis of these studies indicates no simple relationship between the PON1 polymorphisms and the presence of coronary heart disease (CHD). However, at the present moment in time, it seems that PON1 status, i.e., activity and/or concentration, is more closely related to CHD, and indeed, PON1 has shown to be an independent risk factor for CHD in a prospective study, compared to the genetic polymorphisms. PON1 levels can also be modulated by environmental\lifestyle and possibly pharmaceutical factors. Larger, better designed, preferably prospective studies are needed to determine further the association of PON1 genetic polymorphisms and status with CHD. [Copyright &y& Elsevier]

We sought to compare the prevalence of coronary atherosclerosis in a cohort of middle-age African American (black) and non-Hispanic Caucasian (white) men and women from a population-based probability sample.Blacks have a higher mortality from coronary heart disease (CHD) than whites, particularly among younger individuals, and yet several studies have reported that coronary atherosclerosis is less prevalent in blacks than in whites. Data from population-based samples comparing coronary atherosclerotic burden between blacks and whites are limited.The prevalence of coronary atherosclerosis in middle-aged blacks and whites was determined using coronary calcium measured by electron beam computed tomography in 1,289 men and women from a population-based probability sample from Dallas, Texas.The population estimates of the frequency of a positive scan for coronary artery calcium were not statistically different between black and white men (37% vs. 41%, p = 0.36) or between black and white women (29% vs. 23%, p = 0.21). Although the prevalence of most of the coronary risk factors varied significantly between blacks and whites, mean Framingham coronary risk factor scores were identical in black and white men (10 ± 4) but significantly higher in black women (13 ± 4) than in white women (12 ± 4).Blacks in the general population have a prevalence of coronary atherosclerosis similar to whites. Factors other than coronary atherosclerotic burden, which are not reflected in the Framingham risk score, contribute significantly to the higher CHD mortality rate in blacks. [Copyright &y& Elsevier]

The aim of this study was to examine participation in cardiac rehabilitation after myocardial infarction (MI) by age and gender and the association of participation with survival.Lesser participation in cardiac rehabilitation has been reported for women and the elderly.All incident MIs in Olmsted County were validated. Baseline characteristics and outcomes were ascertained from the medical record. Logistic regression examined the association between participation, age, and gender. Propensity scores were used to examine the association between participation and outcome.Among 1,821 persons with incident MI (58% men, 46% age >70 years), 55% participated in cardiac rehabilitation. Participants were more likely to be men, younger, and have fewer comorbidities (p < 0.01 for all comparisons). After adjustment, women were 55% less likely to participate than men (odds ratio [OR] 0.45, 95% confidence interval [CI] 0.34 to 0.60), and persons 70 years or older were 77% less likely to participate than persons younger than 60 (OR 0.23, 95% CI 0.16 to 0.33). Participants had a lower risk of death and recurrent MI at three years (p < 0.001 and p = 0.049, respectively). The survival benefit associated with participation was stronger in more recent years (relative risk [RR] for 1998 vs. 1982 0.28, 95% CI 0.18 to 0.43; RR for 1990 vs. 1982 0.41, 95% CI 0.33 to 0.52).Approximately half of the patients participated in cardiac rehabilitation after MI. Participation did not increase over time. Women and elderly persons were less likely to participate, independently of other characteristics. Participation in rehabilitation was independently associated with decreased mortality and recurrent MI, and its protective effect was stronger in more recent years. [Copyright &y& Elsevier]

The purpose of this double clinical study was (1) to evaluate the effect of one single intake (300 ml) of red wine (RW) on the plasma antioxidant capacity (pAOC) and plasma phenolics over the 24-h time period following the intake, and (2) to compare the long-term effects of daily intakes (250 ml/d) of RW, white wine (WW) and Champagne (CH) on the plasma and LDL characteristics of healthy sujects. In the first part, blood samples were collected just before and after wine consumption. In the second part, subjects received the 3 types of wine successively, only at the mealtime, over 3-week periods separated by a 3-week wash out. Blood samples were drawn in fasting condition before and after each 3-week wine consumption period. The peak of pAOC was at 3-4 h following the single intake of RW, that of catechin was at 4 h (0.13 μmol/l) and that of gallic acid and caffeic acid was earlier (≤1.5 and 0.3 μmol/l, respectively). In plasma, the major form of gallic acid was 4- O -methylated, but a minor form (the 3- O -methyl derivative) appeared. In the long term study, no wine was able to change LDL oxidizability, but some other parameters were modified specifically: RW decreased pAOC (without changing TBARS and uric acid plasma levels), LDL lipids and total cholesterol (TC), and increased plasma apoA1, whereas CH increased plasma vitamin A. The beneficial effect of RW seems to mainly be explained by its action on lipid and lipoprotein constants, and not by its antioxidant one. [ABSTRACT FROM AUTHOR]

Objective: This research examined hemodynamic processes in cardiovascular reactivity (CVR) as a function of task, ethnicity and trait hostility. Method: One hundred and fourteen male patrol officers from the Singapore Police Force participated in this experimental study. Trait hostility was measured using the interpersonal hostility assessment technique to derive a hostile behavior index (HBI). Heart rate, blood pressure and hemodynamic measures were taken while participants performed three tasks: mental arithmetic, number reading and anger recall (AR). Results: AR elicited the greatest blood pressure, vascular and cardiac output reactivity. HBI scores were positively related to systolic blood pressure reactivity during AR for Malays whereas this was not true for Indians and Chinese. Across tasks Indians with high HBI scores appeared to be cardiac reactors whereas the reactivity patterns for Malays and Chinese were undifferentiated. Self-report of negative mood was not related to CVR. Conclusion: These results are consistent with the higher rates of coronary heart disease deaths among Indians as well as the higher rates for hypertension among Malays in Singapore. [Copyright &y& Elsevier]

The concentration of high density lipoprotein-cholesterol (HDL-C) has been found consistently to be a powerful negative predictor of premature coronary heart disease (CHD) in human prospective population studies. There is also circumstantial evidence from human intervention studies and direct evidence from animal intervention studies that HDLs protect against the development of atherosclerosis. HDLs have several documented functions, although the precise mechanism by which they prevent atherosclerosis remains uncertain. Nor is it known whether the cardioprotective properties of HDL are specific to one or more of the many HDL subpopulations that comprise the HDL fraction in human plasma. Several lifestyle and pharmacological interventions have the capacity to raise the level of HDL-C, although it is not known whether all are equally protective. Indeed, despite the large body of information identifying HDLs as potential therapeutic targets for the prevention of atherosclerosis, there remain many unanswered questions that must be addressed as a matter of urgency before embarking wholesale on HDL-C-raising therapies as strategies to prevent CHD. This review summarises what is known and highlights what we still need to know. [Copyright &y& Elsevier]

This population-based cross-sectional study in South London looks at the total homocysteine (tHcy) levels in groups of different ethnic background and the possible role of environmental factors and the 677C→T genetic polymorphism of the methylenetetrahydrofolate reductase (MTHFR). Fasting plasma tHcy was measured in 1392 men and women, age 40–59 years; 475 were white, 465 of African origin (of whom 180 were West Africans and 280 Caribbeans) and 452 South Asian (of whom 222 were Hindus and 167 Muslims). The homozygous MTHFR TT variant had observed frequencies of 0.10 in whites, 0.01 in people of African origin and 0.02 in South Asians (P<0.001). tHcy levels were 16% (95% CI 8–26) higher amongst TT than CC. tHcy levels were 25% (21–29) higher in men than women. Levels were significantly higher in South Asians than whites (8% [3–13]). Vegetarians had higher levels than non-vegetarians (25% [18–33]). These differences were present after adjustments for age, sex, smoking, body mass index (BMI), MTHFR 677C→T polymorphism and socio-economic status. Compared with whites (10.0 [9.7–10.3] μmol/l), and allowing for confounders, Hindus had significantly higher levels of tHcy (12.1 [11.6–12.6] μmol/l). This difference was attenuated by the inclusion of vegetarianism in the model (11.3 [10.8–11.9] μmol/l). In contrast Muslims had similar tHcy levels to whites while both West Africans and Caribbeans had slightly lower levels, though differences were not significant. The reported higher levels of tHcy in South Asians are due to high levels amongst Hindus only. They are in part accounted for by their vegetarianism. These differences in tHcy are large enough to be important contributors to the risk of vascular disease and may be preventable by simple targeted population strategies. [Copyright &y& Elsevier]

We evaluated a 69-year-old Japanese woman with apolipoprotein (apo) A-I deficiency, high levels of low-density lipoprotein (LDL)-cholesterol, hypertension and impaired glucose tolerance. The patient had corneal opacity, but neither xanthomas, xanthelasma, nor tonsillar hypertrophy. She was not symptomatic for coronary heart disease (CHD), and had normal electrocardiograms at rest and exercise using a cycle ergometer. She had severely reduced levels of high-density lipoprotein (HDL)-cholesterol (0.10–0.18 mmol/l) and no apo A-I (<0.6 mg/dl). LDL-cholesterol and apo B as well as apo E were increased even under treatment with 10 mg pravastatin per day. Gel filtration chromatography revealed that in addition to VLDL and LDL fractions, she had apo A-II rich and apo E rich fractions, which were present in the HDL fraction separated by ultracentrifugation. A cytosine deletion was identified by genomic DNA sequencing of the apo A-I gene of the patient at the third base of codon 184 in the fourth exon, which led to a frame shift mutation and early termination at codon 200. This patient is the oldest among those with apo A-I deficiency reported in the literature, and she had no symptoms of CHD despite the accumulated risk for the disease. [Copyright &y& Elsevier]

There is accumulating evidence for a role of tumor necrosis factor-α (TNF-α) in insulin resistance induced by obesity. The purpose of this study was to investigate whether the TNFα/G-308A polymorphism was associated with responses to oral glucose and fat tolerance tests in a case–control study comparing male offspring with a paternal history of premature myocardial infarction (cases, n=335) to age-matched controls (n=340) recruited from 14 European university populations. Genotype frequencies did not significantly differ between cases and controls. Among cases, those carrying the A allele exhibited a higher area under the curve for insulin (64.5 vs 55.9 mU h/l, P=0.009), a higher increment between baseline concentration and peak of insulin (63.1 vs 52.8 mU/l, P=0.005) and a greater decrease between peak and insulin at 120 min (49.1 vs 36.8 mU/l, P=0.003) than those with the GG genotype. No such effect was observed in control subjects. No association was observed with response to a fat tolerance test either in cases or in controls. The present results suggest that the TNFα/G-308A polymorphism might interact with other susceptibility factors to coronary heart disease to predispose to insulin resistance, and that the ability of TNF-α to induce insulin resistance may extend beyond obesity. [Copyright &y& Elsevier]

This review considers the antiatherogenic function of high density lipoprotein (HDL) from the point of view of its dynamics within the sequential steps of reverse cholesterol transport (RCT). It is postulated that the efficiency of cholesterol flux through the RCT pathways is clinically more relevant than the HDL cholesterol concentration. The particular role of preβ1-HDL is reviewed drawing attention to the relationship between its concentration and the flux of cholesterol through the RCT system. [Copyright &y& Elsevier]

The inverse correlation between serum levels of high density lipoprotein (HDL) cholesterol and the risk of coronary heart disease, the protection of susceptible animals from atherosclerosis by transgenic manipulation of HDL metabolism, and several potentially anti-atherogenic in vitro-properties have made HDL metabolism an interesting target for pharmacological intervention in atheroslcerosis. We have previously reviewed the concept of reverse cholesterol transport, which describes both the metabolism and the classic anti-atherogenic function of HDL (Arterioscler. Thromb. Vasc. Biol. 20 2001 13). We here summarize the current understanding of additional biological, potentially anti-atherogenic properties of HDL. HDL inhibits the chemotaxis of monocytes, the adhesion of leukocytes to the endothelium, endothelial dysfunction and apoptosis, LDL oxidation, complement activation, platelet activation and factor X activation but also stimulates the proliferation of endothelial cells and smooth muscle cells, the synthesis of prostacyclin and natriuretic peptide C in endothelial cells, and the activation of proteins C and S. These anti-inflammatory, anti-oxidative, anti-aggregatory, anti-coagulant, and pro-fibrinolytic activities are exerted by different components of HDL, namley apolipoproteins, enzymes, and even specific phospholipids. This complexity further emphasizes that changes in the functionality of HDL rather than changes of plasma HDL-cholesterol levels determine the anti-atherogenicity of therapeutic alterations of HDL metabolism. [Copyright &y& Elsevier]

We studied the value of serum amyloid A (SAA), a first-class acute-phase protein, as a marker for coronary heart disease (CHD) in a middle-aged male population. In a working population of 16 307 men (age, 35–59 years), 446 cases had a history of CHD or prominent Q:QS waves on electrocardiogram. For each case, two matched controls were investigated. SAA, measured by immunonephelometry, was correlated with other acute-phase proteins, cardiovascular risk factors, and infectious serology markers. SAA concentrations were significantly higher in the cases than in controls (P<0.05) and correlated with serum C-reactive protein (CRP) (r=0.61), plasma fibrinogen (r=0.39), serum haptoglobin (r=0.26), and body mass index (r=0.13) (P<0.001). Serum CRP is a better marker for CHD than SAA, which showed discriminative power only in a univariate model comparing highest versus lowest tertile (odds ratio, 1.39; 95% confidence interval, 1.03–1.87). Neither SAA nor other acute-phase proteins correlated with Chlamydia pneumoniae immunoglobulin (Ig)G, Helicobacter pylori IgG and IgA, and cytomegalovirus IgG. In conclusion, although SAA has a discriminative value for CHD, serum CRP is to be preferred as a first-class acute-phase reactant for detection of the disease. [Copyright &y& Elsevier]