Increase In Coronary Heart Disease Research Articles

Blood oxidative stress in taiwan workers exposed to carbon disulfide

Overexposure to carbon disulfide (CS(2) ) has been associated with an increase in coronary heart disease, but the mechanisms mediating this effect remain unclear. We aimed to examine the relationship between CS(2) exposure and oxidative stress markers, in order to clarify the oxidative mechanisms involved in CS(2) -induced atherosclerosis. A total of 89 workers from a viscose rayon plant were recruited for this study, and 111 workers not exposed to CS(2) served as controls. Cholesterol, triglyceride, malondialdehyde (MDA), superoxide dismutase (SOD), catalase, GSH peroxidase, as well as total antioxidants were analyzed. The workers exposed to CS(2) had significantly higher MDA levels and lower SOD levels than the controls. The average MDA levels were 776 ± 268.2 (240-1,220) in the high exposure (≥10 ppm; n = 38), 751.6 ± 274 (170-1,320) in the low exposure (<10 ppm; n = 51), and 550.4 ± 199 (115-1,050) mM in the control group (n = 111). The average SOD levels were 36.5 ± 38.8 (0-223.5), 39.3 ± 38.8 (0-160), and 58.8 ± 60.8 (5.25, 400) U/ml in the high exposure-, low exposure-, and control group, respectively. MDA level increased significantly at a cumulative CS(2) exposure of over 60 ppm-years. Dyslipoproteinemia was borderline significantly associated with CS(2) exposure and MDA level. These results indicate that CS(2) exposure can induce oxidative stress as well as reduce the levels of antioxidative enzymes, and that a cumulative exposure level of 60 ppm-years may be a threshold value for the oxidative and the antioxidant response. Am. J. Ind. Med. 54:637-645, 2011. © 2011 Wiley-Liss, Inc.

Early-life sodium exposure unmasks susceptibility to stroke in hyperlipidemic, hypertensive heterozygous Tg25 rats transgenic for human cholesteryl ester transfer protein.

Early-life risk factor exposure increases aortic atherosclerosis and blood pressure in humans and animal models; however, limited insight has been gained as to end-organ complications. We investigated the effects of early-life Na exposure (0.23% versus 0.4% NaCl regular rat chow) on vascular disease outcomes using the inbred, transgenic [hCETP](25) Dahl salt-sensitive hypertensive rat model of male-predominant coronary atherosclerosis, Tg25. Rather than the expected increase in coronary heart disease, fetal 0.4% Na exposure (< or =2 g of Na per 2-kcal/d diet) induced adult-onset stroke in both sexes (ANOVA P<0.0001), with earlier stroke onset in Tg25 females. Analysis of later onset of 0.4% Na exposure resulted in decreased stroke risk and later stroke onset despite longer 0.4% Na exposure durations, which indicates increasing risk with earlier onset of 0.4% Na exposure. Histological analysis of stroke-positive rat brains revealed cerebral cortical hemorrhagic infarctions, microhemorrhages, neuronal ischemia, and microvascular injury. Ex vivo MRI of stroke-positive rat brains detected cerebral hemorrhages, microhemorrhages, and ischemia with middle cerebral artery distribution and cerebellar noninvolvement. Ultrasound microimaging detected carotid artery disease. Prestroke analysis detected neuronal ischemia and decreased mass of isolated cerebral but not cerebellar microvessels. Early-life Na exposure exacerbated hypertension and unmasked stroke susceptibility, with greater female vulnerability in hypertensive, hyperlipidemic Tg25 rats. The reproducible modeling in stroke-prone Tg25 rats of carotid artery disease, cerebral hemorrhagic infarctions, neuronal ischemia, microhemorrhages, and microvascular alterations suggests a pathogenic spectrum with causal interrelationships. This "mixed-stroke" spectrum could represent paradigms of ischemic-hemorrhagic transformation and/or a microangiopathic basis for the association of ischemic lesions, microhemorrhages, and strokes in humans. Together, the data reveal early-life Na exposure to be a significant modifier of hypertension and stroke disease course and hence a potentially modifiable prevention target that deserves systematic study.

Heart Disease in Asia

People desirous of knowing the diversities of the races of mankind, as well as the diversities of regions of all parts of the East, read through this book and you will find in it the greatest and most marvelous characteristics of the people … From the Prologue to The Travels of Marco Polo With the advent of an aging society, heart disease has become one of the most important health problems worldwide. Heart disease is estimated to increase continuously during the next few decades. In fact, the number of people ≥60 years of age is expected to double by 2025 and to triple by 2050 globally.1 The proportion of this aged population is likely to increase more in the Asian-Pacific region; thus, half of the world’s cardiovascular burden is predicted to occur in this area.2 Increases in levels of risk factors, in particular total cholesterol and blood pressure, appear to account for a substantial amount of the age-related increase in coronary heart disease. This themed issue highlights the perspective for the contributions of risk factors to the excess coronary heart disease mortality in populations of the Asia-Pacific region. Cardiovascular risk factors are traditionally derived from studies in whites. However, relationships between these traditional risk factors and cardiovascular disease may differ in Asian and Western societies. The ethnic differences in the association between diabetes mellitus and ischemic heart disease are noted even within Asian populations.3 In Asian countries, as a consequence of the economic developments, the prevalence of overweight and obesity is increasing, and more important, rates of diabetes are increasing even more quickly. In particular, a moderate increase in body mass index makes South Asians more prone to insulin resistance and related diseases.4 Thus, it has been suggested that lower cutoff points for body mass index …

Otsenka vliyaniya priverzhennosti rekomendatsiyampo profilaktike osteoporoza na mineral'nuyuplotnost' kostey predplech'ya i chastotu komorbidnoypatologii v lechenii osteoporoza

Aim: to assess compliance to osteoporosis (OP) prophylaxis recommendations and its influence on mineral bone density (BMD) and development of comorbid diseases in postmenopause. Methods: prospective cohort study included 404 postmenopausal women aged from 47 to 59 with OP risk factors. BMD was assessed by distant forearm X-ray absorptiometry. Comorbid diseases were registered. Compliance to recommendations was assessed by questionnaire.. Results. Group 1 consisted of 276 non-compliant women. Group 2 (128 persons) changed their lifestyle and consumed recommended amount of daily calcium and vitamin D. Group 1 demonstrated significant increase of coronary heart disease, chronic heart failure and a fraction of persons in whom BMD decreased during 2 years of survey(x2 = 6.986; P = 0.017).. Relative risk of arterial hypertension, coronary heart disease, chronic heart failure and glucose metabolism disorders significantly decreased in group 2. Comclusion: constant co-operation between doctors and patients is necessary to keep the patient compliant and to obtain clinically relevant results in OP prophylaxis.

Paroxetine-induced increase in LDL cholesterol levels

Paroxetine is widely prescribed because it has the indication for multiple psychiatric disorders. Our objective was to assess the effect of short-term administration of paroxetine on low-density lipoprotein cholesterol (LDL-C) levels in both healthy controls (HCs) and in patients with panic disorder (PD). Blood samples for measurement of LDL-C were collected atbaseline, after 8 weeks of paroxetine administration and post-discontinuation in 24 male HCs and nine male patients suffering from PD, for a total of 33 subjects. Paroxetine treatment, both in HCs and PD patients, induced a mean 9% increase per subject in LDL-C that normalized post-discontinuation, suggesting causality. The National Cholesterol Education Program (NCEP) guidelines suggest that this paroxetine-induced increase in LDL-C is clinically significant but would not warrant therapeutic intervention in this population selected to be at low cardiovascular risk. However, the increase in LDL-C levels raised above the threshold of 2.7 mmol/L (100 mg/dL) in 36% of our low-risk subjects. The LDL-C increase in this subgroup would be associated with a minor increase in coronary heart disease (CHD) risk. A similar 9% paroxetine-induced increase in LDL-C observed in the large number of psychiatric patients suffering from comorbid established CHD would be detrimental from a cardiovascular perspective and would oppose the new NCEP therapeutic goals of decreasing LDL-C levels by 30-40% in high and moderately high-risk patients. It is possible that longer treatment duration and use of higher doses of paroxetine would lead to a greater increase in LDL-C.

Long-term consequences of polycystic ovary syndrome on cardiovascular risk

Most available data suggest that the prevalence of cardiovascular diseases in women with polycystic ovary syndrome (PCOS) is smaller than expected based on risk calculations during fertile years; therefore, more studies are needed on long-term cardiovascular consequences. Evidence is accumulating that postmenopausal women with PCOS have an increased risk of cerebrovascular events and cardiovascular morbidity. These events are partially related to persisting hyperandrogenism but are mostly correlated with excessive body weight (mainly visceral obesity); this suggests that our best long-term strategy is to ensure that women with PCOS are informed about their high risk for metabolic and cardiovascular diseases.

Acetaldehyde stimulates monocyte adhesion in a P-selectin- and TNFα-dependent manner

Objective The aim of this study was to determine the effects of acetaldehyde on various steps of the monocyte recruitment cascade. Methods Human umbilical venous endothelial cells (HUVEC), primary blood monocytes (PBM) and THP-1 monocytes, were treated with acetaldehyde (0.1–0 μM) for 6 h. Monocyte adherence experiments were performed using 2′,7′-bis(2-carboxyethyl)-5,6-carboxyfluorescein-acetoxymethylester labeled PBM or 3H-thymidine labeled THP-1 cells. HUVEC TNFα mRNA and protein levels were determined by quantitative real-time PCR and immunoassay, respectively, and HUVEC P-selectin and monocyte CCR2 expression were determined by FACS analysis. Results Acetaldehyde dose-dependently increased the number of CCR2 positive THP-1 monocytes, with a maximal increase of ∼50% observed in the presence of 10 μM acetaldehyde. There was a significant increase in both the number of P-selectin positive cells and P-selectin receptor density when HUVEC were incubated with acetaldehyde. HUVEC TNFα mRNA expression and secretion were enhanced by acetaldehyde. Moreover, acetaldehyde increased THP-1 and PBM adhesion to HUVEC. Inhibition of P-selectin or TNFα, using antibodies or siRNA-directed gene knockdown, attenuated acetaldehyde-induced monocyte adhesion. In conclusion, acetaldehyde increased the number of CCR2 positive monocytes and stimulated endothelial cell P-selectin and TNFα expression. Moreover, acetaldehyde increased monocyte adhesion to endothelial cells, an effect that was both P-selectin- and TNFα-dependent. Conclusion These effects of acetaldehyde may contribute, in part, to the increase in coronary heart disease that is associated with binge patterns of alcohol consumption.

Impact of elevated serum lipoprotein (a) concentrations on the risk of coronary heart disease in patients with type 2 diabetes mellitus

Type 2 diabetes mellitus is associated with a marked increase of coronary heart disease (CHD). We aimed to assess the impact of elevated serum lipoprotein (a) (Lp[a]) concentrations on the risk of CHD in patients with type 2 diabetes mellitus. A consecutive series of 352 outpatients was investigated. We determined the serum lipid profile and checked the patients for a history of CHD and of its traditional risk factors. Furthermore, the patients were divided into 3 groups according to the degree of elevation of the serum Lp(a) concentration: serum Lp(a) concentrations greater than 50 mg/dL, between 30 and 50 mg/dL, and less than 30 mg/dL, a presumed high normal value; and the prevalence of CHD was compared among the 3 groups. The serum Lp(a) concentrations in the subjects varied widely from 0.4 to 163.6 mg/dL. Patients with CHD had significantly higher serum Lp(a) concentrations than those without CHD ( P = .0045). Logistic regression analysis to identify factors associated with the presence of CHD revealed that elevated serum Lp(a) is a significant risk factor ( P = .0246). The prevalence of CHD increased with increasing serum Lp(a) concentrations ( P = .048). Patients with serum Lp(a) concentrations greater than 50 mg/dL had a significantly higher prevalence of CHD than those with serum Lp(a) concentrations less than 30 mg/dL: the odds ratio of an elevated serum Lp(a) concentration was 3.346 ( P = .039). In conclusion, elevated serum Lp(a) is a significant risk factor; and the risk of CHD appears to increase with increasing serum Lp(a) concentrations. Serum Lp(a) concentration of 50 mg/dL might represent a threshold level in relation to the risk of CHD in patients with type 2 diabetes mellitus.

Cardiovascular Risk in Elderly Hypothyroid Patients

Overt hypothyroidism (OH) and subclinical hypothyroidism (SH) are frequently found in the elderly. OH is associated with several functional cardiovascular abnormalities and increased risk of atherosclerosis resulting from hypertension associated to atherogenic lipid profile. Other potential atherogenic factors involved in OH are increased circulating C-reactive protein and homocysteine, increased arterial stiffness, endothelial dysfunction, and altered coagulation parameters. Similar (although mild) cardiovascular abnormalities are present in SH. Since all these abnormalities regress with levothyroxine (L-T4) administration, the cardiovascular benefits of replacement therapy in OH are not questionable, independently from the patient's age or the presence of coexisting cardiovascular disease. On the other hand, in spite of a very large number of studies, no consensus has been reached so far about the actual cardiovascular and/or general health impact of SH, and different recommendations have been recently made about screening and treatment of this condition. Although divergent results have been obtained in several epidemiological studies, recent meta-analyses provide evidence for a slight but significant increase of coronary heart disease (CHD) risk in SH. However, no agreement has been reached in favor or against active screening and/or treatment of mild thyroid failure. Moreover, L-T4 therapy is discouraged in aged subjects, because the increased oxygen consumption consequent to thyroid hormone administration could be dangerous, especially in the presence of coexisting CHD. In keeping with this concept are recent data showing reduced mortality risk in untreated mild hypothyroid subjects aged >85 years, suggesting that some degree of decreased thyroid activity at the tissue level might have favorable effects in the oldest-old. However, the effects of subtle thyroid dysfunction may be different in different age ranges. Since the main studies supporting a role for SH as a risk factor for atherosclerosis, cardiovascular disease, and all-cause mortality have been carried out in populations aged > or =55-60 years, mild thyroid failure could concur to increased cardiovascular risk in middle-aged and "young elderly" subjects, while being devoid of detrimental effects and possibly protective in the oldest-old. Further studies are needed to confirm this hypothesis.

Less Subclinical Atherosclerosis in Japanese Men in Japan than in White Men in the United States in the Post-World War II Birth Cohort

Coronary heart disease incidence and mortality remain very low in Japan despite major dietary changes and increases in risk factors that should have resulted in a substantial increase in coronary heart disease rates (Japanese paradox). Primary genetic effects are unlikely, given the substantial increase in coronary heart disease in Japanese migrating to the United States. For men aged 40-49 years, levels of total cholesterol and blood pressure have been similar in Japan and the United States throughout their lifetimes. The authors tested the hypothesis that levels of subclinical atherosclerosis, coronary artery calcification, and intima-media thickness of the carotid artery in men aged 40-49 years are similar in Japan and the United States. They conducted a population-based study of 493 randomly selected men: 250 in Kusatsu City, Shiga, Japan, and 243 White men in Allegheny County, Pennsylvania, in 2002-2005. Compared with the Whites, the Japanese had a less favorable profile regarding many risk factors. The prevalence ratio for the presence of a coronary calcium score of > or =10 for the Japanese compared with the Whites was 0.52 (95% confidence interval: 0.35, 0.76). Mean intima-media thickness was significantly lower in the Japanese (0.616 mm (standard error, 0.005) vs. 0.672 (standard error, 0.005) mm, p < 0.01). Both associations remained significant after adjusting for risk factors. The findings warrant further investigations.

Explanation for the Japanese Paradox: Prevention of Increase in Coronary Heart Disease and Reduction in Stroke

Japan's age-adjusted rate for mortality from stroke increased after the Second World War until 1965 and then showed a significant decline until 1990; however, the age-adjusted rate for mortality from all heart disease and coronary heart disease (CHD) increased until 1970 and then declined slowly. A puzzling question is why the rate of mortality from CHD declined in spite of an increase in serum total cholesterol level following an increase in fat consumption. It was confirmed that CHD incidence was far lower in several Japanese populations compared to Western countries in the " Monitoring Trends and Determinants in Cardiovascular Disease " (MONICA) project; therefore, the lower CHD mortality in Japan stems from the lower CHD incidence. CHD risk factors based on epidemiologic cohort studies in Japan were no different from those of other industrialized countries: hypertension, hypercholesterolemia, smoking and diabetes mellitus (DM). So, how can we explain this phenomenon?There are three possible explanations. One is the decline in population blood pressure level and the prevalence of hypertension during the years 1965-1990; the second is the decline in smoking rate in men and women; the third is that the serum total cholesterol level for middle-aged and elderly populations remains 5-15 mg/dL lower than that of the US elderly counterpart, although men aged 40-49 in Japan and the US had similar serum total cholesterol levels. It was also noted that elderly people in Japan, as observed in the Seven Countries Study, had far lower serum total cholesterol levels in midlife, i.e., around 160 mg/dL in the 1960s. This was not the case for elderly in the US where a higher serum total cholesterol level was observed in midlife. In conclusion, the lower serum cholesterol level in the past of Japanese middle-aged and elderly people compared to Western counterparts helps to maintain the low CHD incidence and mortality supported by the declining trend in blood pressure level and smoking rate for both men and women.

Skin Autofluorescence Is a Strong Predictor of Cardiac Mortality in Diabetes

Advanced glycation end products (AGEs) are biomarkers of metabolic stress and are thought to contribute to the increase of coronary heart disease (CHD) in diabetes. Tissue autofluorescence is related to the accumulation of AGEs. The aim of the present study was to evaluate the relationship between skin autofluorescence and metabolic burden (hyperglycemia and hyperlipidemia) and its relationship with CHD and mortality. Skin autofluorescence was measured noninvasively with an autofluorescence reader in 48 type 1 and 69 type 2 diabetic patients and 43 control subjects. The presence of CHD was observed at baseline and mortality during a follow-up period of 5 years. Autofluorescence correlated with mean A1C, triglycerides, and LDL. Autofluorescence values further increased with age, microalbuminuria, dialysis treatment, and diabetes duration. Autofluorescence was strongly related to the presence of CHD (odds ratio 7.9) and predicted mortality (3.0). Multivariate analysis showed that autofluorescence was more strongly associated with CHD and mortality compared with A1C, triglycerides, and LDL. Skin autofluorescence is strongly related to cumulative metabolic burden. Skin autofluorescence seems strongly associated with cardiac mortality and may provide important clinical information for risk assessment.

Hormone Replacement Therapy: The Debate over the Risks and Benefits To Women, from Breast Cancer To Quality of Life

The use of hormone replacement therapy, unopposed estrogen or combined estrogen plus progestin, for postmenopausal women has been debated for many years. It has been used for relief from menopausal symptoms and for protective measures from chronic conditions, such as cardiovascular disease and osteoporosis. There have been observational studies and randomized clinical trials undertaken to determine the benefits and risks of these therapies. There are no definite answers among the trials and there are some discrepancies. The major findings, however, have been an increase in breast and endometrial or ovarian cancer, an increase in coronary heart disease, stroke and thromboembolism, a decrease in colorectal cancer, a decrease in bone fractures and an improvement in menopausal symptoms. The current, overall recommendation to women is not to use hormone replacement therapy as a long-term protective measure, but after individual consideration, it may be appropriate on a short-term basis for relief of menopausal symptoms.

Emerging Selective Estrogen Receptor Modulators

Menopause, regardless of age at onset, is associated with a marked increase in coronary heart disease (CHD) risk. On the basis of epidemiological studies that demonstrated mainly positive effects of postmenopausal hormone therapy on CHD as well as on risk markers of CHD, it has been suggested that CHD could be prevented in postmenopausal women with long-term hormone therapy. However, since the publications of the Heart and Estrogen/progestin Replacement Study and the Women's Health Initiative trial, prescription of hormone therapy for the prevention of CHD has become controversial. Major efforts have been made to identify alternatives for hormone therapy. Compounds suggested have included selective estrogen receptor modulators (SERMs), which represent a class with a growing number of compounds that act as either estrogen receptor agonists or antagonists in a tissue-specific manner. This pharmacological profile may offer the opportunity to dissociate favourable estrogenic effects on the bone and cardiovascular system from unfavourable stimulatory effects on the breast and endometrium. Two SERMs presently on the market are tamoxifen and raloxifene. The only data available regarding the effects of tamoxifen on cardiovascular events in postmenopausal women are from breast cancer trials. These trials found fewer fatal myocardial events in women randomly assigned to tamoxifen compared with women assigned to placebo. Raloxifene is a second-generation SERM that has been shown to prevent osteoporotic fractures, is safe for the endometrium and holds high promise for the prevention of breast cancer. The effect of raloxifene on CHD is still uncertain. On the basis of the MORE (Multiple Outcomes of Raloxifene Evaluation) trial, raloxifene may offer some protection to women with CHD or to those who are at high risk of CHD. Proof that raloxifene reduces the risk of CHD requires a clinical trial with hard clinical endpoints. Such a study is currently underway. Next-generation SERMs taken into clinical development include idoxifene, droloxifene, ospemifene, arzoxifene, acolbifene/EM-800, levormeloxifene, lasofoxifene, bazedoxifene and HMR 3339. The aim is to find a compound with the ideal profile, that is, alleviation of climacteric symptoms and prevention of osteoporotic fractures, but without an adverse effect on the breast and endometrium, and no negative effect or even a beneficial effect on the cardiovascular system and the brain. Currently, limited data are available with regard to these next-generation SERMs and CHD. Nevertheless, some of these novel agents provide arguments for continuing the search for an ideal SERM.

Estrogen Plus Progestin, Benefits and Risks: The “Women’s Health Initiative” Trials

The increase in coronary heart disease (CHD) in postmenopausal women continues unabated. Hormone replacement therapy given in an effort to contain this potentially fatal disease has had its successes and failures, but heretofore has not been fully evaluated. Hormone replacement therapy was first advocated in the 1940s for the treatment of menopausal symptoms. Subsequently several observational studies suggested cardiovascular benefits for women who were on hormone therapy. However no high risk clinical trials had been done until the early 1990s, when through the National Institutes of Health, 40 centers in the United States were recruited to enroll the largest number of postmenopausal women in a hormone study. The Women’s Health Initiative (WHI) was a large randomized placebo-controlled trial investigating the effects of estrogen plus progestin on specific potential long-term benefits versus risks. The Heart and Estrogen/progesterone Replacement Study (HERS), an “arm” of the WHI trial, was a randomly compared estrogen plus progestin trial given continuously to 16 000 women who were previously healthy and postmenopausal. A few women that were included in this “arm” had a history of coronary disease but had to have been asymptomatic for 6 months prior to enrollment. At the end of the study, there were no cardiovascular benefits and in fact, there was a significant increased risk in coronary events, primarily nonfatal myocardial infarctions, nearly 25% over 5+ years of follow-up. There was an increase in strokes, deep vein thrombosis, pulmonary emboli, and endometrial cancer. Breast cancer was a major risk after 4 years follow-up. An unusual finding was the increased requirement for gallbladder surgery. Two case presentations highlight key issues involved in hormone replacement therapy in women. Case 1

Diabetes issues in women and children: polycystic ovary syndrome.

At the American Diabetes Postgraduate Course in New York, NY, on 12 January 2003, a number of important topics relating women’s health and diabetes were reviewed. Andrea Dunaif, Chicago, IL, discussed the polycystic ovary syndrome (PCOS), pointing out its frequency in the population and association with type 2 diabetes. PCOS is associated with a 40% decrease in insulin sensitivity (1) and with evidence of relative β-cell dysfunction (2). PCOS is a major risk factor for type 2 diabetes in adolescents (3) and in premenopausal women (4), with ∼40% of individuals with PCOS developing impaired glucose tolerance (IGT) or type 2 diabetes, a rate similar to that seen among Pima Indians. Among women with oligomenorrhea (menses ≤6/year), 77% have PCOS and 33% (vs. 7.7% of control subjects) have glucose intolerance. Using menstrual cycle length ≥40 days as a proxy marker, the Nurses Health Study data showed a 2.18-fold increase in risk of diabetes among women with long cycles (5). The same dataset showed a menstrual cycle ≥40 days to be associated with a 1.53-fold increase in coronary heart disease (CHD) risk (6). Thus, the disease “has substantial health consequences” and represents an important target population for diabetes prevention. Dunaif humorously suggested that as PCOS represents an expression of the metabolic syndrome in women, it should be called “Syndrome XX.” The mechanisms of insulin resistance may include specific genetic abnormalities. Postbinding abnormality in insulin signaling can be shown, with abnormal autophosphorylation of the insulin receptor and of insulin receptor substrate (IRS)-1. Tyrosine phosphorylation is decreased and serine phosphorylation increased at both of these receptors, leading to a decrease in the metabolic actions of insulin. Dunaif noted that cytochrome P450c17 is involved in ovarian androgen synthesis and activated by a serine kinase that may play a role in the abnormal insulin receptor and …

Elevated triglyceride and decreased high density lipoprotein level in carbon disulfide workers in Taiwan.

Carbon disulfide (CS2) is a man-made product utilized primarily in the manufacture of viscose rayon. Overexposure to CS2 has been associated with an increase in coronary heart disease. The aims of this study were to examine the dose-response relationship of CS2 exposure and elevated lipid profile tests among CS2-exposed workers in Taiwan. A total of 132 workers were recruited from two viscose rayon plants. Air sampling was performed to determine the CS2 exposure of workers. Demographic data and work history were gathered by a standard self-administered questionnaire. Lipid profile tests were also performed by routine methods. The average CS2 exposure concentration was 50.6 +/- 25.6 ppm (range: 24-127 ppm) in the high-exposure group, 12.9 +/- 5 ppm (range: 5.2-22.3 ppm) in the mid-exposure group, and 3.5 +/- 1.2 ppm (range 0.97-5.2 ppm) in the low-exposure group. There were 21 out of 33 (63.7%) elevated triglyceride levels among high-CS2-exposure workers, 27 out of 64 (42.2%) among the middle-CS2-exposure, and 14 out of 35 (40%) among low-CS2-exposure workers, respectively. Compared to the low-CS2-exposure workers, the age- and weight-adjusted odds ratios (and 95% confidence intervals) of the prevalence of elevated triglyceride value were 1.12 (0.5, 2.7) for middle-CS2-exposure workers, and 2.81 (1.02, 7.8) for high-CS2-exposure workers. There was a significant linear trend between CS2 exposure and the prevalence of elevated triglyceride value (P = 0.046) after adjusting for other factors. There was also a lower prevalence of elevated HDL level in high-CS2-exposure workers than low-CS2-exposure workers (15.2% versus 31.4%). Compared to the low-CS2-exposure workers, the age- and weight-adjusted odds ratio (and 95% confidence intervals) of elevated HDL level were 0.34 (0.1, 1.18) for high-CS2-exposure workers, which was borderline significant. In conclusion, this study suggests that elevated triglyceride level and decreased HDL level are associated with CS2 exposure. The study also suggests that exposure to CS2 (concentration > 23.2 ppm, which was above the current TLV-TWA of 10 ppm) are significantly associated with increased risk and decreased protective effect for coronary heart disease.

Differences in dietary habits, serum fatty acid compositions and other coronary risk characteristics between freshmen and fourth-year male university students.

Westernization of lifestyles among Japanese, in particular among young generations, is a matter of concern for future increase in coronary heart disease. We surveyed a total of 349 male university students to examine changes in lifestyles and coronary risk factors in campus life. We compared dietary habits and serum fatty acid compositions as well as other coronary risk characteristics between freshmen (n=171) and fourth-year (senior) students (n=178). Serum fatty acid compositions and dietary intakes of selected foods as well as serum lipids, blood pressures and physical characteristics were examined at the 1996 and 1997 annual health examinations.Compared to freshmen, senior students had a lower frequency of fish, vegetable, milk and egg intake, and a higher frequency of oil and fat intake. The proportions of serum saturated and monounsaturated fatty acids were significantly higher among senior students than among freshmen, whereas the proportion of serum polyunsaturated fatty acids was significantly lower among senior students than among freshmen. Senior students also had higher systolic and diastolic blood pressures, percent body fat, smoking rate and alcohol usage than freshmen. Mean body weight and mean body mass index were not different between the two groups.Senior students generally showed Westernized dietary habits and higher coronary risk profiles than freshmen as indicated by the change of serum fatty acid compositions. Modification of these dietary habits and lifestyles may be important for the prevention of future CHD among Japanese young adults.

The prediabetic problem: Development of non-insulin-dependent diabetes mellitus and related abnormalities

Non-insulin-dependent diabetes mellitus (NIDDM) is associated with approximately two fold increase in coronary heart disease (CHD) in men and fourfold increase in CHD in women. In most studies, the duration of diabetes and severity of glycemia are only weakly related to CHD in NIDDM, suggesting that the prediabetic period may be important for the increased CHD in NIDDM subjects. Both hyperinsulinemia and/or insulin resistance predict the development of NIDDM. A number of studies have shown that increased cardiovascular risk factors (especially high triglyceride, blood pressure, and small dense low-density lipoprotein (LDL) and low high-density liproprotein (HDL) cholesterol) precede the onset of NIDDM. Recent data from the San Antonio Heart Study suggest that the atherogenic pattern of cardiovascular risk factors is more marked in prediabetic women than in prediabetic men, thus partially explaining the higher risk of CHD in prediabetic women than in prediabetic men. The atherogenic changes in cardiovascular risk factors appear to be mainly due to increased hyperinsulinemia and insulin resistance in nondiabetic subjects. Interventions to reduce cardiovascular disease in NIDDM subjects should emphasize the primary prevention of NIDDM and very aggressive treatment of traditional cardiovascular risk factors in prediabetic subjects. Treatment of hypertension and dyslipidemia in high-risk patients for NIDDM should avoid agents that further worsen insulin resistance (nicotinic acid, β blockers, and thiazides), as subjects with hypertension and dyslipidemia are already at increased risk of NIDDM.

Should heart attack patients return to stressful jobs?

A paper by Hlatky et al. which appeared in Circulation last August, has received considerable media attention, since it purported to show no relationship between high job stress levels and any increase in coronary heart disease. In a subsequent interview, Hlatky indicated that a major conclusion from the study was that heart attack patients could return to work without any risk. Another author suggested that 'people with a history of heart disease may benefit from working-even in a stressful environment.' I was asked to comment on this by a reporter from Medical Tribune, since most studies have shown a clear correlation between job stess, and coronary morbidity and mortality, as well as hypertension, which was not discussed. My main concern was that the end point was the degree of coronary atherosclerosis as assessed by coronary angiography, which is quite different than conventional clinical criteria. The assumption is made that this measurement is an accurate predictor of future coronary events, and several caveats should be considered. As the authors themselves concede, coronary angiography 'is an imperfect measure of coronary atherosclerosis'. There is also considerable interinterpreter disagreement, and even different conclusions when the identical angiogram is reviewed by the same individual months later. Coronary occlusion often occurs at sites quite different than those predicted by angiography. Many individuals who die from other causes may have severe coronary occlusive disease without ever having experienced angina or any other cardiac symptoms. It is possible to have a coronary occlusion without a myocardial infarction, myocardial necrosis without coronary obstruction, and sudden arrhythmic death without evidence of either. There are other possible methodological flaws based on demographics. This was a 90% white, upper level socioeconomic cohort, from a localized geographical area, studied at only one facility, and marital status was not considered. Job stress was evaluated at only one point in time, and was associated with the stress of hospitalization for angiography. This may have influenced responses based on prior experience with the use of questionnaires to rate Type A behavior in similar settings. Job strain was rated based on the high psychological demand-low decision making model utilized by Karasek and Theorell. It has subsequently been suggested that social support is another factor that should be considered. Since it is not clear that Hlatky et al. actually measured what they thought they were measuring, the results are inconsistent with prior studies, and the conclusions and recommendations are counterintuitive, I have invited the authors of Healthy Work, who developed the questionnaire that was utilized, to add their comments.